Mediating Arboviruses using Wolbachia Bacteria: Difference between revisions
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== | == Wolbachia Cell Structure and Genome== | ||
Wolbachia bacteria were discovered in 1924 when a scientist found the bacteria in Culex pipiens, a mosquito species (Teixeira L, Ferreira Á, Ashburner M., 2008). Studies focusing on Wolbachia became more popular in the 1970s when scientists from UCLA discovered the bacteria’s ability to carry out cytoplasmic incompatibility by looking at mortality in mosquito populations. | Wolbachia bacteria were discovered in 1924 when a scientist found the bacteria in Culex pipiens, a mosquito species (Teixeira L, Ferreira Á, Ashburner M., 2008). Studies focusing on Wolbachia became more popular in the 1970s when scientists from UCLA discovered the bacteria’s ability to carry out cytoplasmic incompatibility by looking at mortality in mosquito populations. | ||
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It is estimated that Wolbachia infects around 20% of all insect species. Wolbachia is a monophyletic clade of alpha-proteobacteria that infects a wide array of invertebrates. Wolbachia is an intracellular bacteria, meaning that it replicates in the cytoplasm of its host (Serbus L. et al 2008). Wolbachia lack many of the genes associated with membrane biogenesis meaning they lack the ability to synthesize lipid A, which is a typical feature of proteobacteria membranes (Foster, J., 2005). Wolbachia is a non-mobile, rod-like, gram-negative bacteria, with a circular chromosome. Wolbachia is closely related to the genus Francisella as well as being closely related to Ehrlichia, Anaplasma and Rickettsia, all disease-causing bacteria. However, Wolbachia, unlike its close bacteria relatives, does not infect vertebrates (Werren Lab Wolbachia Biology). Wolbachia can not be cultured in isolation (Scholz, M et al. 2020). This means that it is particularly difficult to sequence Wolbachia alone, and it is often co-sequenced with the host organism. This can lead to contamination of the Wolbachia genome with the host genome. Mavingui, P et al. (2012) sequenced the Wolbachia wAlbB genome. The study found that the genome has around 1,239,814 bp, with about a 33.7% GC content. There are roughly 1,209 protein-coding sequences each with an average length of 849 bp. Wolbachia has 2 rRNA operons, one of them is used in Wolbachia’s most famous ability, cytoplasmic incompatibility. The study also showed that there are a significant amount of protein families that are present only in the wAlbB strain, suggesting that there are potentially specific genes for specific interactions with other microorganisms and hosts (Mavingui, P. et al. 2012). | It is estimated that Wolbachia infects around 20% of all insect species. Wolbachia is a monophyletic clade of alpha-proteobacteria that infects a wide array of invertebrates. Wolbachia is an intracellular bacteria, meaning that it replicates in the cytoplasm of its host (Serbus L. et al 2008). Wolbachia lack many of the genes associated with membrane biogenesis meaning they lack the ability to synthesize lipid A, which is a typical feature of proteobacteria membranes (Foster, J., 2005). Wolbachia is a non-mobile, rod-like, gram-negative bacteria, with a circular chromosome. Wolbachia is closely related to the genus Francisella as well as being closely related to Ehrlichia, Anaplasma and Rickettsia, all disease-causing bacteria. However, Wolbachia, unlike its close bacteria relatives, does not infect vertebrates (Werren Lab Wolbachia Biology). Wolbachia can not be cultured in isolation (Scholz, M et al. 2020). This means that it is particularly difficult to sequence Wolbachia alone, and it is often co-sequenced with the host organism. This can lead to contamination of the Wolbachia genome with the host genome. Mavingui, P et al. (2012) sequenced the Wolbachia wAlbB genome. The study found that the genome has around 1,239,814 bp, with about a 33.7% GC content. There are roughly 1,209 protein-coding sequences each with an average length of 849 bp. Wolbachia has 2 rRNA operons, one of them is used in Wolbachia’s most famous ability, cytoplasmic incompatibility. The study also showed that there are a significant amount of protein families that are present only in the wAlbB strain, suggesting that there are potentially specific genes for specific interactions with other microorganisms and hosts (Mavingui, P. et al. 2012). | ||
