vgrG Gene as a Virulence Factor in Burkholeria cepacia
2022
- 119Usage
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Usage119
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- Abstract Views31
Lecture / Presentation Description
Burkholderia cepacia is a gram-negative bacterium responsible for causing onion soft rot disease and has been identified as an infectious agent in people with cystic fibrosis. As this bacterium is naturally antibiotic resistant, it is important to understand the virulence factors that contribute to this bacterium’s pathogenicity. Through the use of transposon mutagenesis and bioinformatics, the vgrG gene was identified as a possible virulence factor for B. cepacia ATCC 25416. This gene encodes the tip protein of the Type Six Secretion System (T6SS), a complex structure found in many species of bacteria. In other organisms, this syringe-like system allows a bacterium to inject proteins into neighboring cells as a mechanism of interbacterial competition or for nutrient acquisition during infection. Here, the vgrG gene was disrupted by transposon mutagenesis and tests were performed on both this mutant and the wild-type strain of B. cepacia. I have found that expression of vgrG is not essential for survival of B. cepacia, suggesting that it is used for virulence in our infection model. Similarly, the vgrG mutant strain created smaller lesions compared to the wild-type strain in an onion model of infection, and preliminary data suggests that this mutant cannot establish an infection without a prior wound in the host. I am currently developing genetic methods that will allow me to test whether this gene is required for bacterial interactions, such as those required for biofilm generation and interbacterial competition. Together, these data will describe how vgrG and T6SS contribute to the virulence of B. cepacia.
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