Researchers
from the Max Planck Institute for Terrestrial Microbiology in Marburg have
described a previously unrecognized mechanism of bacterial transcriptional
regulation that is obviously widespread in bacteria. In the future, their
findings could also help fight antibiotic resistance.
Initiation
of transcription in bacteria only occurs upon the binding of a key component
known as the sigma factor (σ factor) to the RNA polymerase (RNAP) core enzyme
in order to form the complete and catalytically active holoenzyme. This
holoenzyme then recognizes key promotor elements and subsequently enables
transcription. During external stress conditions, the primary σ factor is
replaced by an alternative σ factor, which differs from the former with respect
to the promoter sequences that it recognizes. Thus, holoenzyme formation with
this alternative σ factor results in the transcription of corresponding
stress-response genes. Among the various classes of alternative σ factors, the
most abundant ones are the extracytoplasmic function (ECF) σ factors. Sigma
factors are commonly known to be intrinsically active, which means that the
bacterial cell has to keep them in an inactive state until their action is
warranted.
There
are several mechanisms for regulating σ factor activity. Usually, alternative σ
factors stay retained in an inactive state by sequestration into a complex with
an anti-σ factor. Upon a specific stimulus, the inhibitory effect of the anti-σ
factor is alleviated and the σ factor is released for interaction with the RNA
polymerase.
See:
Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)
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