Currently, three strains of Wolbachia have been sequenced. As stated earlier, Wolbachia can not be made into isolated cultures and thus sequenced independently from their host. Therefore, each strain represents Wolbachia infections in different host species. The host species include, Drosophila melanogaster, a common fruit fly, Culex quinquefasciatus, a mosquito, and Brugia malayi, a nematode. The first strain, which infects the common fruit fly, appears to exclusively use cytoplasmic incompatibility. Comparisons of these strains have suggested that recombination and horizontal gene transfer occurs in all of the Wolbachia strains (Klasson et al. 2009). Moreover, a recent study calculated that about three-fourths of the genes that were looked at in the experiment were affected by recombination (Klasson et al. 2009). | Currently, three strains of Wolbachia have been sequenced. As stated earlier, Wolbachia can not be made into isolated cultures and thus sequenced independently from their host. Therefore, each strain represents Wolbachia infections in different host species. The host species include, Drosophila melanogaster, a common fruit fly, Culex quinquefasciatus, a mosquito, and Brugia malayi, a nematode. The first strain, which infects the common fruit fly, appears to exclusively use cytoplasmic incompatibility. Comparisons of these strains have suggested that recombination and horizontal gene transfer occurs in all of the Wolbachia strains (Klasson et al. 2009). Moreover, a recent study calculated that about three-fourths of the genes that were looked at in the experiment were affected by recombination (Klasson et al. 2009). | ||
==Mechanism of Wolbachia Infection== | ==Mechanism of Wolbachia Infection== | ||
Wolbachia infection results in reproductive manipulations in host organisms through male killing, feminization, parthenogenesis (reproduction without male sperm), or cytoplasmic incompatibility (CI) (Klasson et al. 2009). Cytoplasmic incompatibility is the most common reproductive manipulation used by Wolbachia. Reproductive manipulations in the host organism enables further replication of the bacteria. Cytoplasmic incompatibility works to spread Wolbachia bacteria because uninfected females that mate with infected males will not be able to produce offspring. Whereas, offspring from either an infected female and an infected male, will produce viable offspring. Giving a reproductive advantage for insects who carry the Wolbachia infection (Klasson et al. 2009). | Wolbachia infection results in reproductive manipulations in host organisms through male killing, feminization, parthenogenesis (reproduction without male sperm), or cytoplasmic incompatibility (CI) (Klasson et al. 2009). Cytoplasmic incompatibility is the most common reproductive manipulation used by Wolbachia. Reproductive manipulations in the host organism enables further replication of the bacteria. Cytoplasmic incompatibility works to spread Wolbachia bacteria because uninfected females that mate with infected males will not be able to produce offspring. Whereas, offspring from either an infected female and an infected male, will produce viable offspring. Giving a reproductive advantage for insects who carry the Wolbachia infection (Klasson et al. 2009). | ||
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Wolbachia Cell Structure and Genome
Wolbachia bacteria were discovered in 1924 when a scientist found the bacteria in Culex pipiens, a mosquito species (Teixeira L, Ferreira Á, Ashburner M., 2008). Studies focusing on Wolbachia became more popular in the 1970s when scientists from UCLA discovered the bacteria’s ability to carry out cytoplasmic incompatibility by looking at mortality in mosquito populations.
It is estimated that Wolbachia infects around 20% of all insect species. Wolbachia is a monophyletic clade of alpha-proteobacteria that infects a wide array of invertebrates. Wolbachia is an intracellular bacteria, meaning that it replicates in the cytoplasm of its host (Serbus L. et al 2008). Wolbachia lack many of the genes associated with membrane biogenesis meaning they lack the ability to synthesize lipid A, which is a typical feature of proteobacteria membranes (Foster, J., 2005). Wolbachia is a non-mobile, rod-like, gram-negative bacteria, with a circular chromosome. Wolbachia is closely related to the genus Francisella as well as being closely related to Ehrlichia, Anaplasma and Rickettsia, all disease-causing bacteria. However, Wolbachia, unlike its close bacteria relatives, does not infect vertebrates (Werren Lab Wolbachia Biology). Wolbachia can not be cultured in isolation (Scholz, M et al. 2020). This means that it is particularly difficult to sequence Wolbachia alone, and it is often co-sequenced with the host organism. This can lead to contamination of the Wolbachia genome with the host genome. Mavingui, P et al. (2012) sequenced the Wolbachia wAlbB genome. The study found that the genome has around 1,239,814 bp, with about a 33.7% GC content. There are roughly 1,209 protein-coding sequences each with an average length of 849 bp. Wolbachia has 2 rRNA operons, one of them is used in Wolbachia’s most famous ability, cytoplasmic incompatibility. The study also showed that there are a significant amount of protein families that are present only in the wAlbB strain, suggesting that there are potentially specific genes for specific interactions with other microorganisms and hosts (Mavingui, P. et al. 2012).
