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Mechanism to control the cell lysis and the cell survival strategy in stationary phase under heat stress.

Noor R - Springerplus (2015)

Bottom Line: At the elevated temperatures, σ(E) also serves as the transcription factor for σ(H) (the main heat shock sigma factor, encoded by rpoH), which is involved in the expression of several genes whose products deal with the cytoplasmic unfolded proteins.Besides, oxidative stress in form of the reactive oxygen species (ROS) that accumulate due to heat stress, has been found to give rise to viable but non-culturable (VBNC) cells at the early stationary phase, which is in turn lysed by the σ(E)-dependent process.Such lysis of the defective cells may generate nutrients for the remaining population to survive with the capacity of formation of colony forming units (CFUs). σ(H) is also known to regulate the transcription of the major heat shock proteins (HSPs) required for heat shock response (HSR) resulting in cellular survival.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, Stamford University Bangladesh, 51 Siddeswari Road, Dhaka, 1217 Bangladesh.

ABSTRACT
An array of stress signals triggering the bacterial cellular stress response is well known in Escherichia coli and other bacteria. Heat stress is usually sensed through the misfolded outer membrane porin (OMP) precursors in the periplasm, resulting in the activation of σ(E) (encoded by rpoE), which binds to RNA polymerase to start the transcription of genes required for responding against the heat stress signal. At the elevated temperatures, σ(E) also serves as the transcription factor for σ(H) (the main heat shock sigma factor, encoded by rpoH), which is involved in the expression of several genes whose products deal with the cytoplasmic unfolded proteins. Besides, oxidative stress in form of the reactive oxygen species (ROS) that accumulate due to heat stress, has been found to give rise to viable but non-culturable (VBNC) cells at the early stationary phase, which is in turn lysed by the σ(E)-dependent process. Such lysis of the defective cells may generate nutrients for the remaining population to survive with the capacity of formation of colony forming units (CFUs). σ(H) is also known to regulate the transcription of the major heat shock proteins (HSPs) required for heat shock response (HSR) resulting in cellular survival. Present review concentrated on the cellular survival against heat stress employing the harmonized impact of σ(E) and σ(H) regulons and the HSPs as well as their inter connectivity towards the maintenance of cellular survival.

No MeSH data available.


Related in: MedlinePlus

Generation of heat shock and the consequent mechanism of σE-dependent cell lysis. a Functional analysis of sodA and katE genes, involved in the evolution of reactive oxygen species (ROS). Mutation in sodA (encoding superoxide dismutase) and katE (encoding catalase) induces the generation of ROS which may render the viable and culturable cells to be damaged or into the VBNC state, which in turn undergoes the σE-directed lysis. Thus the defective cells are removed and only the culturable cells sustain thereby suggesting the phenomenon of programmed cell death (PCD). The idea is supported by overexpressing the sodA (SodA clone) and katE genes (KatE clone) whereby the ROS accumulation is considerably suppressed with a concomitant downregulation of the rpoE gene (encoding σE). b Possible mechanism of σE-dependent cell lysis whereby the role of ROS has been shown in the formation of the VBNC cells which have further undergone the lysis process with a concominant increased downregulation of peptidyl prolyl isomerise (PpiD) and the simultaneous upregulation of the micA and rybB genes encoding small RNAs. The repression of the expression of the outer membrane porins (OMPs) have also been detected which might be responsible for the impairment of the cell membrane integrity thereby rendering the cells to be lyzed
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Fig5: Generation of heat shock and the consequent mechanism of σE-dependent cell lysis. a Functional analysis of sodA and katE genes, involved in the evolution of reactive oxygen species (ROS). Mutation in sodA (encoding superoxide dismutase) and katE (encoding catalase) induces the generation of ROS which may render the viable and culturable cells to be damaged or into the VBNC state, which in turn undergoes the σE-directed lysis. Thus the defective cells are removed and only the culturable cells sustain thereby suggesting the phenomenon of programmed cell death (PCD). The idea is supported by overexpressing the sodA (SodA clone) and katE genes (KatE clone) whereby the ROS accumulation is considerably suppressed with a concomitant downregulation of the rpoE gene (encoding σE). b Possible mechanism of σE-dependent cell lysis whereby the role of ROS has been shown in the formation of the VBNC cells which have further undergone the lysis process with a concominant increased downregulation of peptidyl prolyl isomerise (PpiD) and the simultaneous upregulation of the micA and rybB genes encoding small RNAs. The repression of the expression of the outer membrane porins (OMPs) have also been detected which might be responsible for the impairment of the cell membrane integrity thereby rendering the cells to be lyzed

Mentions: Afterward, on the basis of the suggestive data of accumulation of oxidative stresses (in the form of reactive oxygen species; i.e., ROS) at the early stationary phase (Desnues et al. 2003; Dukan and Nystrom 1999) to cause formation of VBNC cells (Cuny et al. 2005; Nystrom 2005a, b), the trigger of the lysis process was analyzed using the deletion mutant of katE (encoding catalase) and by over-expressing the sodA (encoding superoxide dismutase) and katE genes (Noor et al. 2009b). The deletion mutant of katE was noticed to result in the elevation of the amounts of intracellular ROS with a concomitant increase in VBNC cells which were further subjected to typical σE-dependent cell lysis (Noor et al. 2009b). Both the amount of ROS and cell lysis level were found to be significantly reduced by the overexpression of sodA and katE genes (Fig. 5a). Thus, together with the knowledge of roles of HSPs under the control of σE and σH regulons (as stated earlier), the discovery of the trigger of the lysis of both VBNC and the damaged cells of E. coli led to model the total survival mechanism under stresses condition (Figs. 2, 4 and 5a).Fig. 5


Mechanism to control the cell lysis and the cell survival strategy in stationary phase under heat stress.

