This coming Friday, Mr. Ahmed M Al-Akash will present his research in Dr. Caguiat's laboratory. The title of his presentation is:
"Increased Expression of ompA, ompX, dedA, and gutS Benes in Enterobacter sp. YSU in the Presence of Selenite"
For background reading, see the following URL:
Mr. Ahmed M Al-Akash presented his research on the increased expression of OmpA, OmpX, DedA, and GutS genes in Enterobacter sp. YSU in the presence of selenite. Enterobacter sp. YSU is resistant to some heavy metal salts such as selenite. Previous studies have shown both specific and nonspecific uptake of selenite into the cell. OmpA, OmpX, DedA, and GutS are some membrane proteins that are involved in selenite uptake. The expression of these proteins increased with selenite presence in previous studies. In this study, RT-PCR of the genes for these proteins was expected to increase when the Enterobacter sp. YSU strain was grown in a selenite culture. RT-PCR concluded that selenite hurt Enterobacter sp. YSU stain growth, but it did not kill the cells. This is a result of selenite resistance. OmpA was heavily expressed with or without selenite while GutS expression was low. OmpX and DedA expression increased with selenite presence.
ReplyDeleteQuestion: Selenite resistance is important for Enterobacter sp. YSU strain survival. How does selenite enter and damage the cell?
Ahmed presented his research on gene expression Enterobacter sp. YSU and heavy metal and salt resistance. Selenite uptake is generally managed by the expression of the genes OmpA, OmpX, DedA, and GutS. In his research, Ahmen found that these genes do provide selenite resistance.
ReplyDeleteSelenite can enter the cell via specific channels or non-specific channels. Inside the cell, gene products and amino acid dimers can influence the uptake of selenite. As selenite, the salt is very toxic and can inhibit cellular growth. Certain proteins interact with selenite to create oxidative compounds that can destroy DNA and cellular structures.
Source:Jasenec, A., Barasa, N., Kulkarni, S., Shaik, N., Moparthi, S., Konda, V., & Caguiat, J. (2009). Proteomic profiling of L-cysteine induced selenite resistance in Enterobacter sp. YSU. Proteome Science, 7(1), 30. doi:10.1186/1477-5956-7-30
Ahmed did a great job presenting his findings on genes OmpA, OmpX, DedA, and GutS having resistance to selenite. I thought he provided great evidence on his findings.
ReplyDeleteAs Andrew said, selenite can enter E. coli cells two ways. Either by a specific pathway or by a non-specific pathway. In the specific pathway, selenite entered the cells through a channel dedicated for selenite. The specifics of this channel have not yet been identified. In the non-specific pathway, selenite entered the cells through a sulfate permease channel.
Source: Jasenec, A., Barasa, N., Kulkarni, S. et al. Proteomic profiling of L-cysteine induced selenite resistance in Enterobacter sp. YSU. Proteome Sci 7, 30 (2009). https://doi.org/10.1186/1477-5956-7-30
Ahmed gave an interesting presentation on increased expression of OmpA, OmpX, DedA, and GutS genes in Enterobacter sp. YSU in the presence of selenite.
ReplyDeleteSome studies show that selenite employs mechanisms involved in transport and metabolic conversion of essential nutrients to enter cells. Some of the transporters include oxyanions and phosphate transporters. Reducing agents like glutathione or other thiols found in growth media reduce selenite to hydrogen selenide, thus internalized into the cells to cause toxicity.
https://www.ncbi.nlm.nih.gov/pubmed/20688911/
I enjoyed the presentation given by Ahmed of the various different genes in Enterobacter sp. YSU while in the presence of selenite.
ReplyDeleteAs stated in the background reading, too much selenium can be toxic and damaging for a cell. Not only can it inhibit growth, but it can cause adverse reactions. For example, selenite racts with proteins containing thiol, like glutathione, to create highly reactice superoxides. These superoxides that were generated can kill cells by damaging DNA and lipids.