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Holdemania filiformis

2012-05-16T01:49:45Z

References:

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	[[File:Pept..jpg\|thumb\|400px\|right\|alt= \|Diagram of unique interpeptide bridge (boxed).<sup>2</sup>]]''H. filiformis'' is a [http://en.wikipedia.org/wiki/Gram_staining Gram positive-staining] bacterium that easily decolorizes. The [http://en.wikipedia.org/wiki/Cell_wall#Bacterial_cell_walls cell wall] contains a group B murein type (B1δ(L-Ala)-D-Glu-L-Asp-L-Lys) that has not been observed in any other bacterial species.<sup>1</sup> Colonies grown on [http://www.anaerobesystems.com/Home/pras-mono-plated-media/Brain-Heart-Infusion-Agar brain heart infusion agar] are 1.0 mm in diameter. They are circular, entire, low convex, and translucent with a granular appearance. PYT-glucose broth cultures were turbid and contained white sediment.<sup>2</sup>		[[File:Pept..jpg\|thumb\|400px\|right\|alt= \|Diagram of unique interpeptide bridge (boxed).<sup>2</sup>]]''H. filiformis'' is a [http://en.wikipedia.org/wiki/Gram_staining Gram positive-staining] bacterium that easily decolorizes. The [http://en.wikipedia.org/wiki/Cell_wall#Bacterial_cell_walls cell wall] contains a group B murein type (B1δ(L-Ala)-D-Glu-L-Asp-L-Lys) that has not been observed in any other bacterial species.<sup>1</sup> Colonies grown on [http://www.anaerobesystems.com/Home/pras-mono-plated-media/Brain-Heart-Infusion-Agar brain heart infusion agar] are 1.0 mm in diameter. They are circular, entire, low convex, and translucent with a granular appearance. PYT-glucose broth cultures were turbid and contained white sediment.<sup>2</sup>
	===Metabolism===		===Metabolism===
−	Strictly [http://en.wikipedia.org/wiki/Anaerobic_organism anaerobic].<sup>2</sup> It is [http://www.biology-online.org/dictionary/Saccharolytic saccharolytic]. Good growth was exhibited in PYT broth media containing esculin, fructose, glucose, salicin, or sucrose. Moderate growth can sometimes be observed in peptone-yeast extract broth with maltose or lactose. Minimal growth was seen in PYT broths with no carbohydrates or with amydalin, arabinose, cellobiose, erythritol, glycogen, inositol, mannitol, mannose, melzitose, melibiose, raffinose, rhamnose, ribose, sorbitol, starch, trehalose, or xylose. In PYT-glucose broth, the consistent end products of fermentation were acetic acid, lactic acid, and succinic acid.<sup>2</sup> Meat, gelatin, and milk are not digested or changed. Esculin is hydrolyzed; nitrate is not reduced; arginine is not deanimated; catalase and indole are not produced. It has been shown to grow in media ranging from a pH of 5.8 to 6.5 ~~.1,~~<sup>2</sup> consistent with ranges found in the human large intestine.	+	Strictly [http://en.wikipedia.org/wiki/Anaerobic_organism anaerobic].<sup>2</sup> It is [http://www.biology-online.org/dictionary/Saccharolytic saccharolytic]. Good growth was exhibited in PYT broth media containing esculin, fructose, glucose, salicin, or sucrose. Moderate growth can sometimes be observed in peptone-yeast extract broth with maltose or lactose. Minimal growth was seen in PYT broths with no carbohydrates or with amydalin, arabinose, cellobiose, erythritol, glycogen, inositol, mannitol, mannose, melzitose, melibiose, raffinose, rhamnose, ribose, sorbitol, starch, trehalose, or xylose. In PYT-glucose broth, the consistent end products of fermentation were acetic acid, lactic acid, and succinic acid.<sup>2</sup> Meat, gelatin, and milk are not digested or changed. Esculin is hydrolyzed; nitrate is not reduced; arginine is not deanimated; catalase and indole are not produced. It has been shown to grow in media ranging from a pH of 5.8 to 6.5 <sup>1,2</sup> consistent with ranges found in the human large intestine.
		+
	===Ecology===		===Ecology===
	''H. filiformis'' is part of the normal human [http://en.wikipedia.org/wiki/Gut_flora gut flora]. It was originally isolated from human feces.<sup>2</sup> It appears to be [http://en.wikipedia.org/wiki/Mesophile mesophilic].		''H. filiformis'' is part of the normal human [http://en.wikipedia.org/wiki/Gut_flora gut flora]. It was originally isolated from human feces.<sup>2</sup> It appears to be [http://en.wikipedia.org/wiki/Mesophile mesophilic].
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	[http://www.ncbi.nlm.nih.gov/bioproject/30361 7] ''Holdemania filiformis'' reference genome for the Human Microbiome Project. http://www.ncbi.nlm.nih.gov/bioproject/30361 May, 2, 2012		[http://www.ncbi.nlm.nih.gov/bioproject/30361 7] ''Holdemania filiformis'' reference genome for the Human Microbiome Project. http://www.ncbi.nlm.nih.gov/bioproject/30361 May, 2, 2012
		+
		+
		+	Edited by a student of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio
		+

	Category: Uncurated Pages		Category: Uncurated Pages

Acetobacter aceti

2012-05-16T01:31:06Z

Genome structure:

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	==Genome structure==		==Genome structure==

−	There are ~~3340429~~ total base pairs of [http://en.wikipedia.org/wiki/DNA DNA] that make up the genome of ''Acetobacter aceti''. There are a total of 3122 genes within Acetobacter aceti. 3050, or ninety seven percent of the [http://en.wikipedia.org/wiki/Genes genes] all code for proteins, meaning that a large portion of ''Acetobacter aceti'' is to produce protein.(4)	+	There are 3,340,429 total base pairs of [http://en.wikipedia.org/wiki/DNA DNA] that make up the genome of ''Acetobacter aceti''. There are a total of 3122 genes within ''Acetobacter aceti''. 3050, or ninety seven percent of the [http://en.wikipedia.org/wiki/Genes genes] all code for proteins, meaning that a large portion of ''Acetobacter aceti'' is to produce protein.(4)

	==Cell and colony structure==		==Cell and colony structure==
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	[http://en.wikipedia.org/wiki/Acetobacter 4] http://en.wikipedia.org/wiki/Acetobacter		[http://en.wikipedia.org/wiki/Acetobacter 4] http://en.wikipedia.org/wiki/Acetobacter
	No DOI		No DOI
−
−
−	[http://ijs.sgmjournals.org/content/62/2/330; Sylvie Cousin, Marie-Laure Gulat-Okalla, Laurence Motreff, Catherine Gouyette, Christiane Bouchier, Dominique Clermont, and Chantal Bizet. Lactobacillus gigeriorum sp. nov., isolated from chicken crop. Int J Syst Evol Microbiol February 2012 62:330-334; published ahead of print March 18, 2011.} [doi:10.1099/ijs.0.028217-0.]


	Edited by David Morin of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio		Edited by David Morin of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio

Nocardia asteroides

2012-05-16T01:27:25Z

Metabolism:

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	{{Uncurated}}		{{Uncurated}}
−	~~{{Catenulispora Genus}}~~	+
	==Classification==		==Classification==

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	==Metabolism==		==Metabolism==
−	Since Nocardia is a soil bacterium, it uses different compounds as its source for carbon and energy. The primary source energy for Nocardia asteroides is acetate and gluconate while its source of carbon and nitrogen is sucrose and acetamide.During nitrogen assimilation glutamate and glutamine is formed .Nocardia asteroides uses the GA/GOGAT pathway to form glutamine which contains the enzymes glutamine synthetase and glutamate synthetase which catalyzes glutamate from α-ketogluterate and ammonia [1, 7].==Ecology==	+	Since Nocardia is a soil bacterium, it uses different compounds as its source for carbon and energy. The primary source energy for Nocardia asteroides is acetate and gluconate while its source of carbon and nitrogen is sucrose and acetamide.During nitrogen assimilation glutamate and glutamine is formed .Nocardia asteroides uses the GS/GOGAT pathway to form glutamine which contains the enzymes glutamine synthetase and glutamate synthetase which catalyzes glutamate from α-ketogluterate and ammonia [1, 7].
		+
		+	==Ecology==
	Vibrio mimicus is a Gram-negative bacterium that is an indigenous member of diverse aquatic environments, including seawater, freshwater, and brackish water, where it has been found both as a free-living bacterium and in association with zooplankton, crustaceans, filter-feeding mollusks, turtle eggs, and fish. [2, 5, 6, 7, and 8].		Vibrio mimicus is a Gram-negative bacterium that is an indigenous member of diverse aquatic environments, including seawater, freshwater, and brackish water, where it has been found both as a free-living bacterium and in association with zooplankton, crustaceans, filter-feeding mollusks, turtle eggs, and fish. [2, 5, 6, 7, and 8].
−		+
	==Pathology and Ecology==		==Pathology and Ecology==
	Nocardia asteroides live on dead decaying organic matter in the soil, water, dust and on vegetation. Nocardiosis is a chronic bacterial disease of humans and many other animals originating in the respiratory tract and disseminated by way of blood to other organs. It is caused by either introduction of the species into the skin or by inhalation of the species from its habitat. Nocardia asteroides accounts for 86% of systematic nocardiosis in humans and 98% of cerebral nocardial abscesses and 2% of all cerebral abscesses [1, 3, and 6].		Nocardia asteroides live on dead decaying organic matter in the soil, water, dust and on vegetation. Nocardiosis is a chronic bacterial disease of humans and many other animals originating in the respiratory tract and disseminated by way of blood to other organs. It is caused by either introduction of the species into the skin or by inhalation of the species from its habitat. Nocardia asteroides accounts for 86% of systematic nocardiosis in humans and 98% of cerebral nocardial abscesses and 2% of all cerebral abscesses [1, 3, and 6].