Noor R - Springerplus (2015)

Generation of heat shock and the consequent mechanism of σE-dependent cell lysis. a Functional analysis of sodA and katE genes, involved in the evolution of reactive oxygen species (ROS). Mutation in sodA (encoding superoxide dismutase) and katE (encoding catalase) induces the generation of ROS which may render the viable and culturable cells to be damaged or into the VBNC state, which in turn undergoes the σE-directed lysis. Thus the defective cells are removed and only the culturable cells sustain thereby suggesting the phenomenon of programmed cell death (PCD). The idea is supported by overexpressing the sodA (SodA clone) and katE genes (KatE clone) whereby the ROS accumulation is considerably suppressed with a concomitant downregulation of the rpoE gene (encoding σE). b Possible mechanism of σE-dependent cell lysis whereby the role of ROS has been shown in the formation of the VBNC cells which have further undergone the lysis process with a concominant increased downregulation of peptidyl prolyl isomerise (PpiD) and the simultaneous upregulation of the micA and rybB genes encoding small RNAs. The repression of the expression of the outer membrane porins (OMPs) have also been detected which might be responsible for the impairment of the cell membrane integrity thereby rendering the cells to be lyzed
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4627973&req=5

Fig5: Generation of heat shock and the consequent mechanism of σE-dependent cell lysis. a Functional analysis of sodA and katE genes, involved in the evolution of reactive oxygen species (ROS). Mutation in sodA (encoding superoxide dismutase) and katE (encoding catalase) induces the generation of ROS which may render the viable and culturable cells to be damaged or into the VBNC state, which in turn undergoes the σE-directed lysis. Thus the defective cells are removed and only the culturable cells sustain thereby suggesting the phenomenon of programmed cell death (PCD). The idea is supported by overexpressing the sodA (SodA clone) and katE genes (KatE clone) whereby the ROS accumulation is considerably suppressed with a concomitant downregulation of the rpoE gene (encoding σE). b Possible mechanism of σE-dependent cell lysis whereby the role of ROS has been shown in the formation of the VBNC cells which have further undergone the lysis process with a concominant increased downregulation of peptidyl prolyl isomerise (PpiD) and the simultaneous upregulation of the micA and rybB genes encoding small RNAs. The repression of the expression of the outer membrane porins (OMPs) have also been detected which might be responsible for the impairment of the cell membrane integrity thereby rendering the cells to be lyzed
Mentions: Afterward, on the basis of the suggestive data of accumulation of oxidative stresses (in the form of reactive oxygen species; i.e., ROS) at the early stationary phase (Desnues et al. 2003; Dukan and Nystrom 1999) to cause formation of VBNC cells (Cuny et al. 2005; Nystrom 2005a, b), the trigger of the lysis process was analyzed using the deletion mutant of katE (encoding catalase) and by over-expressing the sodA (encoding superoxide dismutase) and katE genes (Noor et al. 2009b). The deletion mutant of katE was noticed to result in the elevation of the amounts of intracellular ROS with a concomitant increase in VBNC cells which were further subjected to typical σE-dependent cell lysis (Noor et al. 2009b). Both the amount of ROS and cell lysis level were found to be significantly reduced by the overexpression of sodA and katE genes (Fig. 5a). Thus, together with the knowledge of roles of HSPs under the control of σE and σH regulons (as stated earlier), the discovery of the trigger of the lysis of both VBNC and the damaged cells of E. coli led to model the total survival mechanism under stresses condition (Figs. 2, 4 and 5a).Fig. 5

Bottom Line: At the elevated temperatures, σ(E) also serves as the transcription factor for σ(H) (the main heat shock sigma factor, encoded by rpoH), which is involved in the expression of several genes whose products deal with the cytoplasmic unfolded proteins.Besides, oxidative stress in form of the reactive oxygen species (ROS) that accumulate due to heat stress, has been found to give rise to viable but non-culturable (VBNC) cells at the early stationary phase, which is in turn lysed by the σ(E)-dependent process.Such lysis of the defective cells may generate nutrients for the remaining population to survive with the capacity of formation of colony forming units (CFUs). σ(H) is also known to regulate the transcription of the major heat shock proteins (HSPs) required for heat shock response (HSR) resulting in cellular survival.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, Stamford University Bangladesh, 51 Siddeswari Road, Dhaka, 1217 Bangladesh.

ABSTRACT
An array of stress signals triggering the bacterial cellular stress response is well known in Escherichia coli and other bacteria. Heat stress is usually sensed through the misfolded outer membrane porin (OMP) precursors in the periplasm, resulting in the activation of σ(E) (encoded by rpoE), which binds to RNA polymerase to start the transcription of genes required for responding against the heat stress signal. At the elevated temperatures, σ(E) also serves as the transcription factor for σ(H) (the main heat shock sigma factor, encoded by rpoH), which is involved in the expression of several genes whose products deal with the cytoplasmic unfolded proteins. Besides, oxidative stress in form of the reactive oxygen species (ROS) that accumulate due to heat stress, has been found to give rise to viable but non-culturable (VBNC) cells at the early stationary phase, which is in turn lysed by the σ(E)-dependent process. Such lysis of the defective cells may generate nutrients for the remaining population to survive with the capacity of formation of colony forming units (CFUs). σ(H) is also known to regulate the transcription of the major heat shock proteins (HSPs) required for heat shock response (HSR) resulting in cellular survival. Present review concentrated on the cellular survival against heat stress employing the harmonized impact of σ(E) and σ(H) regulons and the HSPs as well as their inter connectivity towards the maintenance of cellular survival.

No MeSH data available.


Related in: MedlinePlus