Limits...
Adaptation to sustained nitrogen starvation by Escherichia coli requires the eukaryote-like serine/threonine kinase YeaG.

Figueira R, Brown DR, Ferreira D, Eldridge MJ, Burchell L, Pan Z, Helaine S, Wigneshweraraj S - Sci Rep (2015)

Bottom Line: The mechanism by which yeaG acts, involves the transcriptional repression of two toxin/antitoxin modules, mqsR/mqsA and dinJ/yafQ.This, consequently, has a positive effect on the expression of rpoS, the master regulator of the general bacterial stress response.Overall, results indicate that yeaG is required to fully execute the rpoS-dependent gene expression program to allow E. coli to adapt to sustained N starvation and unravels a novel facet to the regulatory basis that underpins adaptive response to N stress.

View Article: PubMed Central - PubMed

Affiliation: MRC Centre for Molecular Microbiology and Infection, Imperial College London, UK.

ABSTRACT
The Escherichia coli eukaryote-like serine/threonine kinase, encoded by yeaG, is expressed in response to diverse stresses, including nitrogen (N) starvation. A role for yeaG in bacterial stress response is unknown. Here we reveal for the first time that wild-type E. coli displays metabolic heterogeneity following sustained periods of N starvation, with the metabolically active population displaying compromised viability. In contrast, such heterogeneity in metabolic activity is not observed in an E. coli ∆yeaG mutant, which continues to exist as a single and metabolically active population and thus displays an overall compromised ability to survive sustained periods of N starvation. The mechanism by which yeaG acts, involves the transcriptional repression of two toxin/antitoxin modules, mqsR/mqsA and dinJ/yafQ. This, consequently, has a positive effect on the expression of rpoS, the master regulator of the general bacterial stress response. Overall, results indicate that yeaG is required to fully execute the rpoS-dependent gene expression program to allow E. coli to adapt to sustained N starvation and unravels a novel facet to the regulatory basis that underpins adaptive response to N stress.

No MeSH data available.


Related in: MedlinePlus

The yeaG-dependent adaptive response to sustained N starvation involves the transcriptional repression of mqsR/mqsA and dinJ/yafQ toxin-antitoxin genes.(A) Expression levels of ten E. coli TA gene pairs in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N-starved conditions and normalised to 16S expression. Error bars represent sd (n = 2; except mqsR/mqsA, where n = 4). (B–D) Expression levels of cspD, rpoS and cspE in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N starved conditions and normalised to 16S expression. Error bars represent sd (n = 4). (E) Levels of RpoS are reduced in ∆yeaG mutant strain following 24 h N starvation. Representative immunoblot of whole-cell extracts of bacterial cells sampled after 20 min and 24 h of N starvation probed with anti-RpoS and anti-DnaK (loading control) antibody. Graph shows quantification of bands by densitometry (n = 3), calculated as the ratio in Optical Density between the bands corresponding to RpoS and DnaK. Error bars represent sd (n = 4). (F) RpoS-dependent catalase activity is impaired in the ∆yeaG mutant strain following 24 h of N starvation. Catalase activity was assessed as a function of concentration of H2O2 remaining in solution after incubation with 24 h N-starved wild-type, ∆yeaG or ∆katE bacterial lysates. Error bars represent sd (n = 3). (G) Deletion of dinJ/yafQ and mqsR/mqsA TA modules in the ∆yeaG strain leads to complementation of the mutant phenotype, whilst deletion of only one TA modules in the ∆yeaG strain leads to only partial complementation. The ‘recovery’ growth curves for wild-type, ∆yeaG, ∆dinJ∆yafQ∆yeaG, ∆mqsR∆mqsA∆yeaG and ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG mutant strains were obtained by OD600nm readings at hourly time points. (H.) Expression levels of sdhB, rpsV, katE, pdhR, bolA and poxB at N-24 calculated as fold change in mRNA between the wild-type and ∆yeaG mutant strain and normalised to 16S expression. Error bars represent sd (n = 3). Statistical analyses for all data-sets were performed by Student’s t test (*P < 0.05; **P < 0.01) relative to the wild-type strain.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4664914&req=5

f5: The yeaG-dependent adaptive response to sustained N starvation involves the transcriptional repression of mqsR/mqsA and dinJ/yafQ toxin-antitoxin genes.(A) Expression levels of ten E. coli TA gene pairs in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N-starved conditions and normalised to 16S expression. Error bars represent sd (n = 2; except mqsR/mqsA, where n = 4). (B–D) Expression levels of cspD, rpoS and cspE in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N starved conditions and normalised to 16S expression. Error bars represent sd (n = 4). (E) Levels of RpoS are reduced in ∆yeaG mutant strain following 24 h N starvation. Representative immunoblot of whole-cell extracts of bacterial cells sampled after 20 min and 24 h of N starvation probed with anti-RpoS and anti-DnaK (loading control) antibody. Graph shows quantification of bands by densitometry (n = 3), calculated as the ratio in Optical Density between the bands corresponding to RpoS and DnaK. Error bars represent sd (n = 4). (F) RpoS-dependent catalase activity is impaired in the ∆yeaG mutant strain following 24 h of N starvation. Catalase activity was assessed as a function of concentration of H2O2 remaining in solution after incubation with 24 h N-starved wild-type, ∆yeaG or ∆katE bacterial lysates. Error bars represent sd (n = 3). (G) Deletion of dinJ/yafQ and mqsR/mqsA TA modules in the ∆yeaG strain leads to complementation of the mutant phenotype, whilst deletion of only one TA modules in the ∆yeaG strain leads to only partial complementation. The ‘recovery’ growth curves for wild-type, ∆yeaG, ∆dinJ∆yafQ∆yeaG, ∆mqsR∆mqsA∆yeaG and ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG mutant strains were obtained by OD600nm readings at hourly time points. (H.) Expression levels of sdhB, rpsV, katE, pdhR, bolA and poxB at N-24 calculated as fold change in mRNA between the wild-type and ∆yeaG mutant strain and normalised to 16S expression. Error bars represent sd (n = 3). Statistical analyses for all data-sets were performed by Student’s t test (*P < 0.05; **P < 0.01) relative to the wild-type strain.

