Science, asked by psingla177, 4 months ago

how do variation provide stability to population?? give example of bacteria population to explain...

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Answered by Anonymous
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Answered by usha1911983
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Bacterial populations can undergo rapid turnover in both time and space, and these can be highly useful in understanding the natural ecological processes, and can act as excellent indicators of eutrophication (Borneman & Triplett, 1997;

From: Freshwater Microbiology, 2019

Related terms:

BiofilmBacteriophagesBacteriumInfectious AgentMutationMicrofloraMicroorganismIntestine FloraEscherichia coli

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Antibiotic Lethality and Membrane Bioenergetics

Martin I. Voskuil, ... Nicholas D. Walter, in Advances in Microbial Physiology, 2018

3.3 Influence of Toxins on pH Homeostasis and Antibiotic Lethality

Bacterial populations employ native defenses against antibiotics that are analogous to the activity of protonophores. These mechanisms disrupt membrane electrochemical gradients that enable bacterial populations to establish subpopulations of drug-tolerant persisters. Foremost among these mechanisms are the toxin–antitoxin modules that slow bacterial growth by a variety of mechanisms (Hall, Gollan, & Helaine, 2017). It is noteworthy that these toxins are generally not lethal, but are bacteriostatic at high levels suggestive that they act more akin to bacteriostatic drugs.

Verstraeten et al. demonstrate that drug tolerance in E. coli and P. aeruginosa emanates from a cascade of events leading to HokB-mediated membrane potential disruption (Verstraeten et al., 2015). The GTPase Obg responds in a stochastic manner to the stringent response through (p)ppGpp and increases levels of the HokB membrane toxin in a small percentage of bacteria. The presence of HokB establishes a bet-hedging strategy to ensure that a portion of the population survives an environmental challenge. In light of the pH homeostasis hypothesis of antibiotic lethality, it appears that HokB permits proton reentry, thereby depolarizing the membrane and relieving intracellular alkalization.

In E. coli, the TisB toxin is induced by the SOS response and confers multiple drug tolerance (Dorr, Vulic, & Lewis, 2010). TisB is an antibiotic peptide that establishes membrane anion channels. This disrupts pmf and ATP synthesis and initiates a dormant state (Dorr et al., 2010; Gurnev, Ortenberg, Dorr, Lewis, & Bezrukov, 2012; Unoson & Wagner, 2008). The SOS response is induced not only by DNA damage but also by alkaline stress (Padan, Bibi, Ito, & Krulwich, 2005), suggesting the SOS response may also assist in countering the effects of alkalization. However, further research is needed to establish whether these toxins confer antibiotic tolerance because of their impact on membrane bioenergetics or solely because they slow growth.

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