The bacterial stress response enables bacteria to survive adverse and fluctuating conditions in their immediate surroundings.
The stress response in bacteria involves a complex network of elements that counteracts the external stimulus.
A complex network of global regulatory systems leads to a coordinated and effective response.
These regulatory systems govern the expression of more effectors that maintain stability of the cellular equilibrium under the various conditions.
[4][5] Stress response systems can play an important role in the virulence of pathogenic organisms.
[5] There are regulatory systems that respond to changes in temperature, pH, nutrients, salts, and oxidation.
The control elements also regulate the expression of genes during various environmental conditions including starvation, sporulation and others.
An initial stress response systems that will likely go into effect against situations that are damaging to the bacterial cell is chaperones.
Without the chaperones as a first line of defense, other stress response systems would not be able to react quickly enough to stop proteins from denaturing in time.
What this involves is proteins binding to promoter regions of DNA to regulate which sections are transcribed into RNA.
The concentration of different RNA transcripts is then altered to favor the production of those that will produce proteins that will mitigate the effects of the stimulus.
This is due to the cell being in a phosphate group, but this new response regulator will start to act like a transcription factor.
[11] When bacteria is in an area of very low and cold temperature, they will have a five hour long phase that will cause them not to grow at all.
The way the bacteria tries to adapt is by creating cold shock proteins that will be transcription factors that will be upregulated during the five hour phase.
And lastly, there is an enhancement when it comes to the survival of bacteria which helps the cell to get the food and nutrients it needs to survive[11] The SOS response is a bacterial adaptive response to DNA damage involving arrest of the cell cycle and the induction of processes that repair DNA damage.