Mentions: Toxin-Antitoxin (TA) genes, which are ubiquitous in bacteria, are key effectors that link bacterial growth to the nutritional status of the bacterial cell16. Most widely studied TA modules consist of two genes in an operon, which encode for a stable toxin that disrupts essential cellular processes, leading to reversible growth arrest, and a labile antitoxin that forms a tight complex with the toxin and neutralises its effect17. The ratio between toxin and antitoxin has important implications in how bacterial cells adapt to stress. During nutritional starvation the antitoxin is degraded, thus generating sufficient free toxin to influence the metabolic status and induce population heterogeneity17. Since results in Fig. 4 reveal that E. coli adjusts its metabolism in response to sustained N starvation, resulting in a metabolically heterogeneous population, we decided to investigate the relative expression levels of ten known E. coli TA gene pairs in ∆yeaG and wild-type cells following 24 h N starvation. Results showed that the mRNA levels of the mqsR/mqsA TA module to be increased by 2.0 ± 0.9/1.8 ± 0.7 fold in wild-type bacteria following 24 h of N starvation compared to N+ conditions (Fig. 5A). Notably, we detected an even larger increase in mRNA levels corresponding to mqsR/mqsA, by 3.7-fold ± 1.6/3.5-fold ± 1.4 fold in the ∆yeaG mutant strain following 24 h of N starvation compared to N+ conditions (Fig. 5A). Further, in the ∆yeaG mutant strain another TA module, dinJ/yafQ, was upregulated by 2.8 ± 0.9/2.7 ± 1.3 fold, following 24 h of N starvation compared to N+ conditions. In contrast, dinJ/yafQ was not upregulated in the wild-type strain (Fig. 5A). We next focused on the biology of mqsR/mqsA and dinJ/yafQ to decipher how both of these TA modules could contribute to the properties of the ∆yeaG mutant strain: The mqsR/mqsA TA module is linked to regulation of the general stress response because it directly represses the transcription of rpoS, which encodes for σ38, the RNA polymerase associated σ factor that is responsible for executing the general bacterial stress response, and cspD, which encodes for the cold-shock protein D, a DNA replication inhibitor1819. Consistent with the increased levels of mqsR/mqsA mRNA levels in 24 h N-starved ∆yeaG mutant compared to wild-type strain (Fig. 5A), mRNA levels of both rpoS and cspD genes were reduced by 2.8 ± 0.8 fold and 3.92 ± 0.77 fold respectively in 24 h N-starved ∆yeaG mutant compared to wild-type strain (Fig. 5B,C). Similarly, DinJ, the toxin component of the dinJ/yafQ TA module, has been implicated in reducing σ38 levels through directly repressing the transcription of cspE, which in turn positively affects σ38 translation through stabilisation of rpoS mRNA20. Consistent with the increased levels of dinJ/yafQ mRNA in the ∆yeaG mutant compared to the wild-type strain following 24 h of N starvation (Fig. 5A), cspE mRNA levels were reduced by 4.26 ± 1.82 fold in the ∆yeaG mutant compared to the wild-type strain (Fig. 5D). To further corroborate these results, we compared σ38 protein levels and activity, which we expected to be reduced in ∆yeaG mutant relative to the wild-type strain following 24 h N starvation: As shown in Fig. 5E, σ38 levels were 1.7 ± 0.3 fold reduced in the ∆yeaG compared to the wild-type strain. Since the transcription of katG and katE, the genes encoding two catalases capable of converting harmful hydrogen peroxide (H2O2) into water and oxygen is σ38-dependent and thus serves as a surrogate for σ38 activity, we compared catalase activity in the wild-type, ∆yeaG and ∆katE mutant bacteria. Levels of H2O2 remaining in solution were quantified following incubation with whole-cell lysates from the three strains following 24 h of N starvation. Although the effect was not as accentuated as with the ∆katE mutant strain, the catalase activity of the ∆yeaG mutant strain was significantly reduced compared to that of the wild-type strain (Fig. 5F), consistent with the reduced levels of σ38 in the ∆yeaG mutant strain (Fig. 5E). Next, to directly link the property of the ∆yeaG mutant strain is mediated by the differences in the levels of expression of mqsR/mqsA and dinJ/yafQ, we constructed ∆dinJ∆yafQ∆yeaG and ∆mqsR∆mqsA∆yeaG triple deletion mutants as well as a ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG quintuple deletion mutant. As shown in Fig. 5G, and as expected, the ‘recovery’ growth curve of the ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG mutant strain almost fully resembled that of the wild-type strain, whilst those of the ∆dinJ∆yafQ∆yeaG and ∆mqsR∆mqsA∆yeaG mutant strains partly resembled that of the mutant strain. Overall, we conclude that the yeaG-dependent adaptive response to sustained N starvation is mediated by the transcriptional repression of both mqsR/mqsA and dinJ/yafQ in E. coli cells that experience sustained N starvation. The absence of yeaG results in the transcriptional de-repression of mqsR/mqsA and dinJ/yafQ transcription, which, as a consequence, has a detrimental effect on σ38-dependent transcriptional programme in the adaptive response to sustained N starvation. To further substantiate this view, we compared the expression levels of selected genes that are either positively (rpsV, katE, pdhR, bolA and poxB) or negatively (sdhB) regulated by the σ38 containing RNA polymerase by qRT-PCR in the ∆yeaG mutant and wild-type strains following 24 h of N starvation. Consistent with the results obtained so far, four out of five of the genes (katE, pdhR, bolA and poxB) that are subjected to positive regulation by σ38 showed reduced levels of expression in the ∆yeaG mutant strain; the expression level of rpsV did not significantly differ in the ∆yeaG mutant and wild-type strains following 24 h of N starvation (Fig. 5H). Whereas sdhB is negatively regulated by the σ38 containing RNA polymerase in the stationary phase of growth in rich medium through promoter occlusion21, it seems that reduced σ38 levels in the ∆yeaG strain does not detectably affect the expression levels of sdhB in 24 h N-starved E. coli.


Adaptation to sustained nitrogen starvation by Escherichia coli requires the eukaryote-like serine/threonine kinase YeaG.

Figueira R, Brown DR, Ferreira D, Eldridge MJ, Burchell L, Pan Z, Helaine S, Wigneshweraraj S - Sci Rep (2015)

The yeaG-dependent adaptive response to sustained N starvation involves the transcriptional repression of mqsR/mqsA and dinJ/yafQ toxin-antitoxin genes.(A) Expression levels of ten E. coli TA gene pairs in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N-starved conditions and normalised to 16S expression. Error bars represent sd (n = 2; except mqsR/mqsA, where n = 4). (B–D) Expression levels of cspD, rpoS and cspE in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N starved conditions and normalised to 16S expression. Error bars represent sd (n = 4). (E) Levels of RpoS are reduced in ∆yeaG mutant strain following 24 h N starvation. Representative immunoblot of whole-cell extracts of bacterial cells sampled after 20 min and 24 h of N starvation probed with anti-RpoS and anti-DnaK (loading control) antibody. Graph shows quantification of bands by densitometry (n = 3), calculated as the ratio in Optical Density between the bands corresponding to RpoS and DnaK. Error bars represent sd (n = 4). (F) RpoS-dependent catalase activity is impaired in the ∆yeaG mutant strain following 24 h of N starvation. Catalase activity was assessed as a function of concentration of H2O2 remaining in solution after incubation with 24 h N-starved wild-type, ∆yeaG or ∆katE bacterial lysates. Error bars represent sd (n = 3). (G) Deletion of dinJ/yafQ and mqsR/mqsA TA modules in the ∆yeaG strain leads to complementation of the mutant phenotype, whilst deletion of only one TA modules in the ∆yeaG strain leads to only partial complementation. The ‘recovery’ growth curves for wild-type, ∆yeaG, ∆dinJ∆yafQ∆yeaG, ∆mqsR∆mqsA∆yeaG and ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG mutant strains were obtained by OD600nm readings at hourly time points. (H.) Expression levels of sdhB, rpsV, katE, pdhR, bolA and poxB at N-24 calculated as fold change in mRNA between the wild-type and ∆yeaG mutant strain and normalised to 16S expression. Error bars represent sd (n = 3). Statistical analyses for all data-sets were performed by Student’s t test (*P < 0.05; **P < 0.01) relative to the wild-type strain.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664914&req=5

f5: The yeaG-dependent adaptive response to sustained N starvation involves the transcriptional repression of mqsR/mqsA and dinJ/yafQ toxin-antitoxin genes.(A) Expression levels of ten E. coli TA gene pairs in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N-starved conditions and normalised to 16S expression. Error bars represent sd (n = 2; except mqsR/mqsA, where n = 4). (B–D) Expression levels of cspD, rpoS and cspE in wild-type and ∆yeaG mutant strain calculated as fold change in mRNA between N+ and N-24 h N starved conditions and normalised to 16S expression. Error bars represent sd (n = 4). (E) Levels of RpoS are reduced in ∆yeaG mutant strain following 24 h N starvation. Representative immunoblot of whole-cell extracts of bacterial cells sampled after 20 min and 24 h of N starvation probed with anti-RpoS and anti-DnaK (loading control) antibody. Graph shows quantification of bands by densitometry (n = 3), calculated as the ratio in Optical Density between the bands corresponding to RpoS and DnaK. Error bars represent sd (n = 4). (F) RpoS-dependent catalase activity is impaired in the ∆yeaG mutant strain following 24 h of N starvation. Catalase activity was assessed as a function of concentration of H2O2 remaining in solution after incubation with 24 h N-starved wild-type, ∆yeaG or ∆katE bacterial lysates. Error bars represent sd (n = 3). (G) Deletion of dinJ/yafQ and mqsR/mqsA TA modules in the ∆yeaG strain leads to complementation of the mutant phenotype, whilst deletion of only one TA modules in the ∆yeaG strain leads to only partial complementation. The ‘recovery’ growth curves for wild-type, ∆yeaG, ∆dinJ∆yafQ∆yeaG, ∆mqsR∆mqsA∆yeaG and ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG mutant strains were obtained by OD600nm readings at hourly time points. (H.) Expression levels of sdhB, rpsV, katE, pdhR, bolA and poxB at N-24 calculated as fold change in mRNA between the wild-type and ∆yeaG mutant strain and normalised to 16S expression. Error bars represent sd (n = 3). Statistical analyses for all data-sets were performed by Student’s t test (*P < 0.05; **P < 0.01) relative to the wild-type strain.
Mentions: Toxin-Antitoxin (TA) genes, which are ubiquitous in bacteria, are key effectors that link bacterial growth to the nutritional status of the bacterial cell16. Most widely studied TA modules consist of two genes in an operon, which encode for a stable toxin that disrupts essential cellular processes, leading to reversible growth arrest, and a labile antitoxin that forms a tight complex with the toxin and neutralises its effect17. The ratio between toxin and antitoxin has important implications in how bacterial cells adapt to stress. During nutritional starvation the antitoxin is degraded, thus generating sufficient free toxin to influence the metabolic status and induce population heterogeneity17. Since results in Fig. 4 reveal that E. coli adjusts its metabolism in response to sustained N starvation, resulting in a metabolically heterogeneous population, we decided to investigate the relative expression levels of ten known E. coli TA gene pairs in ∆yeaG and wild-type cells following 24 h N starvation. Results showed that the mRNA levels of the mqsR/mqsA TA module to be increased by 2.0 ± 0.9/1.8 ± 0.7 fold in wild-type bacteria following 24 h of N starvation compared to N+ conditions (Fig. 5A). Notably, we detected an even larger increase in mRNA levels corresponding to mqsR/mqsA, by 3.7-fold ± 1.6/3.5-fold ± 1.4 fold in the ∆yeaG mutant strain following 24 h of N starvation compared to N+ conditions (Fig. 5A). Further, in the ∆yeaG mutant strain another TA module, dinJ/yafQ, was upregulated by 2.8 ± 0.9/2.7 ± 1.3 fold, following 24 h of N starvation compared to N+ conditions. In contrast, dinJ/yafQ was not upregulated in the wild-type strain (Fig. 5A). We next focused on the biology of mqsR/mqsA and dinJ/yafQ to decipher how both of these TA modules could contribute to the properties of the ∆yeaG mutant strain: The mqsR/mqsA TA module is linked to regulation of the general stress response because it directly represses the transcription of rpoS, which encodes for σ38, the RNA polymerase associated σ factor that is responsible for executing the general bacterial stress response, and cspD, which encodes for the cold-shock protein D, a DNA replication inhibitor1819. Consistent with the increased levels of mqsR/mqsA mRNA levels in 24 h N-starved ∆yeaG mutant compared to wild-type strain (Fig. 5A), mRNA levels of both rpoS and cspD genes were reduced by 2.8 ± 0.8 fold and 3.92 ± 0.77 fold respectively in 24 h N-starved ∆yeaG mutant compared to wild-type strain (Fig. 5B,C). Similarly, DinJ, the toxin component of the dinJ/yafQ TA module, has been implicated in reducing σ38 levels through directly repressing the transcription of cspE, which in turn positively affects σ38 translation through stabilisation of rpoS mRNA20. Consistent with the increased levels of dinJ/yafQ mRNA in the ∆yeaG mutant compared to the wild-type strain following 24 h of N starvation (Fig. 5A), cspE mRNA levels were reduced by 4.26 ± 1.82 fold in the ∆yeaG mutant compared to the wild-type strain (Fig. 5D). To further corroborate these results, we compared σ38 protein levels and activity, which we expected to be reduced in ∆yeaG mutant relative to the wild-type strain following 24 h N starvation: As shown in Fig. 5E, σ38 levels were 1.7 ± 0.3 fold reduced in the ∆yeaG compared to the wild-type strain. Since the transcription of katG and katE, the genes encoding two catalases capable of converting harmful hydrogen peroxide (H2O2) into water and oxygen is σ38-dependent and thus serves as a surrogate for σ38 activity, we compared catalase activity in the wild-type, ∆yeaG and ∆katE mutant bacteria. Levels of H2O2 remaining in solution were quantified following incubation with whole-cell lysates from the three strains following 24 h of N starvation. Although the effect was not as accentuated as with the ∆katE mutant strain, the catalase activity of the ∆yeaG mutant strain was significantly reduced compared to that of the wild-type strain (Fig. 5F), consistent with the reduced levels of σ38 in the ∆yeaG mutant strain (Fig. 5E). Next, to directly link the property of the ∆yeaG mutant strain is mediated by the differences in the levels of expression of mqsR/mqsA and dinJ/yafQ, we constructed ∆dinJ∆yafQ∆yeaG and ∆mqsR∆mqsA∆yeaG triple deletion mutants as well as a ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG quintuple deletion mutant. As shown in Fig. 5G, and as expected, the ‘recovery’ growth curve of the ∆dinJ∆yafQ∆mqsR∆mqsA∆yeaG mutant strain almost fully resembled that of the wild-type strain, whilst those of the ∆dinJ∆yafQ∆yeaG and ∆mqsR∆mqsA∆yeaG mutant strains partly resembled that of the mutant strain. Overall, we conclude that the yeaG-dependent adaptive response to sustained N starvation is mediated by the transcriptional repression of both mqsR/mqsA and dinJ/yafQ in E. coli cells that experience sustained N starvation. The absence of yeaG results in the transcriptional de-repression of mqsR/mqsA and dinJ/yafQ transcription, which, as a consequence, has a detrimental effect on σ38-dependent transcriptional programme in the adaptive response to sustained N starvation. To further substantiate this view, we compared the expression levels of selected genes that are either positively (rpsV, katE, pdhR, bolA and poxB) or negatively (sdhB) regulated by the σ38 containing RNA polymerase by qRT-PCR in the ