Difference between revisions of "Part:BBa K729001"
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===Description=== | ===Description=== | ||
| − | The protein IrrE originates from Deinococcus radiodurans, where it confers resistance to radiation. When transformed into E. Coli however, it protected against salt, oxidative and thermal shock. IrrE appears to function as a global regulator of stress factor genes. So far it has been demonstrated to upregulate transcription of recA and pprA – genes which encode Recombinase A and Radiation Inducible Protein. With respect to salt tolerance, IrrE upregulates the production of several stress responsive proteins, protein kinases, metabolic proteins, and detoxification proteins. It also downregulates glycerol degradation. With this global regulatory effect, E. Coli becomes more salt tolerant. | + | The protein IrrE originates from ''Deinococcus radiodurans'', where it confers resistance to radiation. When transformed into ''E. Coli'' however, it protected against salt, oxidative and thermal shock. IrrE appears to function as a global regulator of stress factor genes. So far it has been demonstrated to upregulate transcription of recA and pprA – genes which encode Recombinase A and Radiation Inducible Protein. With respect to salt tolerance, IrrE upregulates the production of several stress responsive proteins, protein kinases, metabolic proteins, and detoxification proteins. It also downregulates glycerol degradation. With this global regulatory effect, ''E. Coli'' becomes more salt tolerant. |
===Characterisation=== | ===Characterisation=== | ||
Revision as of 22:40, 16 September 2012
irrE from Deinococcus radiodurans
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21COMPATIBLE WITH RFC[21]
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000COMPATIBLE WITH RFC[1000]
Description
The protein IrrE originates from Deinococcus radiodurans, where it confers resistance to radiation. When transformed into E. Coli however, it protected against salt, oxidative and thermal shock. IrrE appears to function as a global regulator of stress factor genes. So far it has been demonstrated to upregulate transcription of recA and pprA – genes which encode Recombinase A and Radiation Inducible Protein. With respect to salt tolerance, IrrE upregulates the production of several stress responsive proteins, protein kinases, metabolic proteins, and detoxification proteins. It also downregulates glycerol degradation. With this global regulatory effect, E. Coli becomes more salt tolerant.
Characterisation
IrrE is deduced to globally regulate gene expression in E. Coli, and to date, no specific assay allows for the convenient determination of IrrE expression. As such, the expression of IrrE will be determined indirectly by determining the increased salt tolerance of our cells. In order to confirm this, we will be conducting growth curve experiments. This will allow us to determine if our cell grow to a higher density in high salinity when compared to the untransformed cells.