Currently, three strains of Wolbachia have been sequenced. As stated earlier, Wolbachia can not be made into isolated cultures and thus sequenced independently from their host. Therefore, each strain represents Wolbachia infections in different host species. The host species include, Drosophila melanogaster, a common fruit fly, Culex quinquefasciatus, a mosquito, and Brugia malayi, a nematode. The first strain, which infects the common fruit fly, appears to exclusively use cytoplasmic incompatibility. Comparisons of these strains have suggested that recombination and horizontal gene transfer occurs in all of the Wolbachia strains (Klasson et al. 2009). Moreover, a recent study calculated that about three-fourths of the genes that were looked at in the experiment were affected by recombination (Klasson et al. 2009).
Mechanism of Wolbachia Infection
Wolbachia infection results in reproductive manipulations in host organisms through male killing, feminization, parthenogenesis (reproduction without male sperm), or cytoplasmic incompatibility (CI) (Klasson et al. 2009). Cytoplasmic incompatibility is the most common reproductive manipulation used by Wolbachia. Reproductive manipulations in the host organism enables further replication of the bacteria. Cytoplasmic incompatibility works to spread Wolbachia bacteria because uninfected females that mate with infected males will not be able to produce offspring. Whereas, offspring from either an infected female and an infected male, will produce viable offspring. Giving a reproductive advantage for insects who carry the Wolbachia infection (Klasson et al. 2009). Until recently many scientists believed that Wolbachia transmission only occurred from mother to offspring. However, recent developments in the field have indicated that Wolbachia participate in horizontal gene transfer. However, it still appears that horizontal gene transfer is relatively rare. The main mode of transmission of Wolbachia remains vertical transmission (Scholz, M et al. 2020).
After infecting a host, Wolbachia disrupts the reproductive development of the host in one of these four ways:
Parthenogenesis occurs when female offspring undergo fertilization without sperm. As a result, all of the offspring are female. Consequently, Wolbachia transmission to the next generation doubles. Parthenogenesis mostly affects Arthropod species (Werren Lab Wolbachia Biology).
Feminization in infected host species results in the conversion of infected males into females. It is possible that feminization infections can be transmitted to the next generation too. Feminization occurs most often in the terrestrial isopod order Oniscidae. Wolbachia-induced feminization in insects also occurs in Lepidoptera and Hemiptera. No other insects are reported to undergo Wolbachia-induced feminization (Werren Lab Wolbachia Biology).
The third mechanism used by the bacteria Wolbachia is male killing, which is, as the name suggests, when males are killed by the infection. This phenotype only evolved as a way to increase the survival of female siblings. Wolbachia, therefore, only uses male killing when competition between siblings is high. Male killing occurs in Diptera, Coleoptera and Lepidoptera, as well as in pseudoscorpions (Werren Lab Wolbachia Biology).
Lastly, Wolbachia induces cytoplasmic incompatibility in host organisms. As described earlier cytoplasmic incompatibility occurs when infected males are unable to produce viable offspring with an uninfected female, while producing surviving offspring with infected females. Cytoplasmic incompatibility affects a wide range of species including Acari, Coleoptera, Diptera, Isopoda, Lepidoptera, Hymenoptera, Homoptera and Orthoptera (Werren Lab Wolbachia Biology).
The exact mechanism by which Wolbachia engages in cytoplasmic incompatibility is unknown, however, there are a few models that might be able to predict how it works. The cif operon in Wolbachia appears to facilitate cytoplasmic incompatibility. CidB and CinB genes downstream on the cif operon induce cytoplasmic incompatibility. Upstream on the cif operon cidA and cinA encode proteins that bind to CidB and CinB genes. It is hypothesized that CidB ubiquitylates a target, such as Kap-α2, limiting its function. Overexpression and duplication of Kap-α2 blocks Y chromosome-bearing sperm from maturing. A process that looks similar to processes associated with cytoplasmic incompatibility (Beckmann et al., 2019).
During cytoplasmic incompatibility the first departure from the normal development of zygotes occurs is an impaired H3.3 histone. The H3 histone proteins facilitate cell division during spindle formation. Next, the activity of kinase CDK1, which prompts the transitions from metaphase to anaphase, is delayed. This delay often leads to chromosome shearing and bridging during anaphase. This error that occurs in anaphase is lethal for diploid insects (Beckmann et al., 2019).
Section 3
Include some current research, with at least one figure showing data.
Section 4
Conclusion
References
Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2022, Kenyon College