Vibrio mimicus

2012-05-16T01:21:07Z

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	{{Uncurated}}		{{Uncurated}}
−	~~{{Catenulispora Genus}}~~	+
	==Classification==		==Classification==

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	11. Aba, Hadi, Soni Priya Valeru, Susan Marouf Sami, Amir Saeed, Saumya Raychaudhuri, and Gunnar Sandström. "Interaction between Vibrio Mimicus and Acanthamoeba Castellanii." Environ Microbiol Rep 2.1 (2010): 166-71. PubMed Central. 24 Nov. 2009. Web. 26 Apr. 2012. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861843/?report=abstract>. doi: 10.1111/j.1758-2229.2009.00129.x		11. Aba, Hadi, Soni Priya Valeru, Susan Marouf Sami, Amir Saeed, Saumya Raychaudhuri, and Gunnar Sandström. "Interaction between Vibrio Mimicus and Acanthamoeba Castellanii." Environ Microbiol Rep 2.1 (2010): 166-71. PubMed Central. 24 Nov. 2009. Web. 26 Apr. 2012. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861843/?report=abstract>. doi: 10.1111/j.1758-2229.2009.00129.x

−	12. Hasan NA, Grim CJ, Haley BJ, Chun J, Alam M, Taviani E, Hoq M, Munk AC, Saunders E, Brettin TS, Bruce DC, Challacombe JF, Detter JC, Han CS, Xie G, Nair GB, Huq A, Colwell RR.Proc Natl Acad Sci U S A. 2010 De	+	12. Hasan NA, Grim CJ, Haley BJ, Chun J, Alam M, Taviani E, Hoq M, Munk AC, Saunders E, Brettin TS, Bruce DC, Challacombe JF, Detter JC, Han CS, Xie G, Nair GB, Huq A, Colwell RR. Comparative genomics of clinical and environmental Vibrio mimicus. Proc Natl Acad Sci U S A. 2010 Dec 7;107(49):21134-9. Epub 2010 Nov 15. doi: 10.1073/pnas.1013825107


	Edited by Raj Patel, Student of Dr. Lisa R Moore, University of Southern Maine		Edited by Raj Patel, Student of Dr. Lisa R Moore, University of Southern Maine

Moraxella bovis

2012-05-16T01:12:26Z

Genome structure:

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	===Higher order taxa===		===Higher order taxa===

−	Bacteria; Proteobacteria; Gammaproteobacteria; Pseudomonadales; Moraxellaceae, Moraxella (2). http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=476	+	Bacteria; Proteobacteria; Gammaproteobacteria; Pseudomonadales; Moraxellaceae, ''Moraxella'' (2). http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=476

	===Species===		===Species===
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	==Genome structure==		==Genome structure==
−	~~Contiguous DNA size is 15826 bp, contigs N50 (4).~~ ''M. bovis'' has circular DNA.	+	''M. bovis'' has circular DNA. The DNA genome sequence of the bacterial strain ''Moraxella bovis'' Epp63 has been or is still being determined with 361 contigs read using Sanger method analysis (3). The largest contiguous (contig N50) DNA size is 15,826 bp (4).
−	The DNA genome sequence of the bacterial strain ''Moraxella bovis'' Epp63 has been or is still being determined with 361 contigs read using Sanger method analysis (3).	+

	==Cell and colony structure==		==Cell and colony structure==

Lymantria dispar mulitinucleocapsid nuclear polyhedrosis virus (LdMNPV)

2012-05-16T01:02:09Z

Genome Structure:

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	==Description and Significance==		==Description and Significance==
−	Lymantria dispar (gypsy moth) is a species that came from Europe and was accidently released into Massachusetts in the late 1860’s. Periodic, high-density outbreaks of gypsy moth have resulted in considerable defoliation of northeastern forests. Furthermore the gypsy moth habitat continues to expand to the south and west at a rate of about 12 miles per year. LdMNPV is a naturally occurring baculovirus that selectively infects gypsy moth larvae (1). In 1978 the EPA trademarked the virus under the name [http://www.fs.fed.us/ne/morgantown/4557/gmoth/manag/gypchek.html Gypchek] and the U.S Forest Service distributes the virus aerially (2). Before 1986, Gypchek was distributed within “whole cadavers”. Since then, inoculated gypsy moth larvae are processed into powder containing a higher concentration of viral occlusion bodies that is more readily mixed with spray additives. Using this method of production requires 500-1000 infected larvae to prepare enough Gypchek to treat one acre of land. Researchers are currently developing an in vitro procedure of growing up and harvesting LdMNPV occlusion bodies from cells in culture, rather than in vivo development and isolation of occlusion bodies from whole larvae (1).	+	''Lymantria dispar'' (gypsy moth) is a species that came from Europe and was accidently released into Massachusetts in the late 1860’s. Periodic, high-density outbreaks of gypsy moth have resulted in considerable defoliation of northeastern forests. Furthermore the gypsy moth habitat continues to expand to the south and west at a rate of about 12 miles per year. LdMNPV is a naturally occurring baculovirus that selectively infects gypsy moth larvae (1). In 1978 the EPA trademarked the virus under the name [http://www.fs.fed.us/ne/morgantown/4557/gmoth/manag/gypchek.html Gypchek] and the U.S Forest Service distributes the virus aerially (2). Before 1986, Gypchek was distributed within “whole cadavers”. Since then, inoculated gypsy moth larvae are processed into powder containing a higher concentration of viral occlusion bodies that is more readily mixed with spray additives. Using this method of production requires 500-1000 infected larvae to prepare enough Gypchek to treat one acre of land. Researchers are currently developing an ''in vitro'' procedure of growing up and harvesting LdMNPV occlusion bodies from cells in culture, rather than ''in vivo'' development and isolation of occlusion bodies from whole larvae (1).

−	[[File:gypchk6.jpg\|thumb\|In vivo processing of Gypchek (2)]]	+	[[File:gypchk6.jpg\|thumb\|''In vivo'' processing of Gypchek (2)]]

	==Genome Structure==		==Genome Structure==
−	The [http://www.ncbi.nlm.nih.gov/nuccore/NC_001973.1 LdMNPV genome] is arranged into a single circular dsDNA chromosome totaling 161,~~046bps~~ with a G+C content of 57% (3). The LdMNPV is distinct from most other MNPV viruses due to its large size and high G+C content. Autographa californica MNPV is well-characterized and considered to be a prototypical MNPV. The [http://www.ncbi.nlm.nih.gov/nuccore/9627742 genomeof AcMNPV] (4) extends 133,~~894bps~~ and has a G+C content of 40.1%; both considerably less than that of LdMNPV. 163 ORFs composed of at least ~~150bps~~ have been identified for LdMNPV. Of the 155 predicted genes for AcMNPV, LdMNPV has 95 gene homologs (5).	+	The [http://www.ncbi.nlm.nih.gov/nuccore/NC_001973.1 LdMNPV genome] is arranged into a single circular dsDNA chromosome totaling 161,046 bp with a G+C content of 57% (3). The LdMNPV is distinct from most other MNPV viruses due to its large size and high G+C content. ''Autographa californica'' MNPV is well-characterized and considered to be a prototypical MNPV. The [http://www.ncbi.nlm.nih.gov/nuccore/9627742 genomeof AcMNPV] (4) extends 133,894 bp and has a G+C content of 40.1%; both considerably less than that of LdMNPV. 163 ORFs composed of at least 150 bp have been identified for LdMNPV. Of the 155 predicted genes for AcMNPV, LdMNPV has 95 gene homologs (5).

	==Virion Structure==		==Virion Structure==
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	5)Kuzio,J., Pearson,M.N., Harwood,S.H., Funk,C.J., Evans,J.T.,		5)Kuzio,J., Pearson,M.N., Harwood,S.H., Funk,C.J., Evans,J.T.,
−	Slavicek,J.M. and Rohrmann,G.F. Sequence and analysis of the genome of a baculovirus pathogenic for Lymantria dispar. <I>Virology</I> 253 (1), 17-34 (1999). PMID9887315	+	Slavicek,J.M. and Rohrmann,G.F. Sequence and analysis of the genome of a baculovirus pathogenic for ''Lymantria dispar''. <I>Virology</I> 253 (1), 17-34 (1999). PMID9887315

	6) Wood, H.A. and Granados, R.R. (1991). Genetically engineered baculoviruses as agents for pest control. <I>Annual Review of Microbiology</I>. 45, 69-87.		6) Wood, H.A. and Granados, R.R. (1991). Genetically engineered baculoviruses as agents for pest control. <I>Annual Review of Microbiology</I>. 45, 69-87.
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	7) Rohrmann, G.F. (2008). Baculovirus Molecular Biology. Bethesda MD: National Center for Biotechnology Information.		7) Rohrmann, G.F. (2008). Baculovirus Molecular Biology. Bethesda MD: National Center for Biotechnology Information.

−	8) Washburn J.O. Chan E.Y. Volkman L.E. Aumiller J.J. Jarvis D.L. Early synthesis of budded virus envelope fusion protein GP64 enhances Autographa californica multicapsidnucleo polyhedrovirus virulence in orally infected Heliothis virescens. <I>J Virol</I> 2003;77(1):280– 90. [PubMed: 12477833]	+	8) Washburn J.O. Chan E.Y. Volkman L.E. Aumiller J.J. Jarvis D.L. Early synthesis of budded virus envelope fusion protein GP64 enhances ''Autographa californica'' multicapsidnucleo polyhedrovirus virulence in orally infected ''Heliothis virescens''. <I>J Virol</I> 2003;77(1):280– 90. [PubMed: 12477833]

	9) Hoover, K.; Grove, M.; Gardner, M.; Hughes, D. P.; McNeil, J.; Slavicek, J. 2011. A Gene for an Extended Phenotype. <I>Science</I>. Vol. 333 no. 6048 p. 1401 DOI: 10.1126/science.1209199		9) Hoover, K.; Grove, M.; Gardner, M.; Hughes, D. P.; McNeil, J.; Slavicek, J. 2011. A Gene for an Extended Phenotype. <I>Science</I>. Vol. 333 no. 6048 p. 1401 DOI: 10.1126/science.1209199

Geomyces Destructans

2012-05-16T00:49:14Z

References:

Veillonella parvula

2012-05-15T16:56:06Z

Cell and colony structure:

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	===Species===		===Species===
−	[[Image:veipa.jpg‎\|frame\|right\|150px\|Te3 strain of V. parvula as show by scanning electron microscope [6]]]	+	[[Image:veipa.jpg‎\|frame\|right\|150px\|Te3 strain of ''V. parvula'' as show by scanning electron microscope [6]]]

	''Veillonella parvula''		''Veillonella parvula''

	==Description and significance==		==Description and significance==
−	Veillonella parvula is a gram negative, strict anaerobic, non-spore-forming coccus-shaped bacterium. It is found in the gut of humans and dental plaque. While considered non-pathogenic, it has been linked with rare cases of meningitis, osteomyelitis, and periodontal disease [7]. It cannot metabolize carbohydrates, but instead uses organic acids like lactate.	+	''Veillonella parvula'' is a gram negative, strict anaerobic, non-spore-forming coccus-shaped bacterium. It is found in the gut of humans and dental plaque. While considered non-pathogenic, it has been linked with rare cases of meningitis, osteomyelitis, and periodontal disease [7]. It cannot metabolize carbohydrates, but instead uses organic acids like lactate.

−	Perhaps the most significant role of V. parvula is its involvement in biofilms. It is able to coaggregate with other organisms, namely Streptococcus mutans, to the dental plaque. The two organisms have a mutualistic relationship with each other; V. parvula cannot adhere to the surface of teeth by itself, and so attaches to S. mutans. It can use the lactate product formed by S. mutans for its metabolism, in the process forming a less corrosive acid. In this particular case, the biofilm has been found to be more resistant to antimicrobials than either of the singular species [1].	+	Perhaps the most significant role of ''V. parvula'' is its involvement in biofilms. It is able to coaggregate with other organisms, namely ''Streptococcus mutans'', to the dental plaque. The two organisms have a mutualistic relationship with each other; ''V. parvula'' cannot adhere to the surface of teeth by itself, and so attaches to ''S. mutans''. It can use the lactate product formed by ''S. mutans'' for its metabolism, in the process forming a less corrosive acid. In this particular case, the biofilm has been found to be more resistant to antimicrobials than either of the singular species [1].

	==Genome structure==		==Genome structure==
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	==Cell and colony structure==		==Cell and colony structure==
−	The cells of V. parvula are coccus shaped, non-motile, roughly 0.4 µm in diameter, and predominantly occur in chains [6]. Like other gram negative bacteria, V. parvula has an outer layer of lipopolysaccharide which is a known virulence factor [4]. Putrescine and cadaverine are major constituents of V. parvula’s peptidoglycan and it cannot live without them [2]. Also present are plasmalogens, ether phospholipids found mainly in mammals and other anaerobic bacteria which may be connected to regulation of membrane fluidity.	+	The cells of ''V. parvula'' are coccus shaped, non-motile, roughly 0.4 µm in diameter, and predominantly occur in chains [6]. Like other gram negative bacteria, ''V. parvula'' has an outer layer of lipopolysaccharide which is a known virulence factor [4]. Putrescine and cadaverine are major constituents of ''V. parvula’s'' peptidoglycan and it cannot live without them [2]. Also present are plasmalogens, ether phospholipids found mainly in mammals and other anaerobic bacteria which may be connected to regulation of membrane fluidity.

	==Metabolism==		==Metabolism==
−	V. parvula cannot ferment carbohydrates. It uses organic acid by-products of carbohydrate processing organisms for its metabolism. Their main source of energy and metabolites is from the conversion of lactate into propionate and acetate as shown in the following stoichiometric equation: [3]	+	''V. parvula'' cannot ferment carbohydrates. It uses organic acid by-products of carbohydrate processing organisms for its metabolism. Their main source of energy and metabolites is from the conversion of lactate into propionate and acetate as shown in the following stoichiometric equation: [3]

	8 lactate > 5 propionate + 3 acetate + 3 CO2 + H2		8 lactate > 5 propionate + 3 acetate + 3 CO2 + H2

−	Oddly, despite a missing hexokinase necessary for the beginning steps of glycolysis, V. parvula still has a functioning pyruvate kinase. It is possible the pyruvate kinase is involved in gluconeogenesis when deactivated by ATP [5].	+	Oddly, despite a missing hexokinase necessary for the beginning steps of glycolysis, ''V. parvula'' still has a functioning pyruvate kinase. It is possible the pyruvate kinase is involved in gluconeogenesis when deactivated by ATP [5].

−	V. parvula can also use the enzyme methylmalonyl-CoA decarboxylase to metabolize succinate in the presence of lactate. The resulting free energy can be used to power a sodium ion pump [7].	+	''V. parvula'' can also use the enzyme methylmalonyl-CoA decarboxylase to metabolize succinate in the presence of lactate. The resulting free energy can be used to power a sodium ion pump [7].

	==Ecology==		==Ecology==
−	V. parvula is found in the gut and oral cavity of humans. In the oral cavity, the microbe is able to form biofilms with other organisms with similar niches [1]. V. parvula gets a large majority of its lactate from the organisms it coaggregates with.	+	''V. parvula'' is found in the gut and oral cavity of humans. In the oral cavity, the microbe is able to form biofilms with other organisms with similar niches [1]. ''V. parvula'' gets a large majority of its lactate from the organisms it coaggregates with.

	==Pathology==		==Pathology==
−	V. parvula is usually not considered a pathogen. However, it has been implicated with rare cases of meningitis, osteomyelitis, and periodontal disease [8]. The lipopolysaccharide has been found as a major virulence factor in some of these diseases [4]. Other more pathogenic microbes such as S. mutans use the biofilm formed with V. parvula as a virulence factor for periodontal disease [1], and therefore V. parvula could be indirectly involved with the pathogenesis of other microbes V. parvula is susceptible to penicillin [6].	+	''V. parvula'' is usually not considered a pathogen. However, it has been implicated with rare cases of meningitis, osteomyelitis, and periodontal disease [8]. The lipopolysaccharide has been found as a major virulence factor in some of these diseases [4]. Other more pathogenic microbes such as ''S. mutans'' use the biofilm formed with ''V. parvula'' as a virulence factor for periodontal disease [1], and therefore ''V. parvula'' could be indirectly involved with the pathogenesis of other microbes ''V. parvula'' is susceptible to penicillin [6].

	==References==		==References==

Borrelia recurrentis

2012-05-15T16:51:42Z

Pathology:

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	===Higher order taxa===		===Higher order taxa===

−	Domain (Bacteria); Phylum (Spirochaetes); Class (Spirochaetes); Order (Spirochaetales); Family (Borreliaceae); Genus (Borrelia)	+	Domain (Bacteria); Phylum (Spirochaetes); Class (Spirochaetes); Order (Spirochaetales); Family (Borreliaceae); Genus (''Borrelia'')

	===Species===		===Species===
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	==Description and significance==		==Description and significance==
−	Borrelia recurrentis is the causative agent of louse borne relapsing fever (LBRF) and is closely related to the ~~bacteria~~ B. duttonii, the source of tick borne relapsing fever. A recent genomic study of the two strains of bacteria found that B. recurrentis is actually a subset of B. duttonii in which the genes of the latter underwent a decaying process that gave rise to B. recurrentis. This process could be due to the inactivation of genes encoding for DNA repair mechanisms ([http://en.wikipedia.org/wiki/RecA recA] and mutS), causing an accumulation of errors in the genome [5]. B. recurrentis is the cause of systemic inflammatory disease, characterized by one to five fever relapses, distinctive hemorrhagic syndrome, a high rate of spontaneous abortion in pregnant women, and a 2-4% mortality rate despite modern antibiotics. B.recurrentis is unlike its counter part (B. duttonii), which produces more relapses and a lower mortality rate [5,6].B. recurrentis is a slender, pathogenic [http://en.wikipedia.org/wiki/Spirochete spirochete] whose habitat is usually associated with humans and is vector borne via lice. LBRF was once a world wide epidemic, but over the last century has since been eradicated due to better personal hygiene and way of living [1]. Now the disease is prevalent in areas that have major lice problems such as the Andean foothills, the highlands of eastern Africa, southern Sudan, and Rwanda [1,2]. The lice become infected by feeding on humans that are infected by the spirochetes. When the lice are transferred to another human, the infection spreads by the contact of the [http://en.wikipedia.org/wiki/Hemolymph hemolymph] (the fluid found in the circulatory system of arthropods) with abraded skin. This contact can occur by scratching, which then opens the skin and crushes the body of the lice, exposing the hemolymph. New evidence suggests that another means of infection can occur through contact with infected feces [2,4].	+	''Borrelia recurrentis'' is the causative agent of louse borne relapsing fever (LBRF) and is closely related to the bacterium ''B. duttonii'', the source of tick borne relapsing fever. A recent genomic study of the two strains of bacteria found that ''B. recurrentis'' is actually a subset of ''B. duttonii'' in which the genes of the latter underwent a decaying process that gave rise to ''B. recurrentis''. This process could be due to the inactivation of genes encoding for DNA repair mechanisms ([http://en.wikipedia.org/wiki/RecA recA] and mutS), causing an accumulation of errors in the genome [5]. ''B. recurrentis'' is the cause of systemic inflammatory disease, characterized by one to five fever relapses, distinctive hemorrhagic syndrome, a high rate of spontaneous abortion in pregnant women, and a 2-4% mortality rate despite modern antibiotics. B.recurrentis is unlike its counter part (''B. duttonii''), which produces more relapses and a lower mortality rate [5,6]. ''B. recurrentis'' is a slender, pathogenic [http://en.wikipedia.org/wiki/Spirochete spirochete] whose habitat is usually associated with humans and is vector borne via lice. LBRF was once a world wide epidemic, but over the last century has since been eradicated due to better personal hygiene and way of living [1]. Now the disease is prevalent in areas that have major lice problems such as the Andean foothills, the highlands of eastern Africa, southern Sudan, and Rwanda [1,2]. The lice become infected by feeding on humans that are infected by the spirochetes. When the lice are transferred to another human, the infection spreads by the contact of the [http://en.wikipedia.org/wiki/Hemolymph hemolymph] (the fluid found in the circulatory system of arthropods) with abraded skin. This contact can occur by scratching, which then opens the skin and crushes the body of the lice, exposing the hemolymph. New evidence suggests that another means of infection can occur through contact with infected feces [2,4].

	==Genome structure==		==Genome structure==
−	According to JGI Genome encyclopedia, the fully sequenced bacteria Borrelia recurrentis has a genome with 1025 genes and 1,242,163 base pairs which contain 8 linear fragments ranging from 6,131 bp to 930,~~981bp~~ [3, 5].This is quite atypical of prokaryotes since they are normally seen having a single, circular chromosome. B. recurrentis contains a linear chromosome with a size of approximately ~~1Mb~~ (27.5 GC%) along with both linear (7) and circular plasmids. All strains contain one large plasmid anywhere from 183 to ~~194kb~~ as well a small one (~~11kb~~). Strains have 5 main differences in the pattern of the other plasmids, which range in size from ~~25kb~~ to ~~62kb~~ [2].	+	According to JGI Genome encyclopedia, the fully sequenced bacteria ''Borrelia recurrentis'' has a genome with 1025 genes and 1,242,163 base pairs which contain 8 linear fragments ranging from 6,131 bp to 930,981 bp [3, 5].This is quite atypical of prokaryotes since they are normally seen having a single, circular chromosome. ''B. recurrentis'' contains a linear chromosome with a size of approximately 1 Mb (27.5 GC%) along with both linear (7) and circular plasmids. All strains contain one large plasmid anywhere from 183 to 194 kb as well a small one (11 kb). Strains have 5 main differences in the pattern of the other plasmids, which range in size from 25 kb to 62 kb [2].

	==Cell and colony structure==		==Cell and colony structure==
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	==Ecology==		==Ecology==
−	B. recurrentis is known for its inhabitance in human hosts and has only successfully been able to infect primates.	+	''B. recurrentis'' is known for its inhabitance in human hosts and has only successfully been able to infect primates.

	==Pathology==		==Pathology==
−	These spirochaetes normally cause a blood infection but they can also infect the nervous system along with other tissues [5]. There are no known [http://en.wikipedia.org/wiki/Virulence_factors virulence factors], but there are a few novel ways that this sneaky pathogen evades the host immune system [5]. The body has its way of recognizing and enhancing the recognition of foreign invaders called [http://en.wikipedia.org/wiki/Opsonin opsonization], which targets them for destruction through a cascade of reactions known as the [http://en.wikipedia.org/wiki/Complement_system complement system]. Recent studies show that B. recurrentis expresses a multifunctional surface lipoprotein, termed HcpA, that exploits the host’s proteins and offers resistance to complement attack and opsonization while increasing the potential to invade the host’s tissues [6]. Since HcpA outlines the high virulence potential of B. recurrentis, it makes a good target for therapeutic treatment of LBRF, however, none have been created yet. It was also found that this spirochete binds to the [http://en.wikipedia.org/wiki/Plasmin PLG](human plasminogen/Plasmin) receptor on endothelium cells and exploits their increased [http://en.wikipedia.org/wiki/Proteolytic proteolytic] capacity to breach tight junctions of endothelium, cross basement membranes, and to initiate patho-physiological processes in the affected organs [6]. Another novel approach is its ability to undergo antigenic variation, meaning that once the innate immune system is able to identify and start fighting off the first antigenic type, another antigenic type appears. This impairs the host immunes system from being able to clear the infection and explains why there are multiple recurrences of fever [6]. To treat LBRF, tetracyclines and penicillins are commonly used and are usually quite effective; however they may cause a severe [http://en.wikipedia.org/wiki/Jarisch-Herxheimer_reaction Jarisch-Herxheimer] reaction, which can be fatal [1] . This reaction causes fever, chills, rigor, hypotension, headache, tachycardia, hyperventilation, vasodilation with flushing, myalgia (muscle pain), and exacerbation of skin lesions because the death of the bacteria causes the release of harmful endotoxins faster than the body can get rid of them.	+	These spirochaetes normally cause a blood infection but they can also infect the nervous system along with other tissues [5]. There are no known [http://en.wikipedia.org/wiki/Virulence_factors virulence factors], but there are a few novel ways that this sneaky pathogen evades the host immune system [5]. The body has its way of recognizing and enhancing the recognition of foreign invaders called [http://en.wikipedia.org/wiki/Opsonin opsonization], which targets them for destruction through a cascade of reactions known as the [http://en.wikipedia.org/wiki/Complement_system complement system]. Recent studies show that ''B. recurrentis'' expresses a multifunctional surface lipoprotein, termed HcpA, that exploits the host’s proteins and offers resistance to complement attack and opsonization while increasing the potential to invade the host’s tissues [6]. Since HcpA outlines the high virulence potential of ''B. recurrentis'', it makes a good target for therapeutic treatment of LBRF, however, none have been created yet. It was also found that this spirochete binds to the [http://en.wikipedia.org/wiki/Plasmin PLG](human plasminogen/Plasmin) receptor on endothelium cells and exploits their increased [http://en.wikipedia.org/wiki/Proteolytic proteolytic] capacity to breach tight junctions of endothelium, cross basement membranes, and to initiate patho-physiological processes in the affected organs [6]. Another novel approach is its ability to undergo antigenic variation, meaning that once the innate immune system is able to identify and start fighting off the first antigenic type, another antigenic type appears. This impairs the host immunes system from being able to clear the infection and explains why there are multiple recurrences of fever [6]. To treat LBRF, tetracyclines and penicillins are commonly used and are usually quite effective; however they may cause a severe [http://en.wikipedia.org/wiki/Jarisch-Herxheimer_reaction Jarisch-Herxheimer] reaction, which can be fatal [1] . This reaction causes fever, chills, rigor, hypotension, headache, tachycardia, hyperventilation, vasodilation with flushing, myalgia (muscle pain), and exacerbation of skin lesions because the death of the bacteria causes the release of harmful endotoxins faster than the body can get rid of them.

	==References==		==References==

Micavibrio

2012-05-15T16:42:49Z

Genome structure:

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	==Description and significance==		==Description and significance==
−	''Micavibrio spp.'' is an obligate predator that exhibits ‘vampire-like’ behavior. It attaches to the surfaces of prey and feeds by "leaching", eventually killing its prey. They prey on Gram-negative micro-organisms known to be pathogenic in humans. <sup>4</sup> Due do its epibiotic lifestyle, obtaining an axenic culture is difficult, limiting potenial research. Currently, research is focused in its application as an antimicrobial.<sup>1</sup>	+	''Micavibrio spp.'' is an obligate predator that exhibits ‘vampire-like’ behavior. It attaches to the surfaces of prey and feeds by "leaching", eventually killing its prey. They prey on Gram-negative micro-organisms known to be pathogenic in humans. <sup>4</sup> Due to its epibiotic lifestyle, obtaining an axenic culture is difficult, limiting potenial research. Currently, research is focused in its application as an antimicrobial.<sup>1</sup>

	==Genome structure==		==Genome structure==
	[[Image:chromosome.jpg\|thumb\|400px\|right\| ''Micavibrio aerurinosavorus'' ARL-13 genome. [http://www.biomedcentral.com/1471-2164/12/453 From BMC Genomics.]]]		[[Image:chromosome.jpg\|thumb\|400px\|right\| ''Micavibrio aerurinosavorus'' ARL-13 genome. [http://www.biomedcentral.com/1471-2164/12/453 From BMC Genomics.]]]

−	The genome of ''M. aeruginosavorus'' ARL-13 has been completely sequenced and is a single circular molecule consisting of 2,481,983 bp and a 54.7% G+C content.<sup>4</sup> It is predicted that 90.3% of the genome codes for 1 rRNA operon, 40 tRNA genes and 2,434 open reading frames (ORFs). <sup>4</sup> There were no extragenomic DNA molecules (phage or plasmid) identified from the sequence and there was a complete absence of mobile genetic elements including insertion sequences, transposons and retrotransposons.<sup>4</sup> Numerous genes are encoded which have an important role in predator-prey interaction, for example, hemolysin-related proteins.<sup>4</sup> RNA-Seq analysis has shown a substantial difference in transcriptome between the attack phase (seeking prey) and attachment phase (feeding on prey and replicating). <sup>4</sup> ''M. aeruginosavorus'' ARL-13 encodes six hemolysin related proteins belonging to the RTX family of toxins which are suggested to contribute to recognizing and adhering to prey.<sup>4</sup> The genome of ''M. aeruginosavorus'' ARL-13 is a moderate size at 2.4 Mbp and is almost twice the size of most obligatory intracellular alphaproteobacteria and is smaller, by comparison, to most free living alphaproteobacteria.<sup>4</sup> The genome also encodes a large selection of hydrolytic enzymes with 4.3% of the genome predicting to encode 49 peptidases and proteases, 12 lipases, 4 RNAses, 2 DNAses and 37 additional hydrolases.<sup>4</sup> The genome of ''M. admirandus'' ARL-14 has a G+C content of 57.1%..<sup>5</sup>	+	The genome of ''M. aeruginosavorus'' ARL-13 has been completely sequenced and is a single circular molecule consisting of 2,481,983 bp and a 54.7% G+C content.<sup>4</sup> It is predicted that 90.3% of the genome codes for 1 rRNA operon, 40 tRNA genes and 2,434 open reading frames (ORFs). <sup>4</sup> There were no extragenomic DNA molecules (phage or plasmid) identified from the sequence and there was a complete absence of mobile genetic elements including insertion sequences, transposons and retrotransposons.<sup>4</sup> Numerous genes are encoded which have an important role in predator-prey interaction, for example, hemolysin-related proteins.<sup>4</sup> RNA-Seq analysis has shown a substantial difference in transcriptome between the attack phase (seeking prey) and attachment phase (feeding on prey and replicating). <sup>4</sup> ''M. aeruginosavorus'' ARL-13 encodes six hemolysin related proteins belonging to the RTX family of toxins which are suggested to contribute to recognizing and adhering to prey.<sup>4</sup> The genome of ''M. aeruginosavorus'' ARL-13 is a moderate size at 2.4 Mbp and is almost twice the size of most obligatory intracellular alphaproteobacteria and is smaller, by comparison, to most free living alphaproteobacteria.<sup>4</sup> The genome also encodes a large selection of hydrolytic enzymes with 4.3% of the genome predicting to encode 49 peptidases and proteases, 12 lipases, 4 RNAses, 2 DNAses and 37 additional hydrolases.<sup>4</sup> The genome of ''M. admirandus'' ARL-14 has a G+C content of 57.1%.<sup>5</sup>

	==Cell and colony structure==		==Cell and colony structure==

Nitrogen Fixation and Agriculture

2012-05-14T18:04:09Z

Current Use:

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	===Yield Concerns===		===Yield Concerns===
−	There are a few reasons why there needs to be a move towards more plants being able to fix their own nitrogen. The first reason is the need for increased yields in crops over the next few decades combined with the expensive nature of nitrogen fertilizers. ~~Yields of grain crops~~ have increased ~~substantial~~ over the last thirty years while the area of land harvested has stayed relatively flat. For example, in 1975 the area harvest for grains was ~~a little~~ over 700 million hectares for a total production of roughly 1,250 metric tonnes. This comes out to a yield of roughly 1.75 tonnes per hectare.[7] In 2010, the total harvested ~~Area~~ remained flat around 700 million hectares while the global grain production had risen to roughly 2,500 million metric tonnes. This comes to a yield of roughly 3.5 metric tonnes per hectare~~. This is~~ a very significant increase ~~in yield~~. A lot of the increased in yields can be attributed to ~~increase~~ fertilizer use, in some cases as much as 75%. With the population doubling in the last 30 years, the increase in yield has been essential to our survival.[8] Over the next few decades, the population is expected to rise even further, which will require yields to rise ~~too~~.	+	There are a few reasons why there needs to be a move towards more plants being able to fix their own nitrogen. The first reason is the need for increased yields in crops over the next few decades combined with the expensive nature of nitrogen fertilizers. Grain crop yields have increased substantially over the last thirty years while the area of land harvested has stayed relatively flat. For example, in 1975 the area harvest for grains was just over 700 million hectares for a total production of roughly 1,250 metric tonnes. This comes out to a yield of roughly 1.75 tonnes per hectare.[7] In 2010, the total harvested area remained flat around 700 million hectares while the global grain production had risen to roughly 2,500 million metric tonnes. This comes to a yield of roughly 3.5 metric tonnes per hectare, a very significant increase. A lot of the increased in yields can be attributed to increased fertilizer use, in some cases as much as 75%. With the population doubling in the last 30 years, the increase in yield has been essential to our survival.[8] Over the next few decades, the population is expected to rise even further, which will require yields to rise even further.

	===Costs===		===Costs===
−	Secondly, fertilizer costs are a large part of farmers’ budgets. In 2011, ~~fertilizer~~ for corn and wheat were roughly 20% of a farmer’s budget, compared to less than 10% for soybeans. This is due to the fact that soybeans ~~don’t~~ need as much fertilizer because of ~~the~~ nitrogen fixing bacteria ~~with which they can establish a relationship with~~. Fertilizer costs have increased nearly 50% in the previous years, putting pressure on farmers.[9]	+	Secondly, fertilizer costs are a large part of farmers’ budgets. In 2011, fertilizers for corn and wheat were roughly 20% of a farmer’s budget, compared to less than 10% for soybeans. This is due to the fact that soybeans do not need as much fertilizer because of their symbiotic relationship with nitrogen fixing bacteria. Fertilizer costs have increased nearly 50% in the previous years, putting pressure on farmers to find alternative methods of providing nitrogen to their crops.[9]

	===Environmental Concerns===		===Environmental Concerns===
−	Finally, there are environmental costs associated with the excessive use of fertilizer. The nitrogen that is not taken up by plants can ~~run~~ “accumulate in soil, water, the atmosphere and coastal oceanic waters [and] contribute to the greenhouse effect, smog, haze, acid rain, coastal ‘dead zones’ and stratospheric ozone depletion.”[10] Crops are only able to harness somewhere between 30% and 50% of the fertilizer that is applied.[11] Fossil fuels are another factor in the environmental costs of fertilizers. Roughly 2% of the world’s fossil fuel consumption is used in producing fertilizers. ~~Nitrogen fertilizers, again, are made by burning natural.~~	+	Finally, there are environmental costs associated with the excessive use of fertilizer. The nitrogen that is not taken up by plants can “accumulate in soil, water, the atmosphere and coastal oceanic waters [and] contribute to the greenhouse effect, smog, haze, acid rain, coastal ‘dead zones’ and stratospheric ozone depletion.”[10] Crops are only able to harness somewhere between 30% and 50% of the fertilizer that is applied.[11] Fossil fuels are another factor in the environmental costs of fertilizers. Roughly 2% of the world’s fossil fuel consumption is used in producing fertilizers.
−	If ~~the~~ major crops ~~that are grown~~ can be enhanced to become nitrogen fixers, then the world ~~will cut down on a lot of excess~~. We would be able to decrease ~~our use of producing~~ fertilizer and ~~having to transport it~~ to the farmland. We would cut down the costs of ~~needing~~ fertilizer because the plants would ~~make it themselves~~. The increase in yield that is needed would not be sacrificed, and there would be less excess nitrogen in water and soil because plants that fix nitrogen themselves make the necessary amount.	+	If major crops can be enhanced to become nitrogen fixers, then the world would use substantially less fossil fuels. We would be able to decrease fertilizer production and limit the cost of transportation to the farmland. We would cut down the costs of fertilizer because the plants would be able to biologically fix nitrogen. The increase in yield that is needed would not be sacrificed, and there would be less excess nitrogen in water and soil because plants that fix nitrogen themselves make the necessary amount.

	==What is being done==		==What is being done==
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	===Rhizospheric Relationship===		===Rhizospheric Relationship===
−	Within the past decade or so, scientists have been actively trying to make our crops capable of being nitrogen fixers, and therefore less reliant on inorganic fertilizers. The most significant crop for us to achieve nitrogen fixation with would be corn. The US produces more corn than any other crop. It has been shown that corn can establish a relationship with nitrogen fixing bacteria. Rhizospheric or endophytic relationships can be established “with various nitrogen-fixing bacteria such as azospirillum, Klebsiella, Pantoea, Herbaspirillum, Bacillus, Rhizobium etli, and Burkholderia. Establishing relationships means less nitrogen fertilizer and lower costs for farmers. This can be extremely beneficial to poor farmers in developing countries.[12] This, from a study in 2010, may have been a little optimistic.	+	Within the past decade or so, scientists have been actively trying to make our crops capable of being nitrogen fixers, and therefore less reliant on inorganic fertilizers. The most significant crop for us to achieve nitrogen fixation with would be corn. The US produces more corn than any other crop. It has been shown that corn can establish a relationship with nitrogen fixing bacteria. Rhizospheric or endophytic relationships can be established “with various nitrogen-fixing bacteria such as azospirillum, Klebsiella, Pantoea, Herbaspirillum, Bacillus, Rhizobium etli, and Burkholderia." Establishing relationships means less nitrogen fertilizer and lower costs for farmers. This can be extremely beneficial to poor farmers in developing countries.[12] This, from a study in 2010, may have been a little optimistic.

	===G. diazotrophicus===		===G. diazotrophicus===
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	===Current Use===		===Current Use===
−	There ~~is a website~~ that ~~is selling~~ nitrogen fixing bacteria that ~~claims to be~~ for all crops. It is called TwinN ~~and is~~ “free living Nitrogen fixing bacteria that will infect all crops, and make available large quantities of nitrogen while improving root growth and solid health.”[15] The bacteria “produce nitrogen ‘in tune’ with the plant, so the plant is never under nor over supplied with nitrogen.” The costs of using these bacteria versus normal inorganic fertilizer are cut in half.[16] This does not conclude a solution has been found though because of the ~~crops~~ inability to pass on the bacteria to the next generation. More research and study will be needed to make nitrogen fixation a widespread reality and to decrease our need for inorganic fertilizers.	+	There are some websites that claim to sell nitrogen fixing bacteria that work for all crops. One of these is called TwinN, a “free living Nitrogen fixing bacteria that will infect all crops, and make available large quantities of nitrogen while improving root growth and solid health.”[15] The bacteria “produce nitrogen ‘in tune’ with the plant, so the plant is never under nor over supplied with nitrogen.” The costs of using these bacteria versus normal inorganic fertilizer are cut in half.[16] This does not conclude a solution has been found though because of the crop's inability to pass on the bacteria to the next generation. More research and study will be needed to make nitrogen fixation a widespread reality and to decrease our need for inorganic fertilizers.

	==References==		==References==
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Lymantria dispar mulitinucleocapsid nuclear polyhedrosis virus (LdMNPV)

2012-05-14T06:00:09Z

File:Gypchk6.jpg

2012-05-14T05:52:50Z

uploaded "[[File:Gypchk6.jpg]]"

Lymantria dispar mulitinucleocapsid nuclear polyhedrosis virus (LdMNPV)

2012-05-14T05:49:25Z

← Older revision		Revision as of 05:49, 14 May 2012
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−
	[[File:gypck4.jpeg\|frame\|Gypsy moth virus life cycle: viral occlusion bodies (OB) (A) dissolve in the insect's gut liberating nonoccluded virus (NOV) that enters the midgut (B) and eventually passes through to the hemocoel. There NOV enters hemocytes and other cell types and replicates (C), producing more NOV (D) and OB (E). Cells eventually rupture releasing NOV and OB into the hemocoel. The insect dies (F) 10-14 days after consuming the virus.(photo from Reardon, Podgwaite, Zerillo. 1996. Gypcheck - The Gypsy Moth Nucleopolyhedrosis Virus Product. USDA FS FHTET-96-16.)]]		[[File:gypck4.jpeg\|frame\|Gypsy moth virus life cycle: viral occlusion bodies (OB) (A) dissolve in the insect's gut liberating nonoccluded virus (NOV) that enters the midgut (B) and eventually passes through to the hemocoel. There NOV enters hemocytes and other cell types and replicates (C), producing more NOV (D) and OB (E). Cells eventually rupture releasing NOV and OB into the hemocoel. The insect dies (F) 10-14 days after consuming the virus.(photo from Reardon, Podgwaite, Zerillo. 1996. Gypcheck - The Gypsy Moth Nucleopolyhedrosis Virus Product. USDA FS FHTET-96-16.)]]

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	===Genus:Nucleopolyhedrosis virus (NPV)===		===Genus:Nucleopolyhedrosis virus (NPV)===
	===Group II NPV===		===Group II NPV===
		+
	==Description and Significance==		==Description and Significance==
−	Lymantria dispar (gypsy moth) is a species that came from Europe and was accidently released into Massachusetts in the late 1860’s. Periodic, high-density outbreaks of gypsy moth have resulted in considerable defoliation of northeastern forests. Furthermore the gypsy moth habitat continues to expand to the south and west at a rate of about 12 miles per year. LdMNPV is a naturally occurring baculovirus that selectively infects gypsy moth larvae (1). In 1978 the EPA trademarked the virus under the name Gypchek and the U.S Forest Service distributes the virus aerially (2). Before 1986, Gypchek was distributed within “whole cadavers”. Since then, inoculated gypsy moth larvae are processed into powder containing a higher concentration of viral occlusion bodies that is more readily mixed with spray additives. Using this method of production requires 500-1000 infected larvae to prepare enough Gypchek to treat one acre of land. Researchers are currently developing an in vitro procedure of growing up and harvesting LdMNPV occlusion bodies from cells in culture, rather than in vivo development and isolation of occlusion bodies from whole larvae (1).	+	Lymantria dispar (gypsy moth) is a species that came from Europe and was accidently released into Massachusetts in the late 1860’s. Periodic, high-density outbreaks of gypsy moth have resulted in considerable defoliation of northeastern forests. Furthermore the gypsy moth habitat continues to expand to the south and west at a rate of about 12 miles per year. LdMNPV is a naturally occurring baculovirus that selectively infects gypsy moth larvae (1). In 1978 the EPA trademarked the virus under the name [http://www.fs.fed.us/ne/morgantown/4557/gmoth/manag/gypchek.html Gypchek] and the U.S Forest Service distributes the virus aerially (2). Before 1986, Gypchek was distributed within “whole cadavers”. Since then, inoculated gypsy moth larvae are processed into powder containing a higher concentration of viral occlusion bodies that is more readily mixed with spray additives. Using this method of production requires 500-1000 infected larvae to prepare enough Gypchek to treat one acre of land. Researchers are currently developing an in vitro procedure of growing up and harvesting LdMNPV occlusion bodies from cells in culture, rather than in vivo development and isolation of occlusion bodies from whole larvae (1).

	==Genome Structure==		==Genome Structure==
−	LdMNPV ~~genetic material~~ is arranged into a single circular dsDNA chromosome totaling 161,046bps with a G+C content of 57% (3). The LdMNPV is distinct from most other MNPV viruses due to its large size and high G+C content. Autographa californica MNPV is well-characterized and considered to be a prototypical MNPV. The genomeof AcMNPV (4) extends 133,894bps and has a G+C content of 40.1%; both considerably less than that of LdMNPV. 163 ORFs composed of at least 150bps have been identified for LdMNPV. Of the 155 predicted genes for AcMNPV, LdMNPV has 95 gene homologs (5).	+	The [http://www.ncbi.nlm.nih.gov/nuccore/NC_001973.1 LdMNPV genome] is arranged into a single circular dsDNA chromosome totaling 161,046bps with a G+C content of 57% (3). The LdMNPV is distinct from most other MNPV viruses due to its large size and high G+C content. Autographa californica MNPV is well-characterized and considered to be a prototypical MNPV. The [http://www.ncbi.nlm.nih.gov/nuccore/9627742 genomeof AcMNPV] (4) extends 133,894bps and has a G+C content of 40.1%; both considerably less than that of LdMNPV. 163 ORFs composed of at least 150bps have been identified for LdMNPV. Of the 155 predicted genes for AcMNPV, LdMNPV has 95 gene homologs (5).

	==Virion Structure==		==Virion Structure==
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	==Reproductive Cycle in a Host Cell==		==Reproductive Cycle in a Host Cell==
	LdMNPV virions are found dispersed throughout the foliage that Lymantia dispar larvae feed upon and therefore enter the host through ingestion. The infection course is initiated once OBs reach the midgut of the host. The lepidopteran midgut is an alkaline environment that breaks down the polyhedra surrounding nucleocapsids. Following release from occlusion bodies, nucleocapsids enter surrounding midgut epithelium cells. However cells lining the midgut are regularly sloughed off, systemic infection must be initiated promptly. It has been purposed that MNPV nucleocapsids are capable of transmitting through midgut epithelium cells without replicating DNA and directly budding off to promote the spread of infection into hemolymph and tracheal tissues (7).		LdMNPV virions are found dispersed throughout the foliage that Lymantia dispar larvae feed upon and therefore enter the host through ingestion. The infection course is initiated once OBs reach the midgut of the host. The lepidopteran midgut is an alkaline environment that breaks down the polyhedra surrounding nucleocapsids. Following release from occlusion bodies, nucleocapsids enter surrounding midgut epithelium cells. However cells lining the midgut are regularly sloughed off, systemic infection must be initiated promptly. It has been purposed that MNPV nucleocapsids are capable of transmitting through midgut epithelium cells without replicating DNA and directly budding off to promote the spread of infection into hemolymph and tracheal tissues (7).
−	In AcMNPV, the GP64 envelope fusion protein is essential for the spread of infection. Within the genomes of Group 1 NPV viruses, including AcMNPV, both early and late promoter sequences have been identified within the regulatory regions upstream of gp64 coding region Washburn et al. () found that deletion of the early promoter sequence from the AcMNPV gp64 regulatory region produced a delay in infection time course when following virion ingestion, but not when infections were initiated by injection directly into hemolymph tissue. The genomes of group II NPVs do not include a gp64 ORF, but do have F genes that encode a protein with a function analogous to the GP64 fusion protein. Interestingly, early and late promoter consensus sequences were identified in the regulatory region F genes, suggesting a similar capability in LdMNPV(7).	+
−	The most characteristic feature of LdMNPV and other baculoviruses that infect Lepoditera is the manipulation of host behavior to maximize viral prodigy as well as increase the likeliness of spreading infection . The egt gene of LdMNPV and others encodes the EGT enzyme that inactivates 20-hydroxyecdysone, which is a hormone that initiates molting. Inhibition of molting extends the period of time lepidopteran larvae feeds upon tree vegetation. As a result there is more biomass to convert into OBs. Furthermore, this manipulation changes the climbing behavior of the gypsy moth larvae. Healthy larvae typically hide from birds in bark crevices or on the ground during the day and feed in the treetops at night. Catepillars infected with LdMNPV remain in the treetops until death. Therefore upon death of the insect host, OBs can be distributed in the foliage below, where other gypsy moth larvae are likely present (9).	+	In AcMNPV, the GP64 envelope fusion protein is essential for the spread of infection. Within the genomes of Group 1 NPV viruses, including AcMNPV, both early and late promoter sequences have been identified within the regulatory regions upstream of <I>gp64</I> coding region Washburn et al.(8) found that deletion of the early promoter sequence from the AcMNPV <I>gp64</I> regulatory region produced a delay in infection time course when following virion ingestion, but not when infections were initiated by injection directly into hemolymph tissue. The genomes of group II NPVs do not include a <I>gp64</I> ORF, but do have <I>f</I> genes that encode a protein with a function analogous to the GP64 fusion protein. Interestingly, early and late promoter consensus sequences were identified in the regulatory region F genes, suggesting a similar capability in LdMNPV(7).
−	Early in the course of baculovirus infection, a non-occulated form of the virus is exclusively produced. Later in infection, nucleocapsids are occulated within a protein matrix predominately composed of the protein polyhedron. This protein shell allows for the stability of released multinucleocapsids into the environment. Studies on AcMNPV, as well as other NPVs, has led to the characterization of a pattern of gene expression cascades with common chronology across all NPVs. Gene expression throughout baculovirus infection is organized into three phases: early, late and hyper-expressed. The early phase of gene expression, which occurs before DNA replication, is further organized into two stages; immediant early and delayed early gene expression. Genes expressed during the immediate early stage do not require the presence of trans-activators for sufficient expression levels. In contrast, genes expressed during the delayed-early phase, as well as later phases of gene expression rely on the presence of trans-activators and other genes expressed throughout the immediate early stage of gene expression (10). The immediate early expression of the g22 gene, which codes for a promoter of the RNA polymerase II gene, is required for subsequent DNA replication (11). The late stage of gene expression begins following the onset of DNA replication. The p39 capsid protein and polyhedral envelope protein are expressed throughout the late phase of gene expression (12). The hyperexpressed (also termed very late) stage of infection is characterized by expression of polyhedrin and p10 genes. Polyhedrin and P10 accumulate in the nuclei of infected cells throughout the hyperexpressed stage. Polyhedrin molecules interact to form occlusion bodies that package multiple nucleocapsids. At a later point in infection, p10 fibrils form on the surface of occlusion bodies and are thought to be a key component to the formation of the polyhedron envelope. Studies of NPV infection where the p10 gene has been deleted result in polyhedrons with uneven surfaces and from which virions are readily dislodged (7).	+
		+	The most characteristic feature of LdMNPV and other baculoviruses that infect Lepoditera is the manipulation of host behavior to maximize viral prodigy as well as increase the likeliness of spreading infection . The <I>egt</I> gene of LdMNPV and others encodes the EGT enzyme that inactivates 20-hydroxyecdysone, which is a hormone that initiates molting. Inhibition of molting extends the period of time lepidopteran larvae feeds upon tree vegetation. As a result there is more biomass to convert into OBs. Furthermore, this manipulation changes the climbing behavior of the gypsy moth larvae. Healthy larvae typically hide from birds in bark crevices or on the ground during the day and feed in the treetops at night. Catepillars infected with LdMNPV remain in the treetops until death. Therefore upon death of the insect host, OBs can be distributed in the foliage below, where other gypsy moth larvae are likely present (9).
		+
		+	Early in the course of baculovirus infection, a non-occulated form of the virus is exclusively produced. Later in infection, nucleocapsids are occulated within a protein matrix predominately composed of the protein polyhedron. This protein shell allows for the stability of released multinucleocapsids into the environment. Studies on AcMNPV, as well as other NPVs, has led to the characterization of a pattern of gene expression cascades with common chronology across all NPVs. Gene expression throughout baculovirus infection is organized into three phases: early, late and hyper-expressed. The early phase of gene expression, which occurs before DNA replication, is further organized into two stages; immediant early and delayed early gene expression. Genes expressed during the immediate early stage do not require the presence of trans-activators for sufficient expression levels. In contrast, genes expressed during the delayed-early phase, as well as later phases of gene expression rely on the presence of trans-activators and other genes expressed throughout the immediate early stage of gene expression (10). The immediate early expression of the <I>g22</I> gene, which codes for a promoter of the RNA polymerase II gene, is required for subsequent DNA replication (11). The late stage of gene expression begins following the onset of DNA replication. The p39 capsid protein and polyhedral envelope protein are expressed throughout the late phase of gene expression (12). The hyperexpressed (also termed very late) stage of infection is characterized by expression of <I>polyhedrin</I> and <I>p10</I> genes. Polyhedrin and P10 accumulate in the nuclei of infected cells throughout the hyperexpressed stage. Polyhedrin molecules interact to form occlusion bodies that package multiple nucleocapsids. At a later point in infection, p10 fibrils form on the surface of occlusion bodies and are thought to be a key component to the formation of the polyhedron envelope. Studies of NPV infection where the p10 gene has been deleted result in polyhedrons with uneven surfaces and from which virions are readily dislodged (7).

	==References==		==References==

← Older revision		Revision as of 00:49, 16 May 2012
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	==References==		==References==

−	[1] Chaturvedi V, Springer DJ, Behr MJ, Ramani R, Li X, et al. (2010) Morphological and Molecular Characterizations of Psychrophilic Fungus Geomyces destructans from New York Bats with White Nose Syndrome (WNS). PLoS ONE 5(5): e10783. doi:10.1371/journal.pone.0010783	+	[1] Chaturvedi V, Springer DJ, Behr MJ, Ramani R, Li X, et al. (2010) Morphological and Molecular Characterizations of Psychrophilic Fungus ''Geomyces destructans'' from New York Bats with White Nose Syndrome (WNS). PLoS ONE 5(5): e10783. doi:10.1371/journal.pone.0010783

	[2] G. G. Turner, D. M. Reeder, and J. T. H. Coleman. 2011. A Five-year Assessment of Mortality and Geographic Spread of White-Nose Syndrome in North American Bats, with a Look at the Future. Update of White-Nose Syndrome in bats. Bat Research News, 52:13-27.pdf		[2] G. G. Turner, D. M. Reeder, and J. T. H. Coleman. 2011. A Five-year Assessment of Mortality and Geographic Spread of White-Nose Syndrome in North American Bats, with a Look at the Future. Update of White-Nose Syndrome in bats. Bat Research News, 52:13-27.pdf

−	[3] Gargas, A., M.T. Trest, M. Christensen, T.J. Volk, and D.S. Blehert. "Geomyces Destructans sp. nov. associated with bat white-nose syndrome." Mycotaxon 108.1 (2009): 147-54. Print.	+	[3] Gargas, A., M.T. Trest, M. Christensen, T.J. Volk, and D.S. Blehert. "''Geomyces Destructans'' sp. nov. associated with bat white-nose syndrome." Mycotaxon 108.1 (2009): 147-54. Print.

−	[4] KUBÁTOVÁ1, ALENA, ONDŘEJ KOUKOL, ALENA NOVÁKOVÁ, and CZECH MYCOL. "Geomyces Destructans, Phenotypic Features of Some Czech Isolates." CZECH MYCOL 63(1): (2011): 65-75. Print.	+	[4] KUBÁTOVÁ1, ALENA, ONDŘEJ KOUKOL, ALENA NOVÁKOVÁ, and CZECH MYCOL. "''Geomyces Destructans'', Phenotypic Features of Some Czech Isolates." CZECH MYCOL 63(1): (2011): 65-75. Print.

	[5] Courtin, F., WB Stone, G. Risatti, and K. Gilbert. "Pathologic Findings and Liver Elements in Hibernating Bats With White-Nose Syndrome." Veterinary Pathology. Veterinary Patholog, doi: 10.1177/0300985809358614 Mar. 2010. accessed Web. 03 May 2012. <http://vet.sagepub.com/content/47/2/214.full>.		[5] Courtin, F., WB Stone, G. Risatti, and K. Gilbert. "Pathologic Findings and Liver Elements in Hibernating Bats With White-Nose Syndrome." Veterinary Pathology. Veterinary Patholog, doi: 10.1177/0300985809358614 Mar. 2010. accessed Web. 03 May 2012. <http://vet.sagepub.com/content/47/2/214.full>.
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	http://www.ncbi.nlm.nih.gov/		http://www.ncbi.nlm.nih.gov/

−	[7] Amy Whistle1, Evan Pannkuk2,3, David Gilmore1, Ellis Benjamin3, Earl Benjamin3, FATTY ACID METABOLISM BY GEOMYCES DESTRUCTANS. Department of Biological Sciences, Graduate Program in Environmental Science, Department of Chemistry and Physical Sciences Arkansas State University, State University https://ncur.weber.edu/ncur/archive/Display_NCUR.aspx?id=52845	+	[7] Amy Whistle1, Evan Pannkuk2,3, David Gilmore1, Ellis Benjamin3, Earl Benjamin3, FATTY ACID METABOLISM BY ''GEOMYCES DESTRUCTANS''. Department of Biological Sciences, Graduate Program in Environmental Science, Department of Chemistry and Physical Sciences Arkansas State University, State University https://ncur.weber.edu/ncur/archive/Display_NCUR.aspx?id=52845

	[8]Wing pathology of white-nose syndrome in bats suggests life-threatening disruption of physiology. Paul M Cryan1, Carol U Meteyer2*, Justin G Boyles3 and David S Blehert.November 2010		[8]Wing pathology of white-nose syndrome in bats suggests life-threatening disruption of physiology. Paul M Cryan1, Carol U Meteyer2*, Justin G Boyles3 and David S Blehert.November 2010
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	[9]Serological, hematological and immunological research on hibernating bats. Jaeger R Experientia 1963, 19:596-598.		[9]Serological, hematological and immunological research on hibernating bats. Jaeger R Experientia 1963, 19:596-598.

−	[10] Wibbelt G, Kurth A, Hellmann D, Weishaar M, Barlow A, Veith M, Pruger J, Gorfol T, Grosche L, Bontadina F, et al: White-nose syndrome fungus (Geomyces destructans) in bats, Europe. Emerg Infect Dis 2010, 16:1237-1243.	+	[10] Wibbelt G, Kurth A, Hellmann D, Weishaar M, Barlow A, Veith M, Pruger J, Gorfol T, Grosche L, Bontadina F, et al: White-nose syndrome fungus (''Geomyces destructans'') in bats, Europe. Emerg Infect Dis 2010, 16:1237-1243.

← Older revision		Revision as of 06:00, 14 May 2012
(3 intermediate revisions not shown)
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−	[[File:gypck4.jpeg\|frame\|Gypsy moth virus life cycle: viral occlusion bodies (OB) (A) dissolve in the insect's gut liberating nonoccluded virus (NOV) that enters the midgut (B) and eventually passes through to the hemocoel. There NOV enters hemocytes and other cell types and replicates (C), producing more NOV (D) and OB (E). Cells eventually rupture releasing NOV and OB into the hemocoel. The insect dies (F) 10-14 days after consuming the virus.(photo from Reardon, Podgwaite, Zerillo. 1996. Gypcheck - The Gypsy Moth Nucleopolyhedrosis Virus Product. USDA FS FHTET-96-16.)]]	+	[[File:gypck4.jpeg\|frame\|Gypsy moth virus life cycle: viral occlusion bodies (OB) (A) dissolve in the insect's gut liberating nonoccluded virus (NOV) that enters the midgut (B) and eventually passes through to the hemocoel. There NOV enters hemocytes and other cell types and replicates (C), producing more NOV (D) and OB (E). Cells eventually rupture releasing NOV and OB into the hemocoel. The insect dies (F) 10-14 days after consuming the virus.(photo from Reardon, Podgwaite, Zerillo. 1996. Gypcheck - The Gypsy Moth Nucleopolyhedrosis Virus Product. USDA FS FHTET-96-16.)(1)]]

	==Baltimore Classification==		==Baltimore Classification==
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	==Description and Significance==		==Description and Significance==
	Lymantria dispar (gypsy moth) is a species that came from Europe and was accidently released into Massachusetts in the late 1860’s. Periodic, high-density outbreaks of gypsy moth have resulted in considerable defoliation of northeastern forests. Furthermore the gypsy moth habitat continues to expand to the south and west at a rate of about 12 miles per year. LdMNPV is a naturally occurring baculovirus that selectively infects gypsy moth larvae (1). In 1978 the EPA trademarked the virus under the name [http://www.fs.fed.us/ne/morgantown/4557/gmoth/manag/gypchek.html Gypchek] and the U.S Forest Service distributes the virus aerially (2). Before 1986, Gypchek was distributed within “whole cadavers”. Since then, inoculated gypsy moth larvae are processed into powder containing a higher concentration of viral occlusion bodies that is more readily mixed with spray additives. Using this method of production requires 500-1000 infected larvae to prepare enough Gypchek to treat one acre of land. Researchers are currently developing an in vitro procedure of growing up and harvesting LdMNPV occlusion bodies from cells in culture, rather than in vivo development and isolation of occlusion bodies from whole larvae (1).		Lymantria dispar (gypsy moth) is a species that came from Europe and was accidently released into Massachusetts in the late 1860’s. Periodic, high-density outbreaks of gypsy moth have resulted in considerable defoliation of northeastern forests. Furthermore the gypsy moth habitat continues to expand to the south and west at a rate of about 12 miles per year. LdMNPV is a naturally occurring baculovirus that selectively infects gypsy moth larvae (1). In 1978 the EPA trademarked the virus under the name [http://www.fs.fed.us/ne/morgantown/4557/gmoth/manag/gypchek.html Gypchek] and the U.S Forest Service distributes the virus aerially (2). Before 1986, Gypchek was distributed within “whole cadavers”. Since then, inoculated gypsy moth larvae are processed into powder containing a higher concentration of viral occlusion bodies that is more readily mixed with spray additives. Using this method of production requires 500-1000 infected larvae to prepare enough Gypchek to treat one acre of land. Researchers are currently developing an in vitro procedure of growing up and harvesting LdMNPV occlusion bodies from cells in culture, rather than in vivo development and isolation of occlusion bodies from whole larvae (1).
		+
		+	[[File:gypchk6.jpg\|thumb\|In vivo processing of Gypchek (2)]]

	==Genome Structure==		==Genome Structure==
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	5)Kuzio,J., Pearson,M.N., Harwood,S.H., Funk,C.J., Evans,J.T.,		5)Kuzio,J., Pearson,M.N., Harwood,S.H., Funk,C.J., Evans,J.T.,
−	Slavicek,J.M. and Rohrmann,G.F. Sequence and analysis of the genome of a baculovirus pathogenic for Lymantria dispar. Virology 253 (1), 17-34 (1999). PMID9887315	+	Slavicek,J.M. and Rohrmann,G.F. Sequence and analysis of the genome of a baculovirus pathogenic for Lymantria dispar. <I>Virology</I> 253 (1), 17-34 (1999). PMID9887315

−	6) Wood, H.A. and Granados, R.R. (1991). Genetically engineered baculoviruses as agents for pest control. Annual Review of Microbiology. 45, 69-87.	+	6) Wood, H.A. and Granados, R.R. (1991). Genetically engineered baculoviruses as agents for pest control. <I>Annual Review of Microbiology</I>. 45, 69-87.

	7) Rohrmann, G.F. (2008). Baculovirus Molecular Biology. Bethesda MD: National Center for Biotechnology Information.		7) Rohrmann, G.F. (2008). Baculovirus Molecular Biology. Bethesda MD: National Center for Biotechnology Information.

−	8) Washburn J.O. Chan E.Y. Volkman L.E. Aumiller J.J. Jarvis D.L. Early synthesis of budded virus envelope fusion protein GP64 enhances Autographa californica multicapsidnucleo polyhedrovirus virulence in orally infected Heliothis virescens. J Virol 2003;77(1):280– 90. [PubMed: 12477833]	+	8) Washburn J.O. Chan E.Y. Volkman L.E. Aumiller J.J. Jarvis D.L. Early synthesis of budded virus envelope fusion protein GP64 enhances Autographa californica multicapsidnucleo polyhedrovirus virulence in orally infected Heliothis virescens. <I>J Virol</I> 2003;77(1):280– 90. [PubMed: 12477833]

−	9) Hoover, K.; Grove, M.; Gardner, M.; Hughes, D. P.; McNeil, J.; Slavicek, J. 2011. A Gene for an Extended Phenotype. Science. Vol. 333 no. 6048 p. 1401 DOI: 10.1126/science.1209199	+	9) Hoover, K.; Grove, M.; Gardner, M.; Hughes, D. P.; McNeil, J.; Slavicek, J. 2011. A Gene for an Extended Phenotype. <I>Science</I>. Vol. 333 no. 6048 p. 1401 DOI: 10.1126/science.1209199

−	10) Reigel, C.I. and Slavicek, J.M. (1997). Characterization of the replication cycle of the Lymantria dispar nuclear polyhedrosis virus. Virus Research 51, 9-17.	+	10) Reigel, C.I. and Slavicek, J.M. (1997). Characterization of the replication cycle of the Lymantria dispar nuclear polyhedrosis virus. <I>Virus Research</I> 51, 9-17.

−	11)Bischoff, David S.; Slavicek, James M. 1995. Identification and characterization of an early gene in the Lymantria dispar multinucleocapsid nuclear polyhedrosis virus. Journal of General Virology. 76: 2933-2940.	+	11)Bischoff, David S.; Slavicek, James M. 1995. Identification and characterization of an early gene in the Lymantria dispar multinucleocapsid nuclear polyhedrosis virus. <I>Journal of General Virology</I>. 76: 2933-2940.

−	12)12) Thiem, S. M. & Miller, L. K. (1989a). Identification, sequence and transcriptional mapping of the major capsid protein of the baculovirus Autographa californica nuclear polyhedrosis virus. Journal of Virology 63, 2008-2018.	+	12)12) Thiem, S. M. & Miller, L. K. (1989a). Identification, sequence and transcriptional mapping of the major capsid protein of the baculovirus Autographa californica nuclear polyhedrosis virus. <I>Journal of Virology</I> 63, 2008-2018.