Xanthomonas axonopodis: Difference between revisions
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Xanthomonas axonopodis | Xanthomonas axonopodis | ||
Bacteria; | Bacteria; Proteobaceria; Gammaproteobacteria, Xanthomonadales; Xanthomonadaceae; Xanthomonas(1) | ||
===Species=== | ===Species=== | ||
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''Genus species'' | ''Genus species:'' | ||
axonopodis | |||
==Description and significance== | ==Description and significance== | ||
Xanthomonas axonopodis are proteobacteria and as with all proteobacteria they have a gram negative wall consisting of an outer membrane made up of lipopolysaccharide (LPS) and a phospholipid inner membrane (4). Their appearances are aerobic rod shape with polar flagella. X. axonopodis can be found cultivating on the leaves, stems, and fruit of citrus trees all around the world. They are mostly found in heavily citrus agricultural countries such as the United States, Australia, and Brazil. These bacteria are mainly known as plant pathogens that causes citrus cankers. The leaves, stems, and fruits that are infected with X. axonopodis display lesions which take on yellow halo or ring shaped appearances. They are so persistent that whole orchards have to be destroyed if X. axonopodis are present (5). In 1910, Xanthomonas were first reported and studied in the United States. | |||
==Genome structure== | ==Genome structure== | ||
Their genome was sequenced in Sao Paulo, Brazil where they found X. axonopodis genome structures to contain a circular dsDNA chromosome with 5 mega base pairs and 4374 genes. Furthermore, the bacterium carries two plasmids, referred to as pXAC33 and pXAC64 (2). The two plasmids are 33 and 64 kilo base pairs long (3). | |||
==Cell structure and metabolism== | ==Cell structure and metabolism== | ||
The cell of X. axonopodis is a rod-shaped gram negative membrane with a polar flagella attached onto the membrane (3). The flagella allows the bacteria to move from lesion leaves of citrus trees to others trees infecting its host. | |||
Cellualse, protease and pectate lyase from Xanthomonas species have been suggested to play crucial roles in virulence and in bacterial nutrition. Xanthomonas possesses a Type III protein secretion system that is essential for pathogenicity in plants. This system is what causes the plants to become infected by inducing the hypersensitive response in resistant plants. The Type III protein system infects plants by inducing the expression of the host gene Os8N3, resulting in an increase of the host susceptibility (6). | |||
==Ecology== | ==Ecology== | ||
X. axonopodis have a parasitic relationship exclusively in plants where they cause citrus cankers on plants. They are most likely originated from southeastern Asia and spread to Japan, South Africa, Australia, the Pacific Islands, South America, and the United States (7). Usually trees that are infected with citrus canker bacteria, such as the X. axonopodis, are burned to prevent the spread of infection because it is difficult to control their rapidly spreading nature. Xanthomonas are an agriculturally devastating bacteria, in 1933 they caused more than 6 million dollars in damage in Florida alone which destroyed about 258,000 grove trees and 3 million nursery trees that had become infected. In 1998, Sao Paulo, Brazil suffered from a citrus canker outbreak where they had no choice but to destroy all infected trees as well as trees that were within a 30 meter radius of the infected trees. | |||
==Pathology== | ==Pathology== | ||
Xanthomonas are exclusively pathogenic to a large group of plants such as citrus trees, rice, cotton, beans, and grapes. They cause a highly contagious disease called citrus canker. Citrus canker can destroy an entire crop field, but does not pose any danger to humans or animals. The infection has a wide range of effects which include: defoliation, dieback, severely blemished fruit, reduced fruit quality, and premature fruit drop (8). Once the hosts are infected, X. axonopodis can spread like wildfire because of the many ways it can travel. Some examples of how it’s spread are by human movement of diseased citrus plants, use of contaminated equipment, or by fallen lesion leaves and fruits. Diseased leaves and fruits with lesions have a yellow halo or ring appearance. X. axonopodis would multiply if the lesions were expanding, but would die if it was on a surface facing sunlight. When the bacteria are not on leaves or fruits, it can survive by taking residence inside tree bark until it can transfer itself onto leaves or fruits. However, it can only survive for a few days if its host has fallen to the ground because its natural habitat has changed. This results because the bacteria now has to adapt to a new environment and find new sources for growth and reproduction. | |||
The two fundamental host determinants for citrus canker are the stage of leaf expansion and the resistance of mesophyll tissue. The host is most susceptible when its leaves expand ½ to 2/3, at this point the stomata open, but the leaf cuticle is not fully developed. During this time, the bacteria would take advantage of this opening and invade the leaves. | |||
==Current Research== | ==Current Research== | ||
1. Regulation of Resistance to copper in Xanthomonas axonopodis pv. Vesicatoria. (9) | |||
In this research, the scientist at the University of California, Riverside, attempt to identified the plasmid-borne copper resistance genes of X. axonopodis. Copper is required for eukaryotic and prokaryotic cells to maintain cell growth. However, having too much copper can be harmful to cells because it has the ability to generate free radicals which are able to damage DNA and lipid membranes. This is the reason why farmers spray copper on their plants in order to limit the bacteria population preying on plants. Unfortunately, as with all excessive use of chemicals on microorganisms, there are drawbacks that the bacteria would develop a detoxification system to protect themselves. As such, there are strains of X. axonopodis able to develop a copper resistance in their plasmid (9). The copABCD operon of X. axonopodis is specifically induced by copper. Thereby, expression of resistance to toxic levels of copper involves complex interactions between both plasmid and chromosomal genes (9). The experiment was conducted by isolating copper resistant strains of X. axonopodis from the tomato field of California. Then, dissemination of the plasmid copper resistance strands is needed in order to observe which cop genes are expressed for copper resistance. The result was copA express only in the presence of copper. However, full copper resistance is dependent on the presence of an intact copL gene, coupled with the ability to translate CopL. | |||
2. Comparative analysis of three indigenous plasmids from Xanthomonas axonopodis pv. Glycines. (10) | |||
In this experiment, the nucleotide sequences of three plasmids in X. axonopodis pv. Glycines were completed. These plasmids were named pAG1, pXAG81,and pXAG82. By determining the sequences of these plasmids from X. axonopodis, scientist will be able to understand how each gene is expressed. Therefore, they can figure out how to stop these bacteria and others like it from destroying crop fields. What makes X. axonopodis special is that its indigenous plasmids are temperate phage and cryptic, instead of just being cryptic like others plant pathogenic bacteria (10). In the study, 255 isolated X. axonopodis pv. Glycines were used and each subject had 3 of their plasmids sequenced. The result was shocking; two plasmids ( pAG1 and pXAG82) are variants of one prototype plasmid pXAG81. The plasmid pXAG81 was suggested to have gone through genetic rearrangement, resulting in the creation of the others two plasmids. | |||
3. Linkage and mapping of resistance genes to Xanthomonas axonopodis pv. Passiflorae in yellow passon fruit. (11) | |||
This experiment was conducted in order to determine if crosses between F1 population of passion fruit clones IAPAR-06 and IAPAR-123 can map resistance genes to X. axonopodis pv. Passiflorae (11). The method used was a 2-way pseudo-testcross mapping using markers that segregated in a 1:1 ratio. To determine the magnitude of bacteria resistance, the diseased leaf area was measured. Data concluded a bacteria resistance loci was found named QRLs, however more tests need to be done in order to discover more bacteria resistant genes. | |||
==References== | ==References== | ||
1) Taxnomoy. 1995. Xanthomonas [ncbi] | |||
2) The Genome Project. 2004. Xanthomomnas axonopodis [ncbi] | |||
3) Alegria, M, Souza, D., Andrade, M., Docena, C., Khater, L. “Identification of New Protein-Protein Interactions involving the products of the chromosome and plasmid-encoded type IV secretion loci of the Phytopathogen Xanthomonas axonopdis pv. Citri”. Journal of Bacteriology. 2005. Vol. 187. p.2315-2325. | |||
4) Citrus canker. 2005. [Wikipedia] | |||
5) Silva, D, Ferro, J., Reinach, F, Farah, C. “Comparison of the genomes of two Xantomonas pathogens with differing host specificities”. Nature. 2002. Vol. 417. p.459-463. | |||
6) Sugio, A., Yang, B., Zhu, T., White F. “Two type III effector genes of Xanthomona oryzae pv. Oryzae control the induction of the host genes OsTFIIAgamma1 and OsTFX1 during the bacterial blight of rice”. PubMed. 2007. | |||
7) Citrus canker. 1997. [Animal and Plant Health Inspction Service] | |||
8) Graham, J., Gottwald, T., Cuero, J., Achor, D. “Xanthomonas axonopodis pv. Citri: factors affecting successful eradication of citrus canker”. Molecular Plant Pathology. 2004. Vol. 5. p.1-15 | |||
9) Voloudakis, A., Reignier, T., Coksey, D. “Regulation of resistance to copper in Xanthomonas axonopodis pv. Vesicatoria”. Department of Plant Pathology, University of California, Riverside. 2004. | |||
10) Kim, J., Choi, S., Oh, J., Moon, J., Hwang, I. “Comparative analysis of three indigenous plasmids from Xanthomonas axonopodis pv. Glycines” Seoul National University. 2006. Vol. 56. p.79-87. | |||
11) Lopes, R., Lopes, M, Carneiro, M, Matta, P., Camargo, L., Vieira, M. “Linkage and mapping of resistance genes to Xanthomonas axonopodis pv. Passiflorae in yellow passion fruit”. Genome. 2006. Vol. 49. p.17-29. | |||
Edited by student of | Edited by Richard Phan, student of Rachel Larsen | ||
Latest revision as of 15:59, 16 September 2010
A Microbial Biorealm page on the genus Xanthomonas axonopodis
Classification
Higher order taxa
Xanthomonas axonopodis
Bacteria; Proteobaceria; Gammaproteobacteria, Xanthomonadales; Xanthomonadaceae; Xanthomonas(1)
Species
|
NCBI: Taxonomy |
Genus species: axonopodis
Description and significance
Xanthomonas axonopodis are proteobacteria and as with all proteobacteria they have a gram negative wall consisting of an outer membrane made up of lipopolysaccharide (LPS) and a phospholipid inner membrane (4). Their appearances are aerobic rod shape with polar flagella. X. axonopodis can be found cultivating on the leaves, stems, and fruit of citrus trees all around the world. They are mostly found in heavily citrus agricultural countries such as the United States, Australia, and Brazil. These bacteria are mainly known as plant pathogens that causes citrus cankers. The leaves, stems, and fruits that are infected with X. axonopodis display lesions which take on yellow halo or ring shaped appearances. They are so persistent that whole orchards have to be destroyed if X. axonopodis are present (5). In 1910, Xanthomonas were first reported and studied in the United States.
Genome structure
Their genome was sequenced in Sao Paulo, Brazil where they found X. axonopodis genome structures to contain a circular dsDNA chromosome with 5 mega base pairs and 4374 genes. Furthermore, the bacterium carries two plasmids, referred to as pXAC33 and pXAC64 (2). The two plasmids are 33 and 64 kilo base pairs long (3).
Cell structure and metabolism
The cell of X. axonopodis is a rod-shaped gram negative membrane with a polar flagella attached onto the membrane (3). The flagella allows the bacteria to move from lesion leaves of citrus trees to others trees infecting its host. Cellualse, protease and pectate lyase from Xanthomonas species have been suggested to play crucial roles in virulence and in bacterial nutrition. Xanthomonas possesses a Type III protein secretion system that is essential for pathogenicity in plants. This system is what causes the plants to become infected by inducing the hypersensitive response in resistant plants. The Type III protein system infects plants by inducing the expression of the host gene Os8N3, resulting in an increase of the host susceptibility (6).
Ecology
X. axonopodis have a parasitic relationship exclusively in plants where they cause citrus cankers on plants. They are most likely originated from southeastern Asia and spread to Japan, South Africa, Australia, the Pacific Islands, South America, and the United States (7). Usually trees that are infected with citrus canker bacteria, such as the X. axonopodis, are burned to prevent the spread of infection because it is difficult to control their rapidly spreading nature. Xanthomonas are an agriculturally devastating bacteria, in 1933 they caused more than 6 million dollars in damage in Florida alone which destroyed about 258,000 grove trees and 3 million nursery trees that had become infected. In 1998, Sao Paulo, Brazil suffered from a citrus canker outbreak where they had no choice but to destroy all infected trees as well as trees that were within a 30 meter radius of the infected trees.
Pathology
Xanthomonas are exclusively pathogenic to a large group of plants such as citrus trees, rice, cotton, beans, and grapes. They cause a highly contagious disease called citrus canker. Citrus canker can destroy an entire crop field, but does not pose any danger to humans or animals. The infection has a wide range of effects which include: defoliation, dieback, severely blemished fruit, reduced fruit quality, and premature fruit drop (8). Once the hosts are infected, X. axonopodis can spread like wildfire because of the many ways it can travel. Some examples of how it’s spread are by human movement of diseased citrus plants, use of contaminated equipment, or by fallen lesion leaves and fruits. Diseased leaves and fruits with lesions have a yellow halo or ring appearance. X. axonopodis would multiply if the lesions were expanding, but would die if it was on a surface facing sunlight. When the bacteria are not on leaves or fruits, it can survive by taking residence inside tree bark until it can transfer itself onto leaves or fruits. However, it can only survive for a few days if its host has fallen to the ground because its natural habitat has changed. This results because the bacteria now has to adapt to a new environment and find new sources for growth and reproduction. The two fundamental host determinants for citrus canker are the stage of leaf expansion and the resistance of mesophyll tissue. The host is most susceptible when its leaves expand ½ to 2/3, at this point the stomata open, but the leaf cuticle is not fully developed. During this time, the bacteria would take advantage of this opening and invade the leaves.
Current Research
1. Regulation of Resistance to copper in Xanthomonas axonopodis pv. Vesicatoria. (9) In this research, the scientist at the University of California, Riverside, attempt to identified the plasmid-borne copper resistance genes of X. axonopodis. Copper is required for eukaryotic and prokaryotic cells to maintain cell growth. However, having too much copper can be harmful to cells because it has the ability to generate free radicals which are able to damage DNA and lipid membranes. This is the reason why farmers spray copper on their plants in order to limit the bacteria population preying on plants. Unfortunately, as with all excessive use of chemicals on microorganisms, there are drawbacks that the bacteria would develop a detoxification system to protect themselves. As such, there are strains of X. axonopodis able to develop a copper resistance in their plasmid (9). The copABCD operon of X. axonopodis is specifically induced by copper. Thereby, expression of resistance to toxic levels of copper involves complex interactions between both plasmid and chromosomal genes (9). The experiment was conducted by isolating copper resistant strains of X. axonopodis from the tomato field of California. Then, dissemination of the plasmid copper resistance strands is needed in order to observe which cop genes are expressed for copper resistance. The result was copA express only in the presence of copper. However, full copper resistance is dependent on the presence of an intact copL gene, coupled with the ability to translate CopL.
2. Comparative analysis of three indigenous plasmids from Xanthomonas axonopodis pv. Glycines. (10) In this experiment, the nucleotide sequences of three plasmids in X. axonopodis pv. Glycines were completed. These plasmids were named pAG1, pXAG81,and pXAG82. By determining the sequences of these plasmids from X. axonopodis, scientist will be able to understand how each gene is expressed. Therefore, they can figure out how to stop these bacteria and others like it from destroying crop fields. What makes X. axonopodis special is that its indigenous plasmids are temperate phage and cryptic, instead of just being cryptic like others plant pathogenic bacteria (10). In the study, 255 isolated X. axonopodis pv. Glycines were used and each subject had 3 of their plasmids sequenced. The result was shocking; two plasmids ( pAG1 and pXAG82) are variants of one prototype plasmid pXAG81. The plasmid pXAG81 was suggested to have gone through genetic rearrangement, resulting in the creation of the others two plasmids.
3. Linkage and mapping of resistance genes to Xanthomonas axonopodis pv. Passiflorae in yellow passon fruit. (11) This experiment was conducted in order to determine if crosses between F1 population of passion fruit clones IAPAR-06 and IAPAR-123 can map resistance genes to X. axonopodis pv. Passiflorae (11). The method used was a 2-way pseudo-testcross mapping using markers that segregated in a 1:1 ratio. To determine the magnitude of bacteria resistance, the diseased leaf area was measured. Data concluded a bacteria resistance loci was found named QRLs, however more tests need to be done in order to discover more bacteria resistant genes.
References
1) Taxnomoy. 1995. Xanthomonas [ncbi]
2) The Genome Project. 2004. Xanthomomnas axonopodis [ncbi]
3) Alegria, M, Souza, D., Andrade, M., Docena, C., Khater, L. “Identification of New Protein-Protein Interactions involving the products of the chromosome and plasmid-encoded type IV secretion loci of the Phytopathogen Xanthomonas axonopdis pv. Citri”. Journal of Bacteriology. 2005. Vol. 187. p.2315-2325.
4) Citrus canker. 2005. [Wikipedia]
5) Silva, D, Ferro, J., Reinach, F, Farah, C. “Comparison of the genomes of two Xantomonas pathogens with differing host specificities”. Nature. 2002. Vol. 417. p.459-463.
6) Sugio, A., Yang, B., Zhu, T., White F. “Two type III effector genes of Xanthomona oryzae pv. Oryzae control the induction of the host genes OsTFIIAgamma1 and OsTFX1 during the bacterial blight of rice”. PubMed. 2007.
7) Citrus canker. 1997. [Animal and Plant Health Inspction Service]
8) Graham, J., Gottwald, T., Cuero, J., Achor, D. “Xanthomonas axonopodis pv. Citri: factors affecting successful eradication of citrus canker”. Molecular Plant Pathology. 2004. Vol. 5. p.1-15
9) Voloudakis, A., Reignier, T., Coksey, D. “Regulation of resistance to copper in Xanthomonas axonopodis pv. Vesicatoria”. Department of Plant Pathology, University of California, Riverside. 2004.
10) Kim, J., Choi, S., Oh, J., Moon, J., Hwang, I. “Comparative analysis of three indigenous plasmids from Xanthomonas axonopodis pv. Glycines” Seoul National University. 2006. Vol. 56. p.79-87.
11) Lopes, R., Lopes, M, Carneiro, M, Matta, P., Camargo, L., Vieira, M. “Linkage and mapping of resistance genes to Xanthomonas axonopodis pv. Passiflorae in yellow passion fruit”. Genome. 2006. Vol. 49. p.17-29.
Edited by Richard Phan, student of Rachel Larsen
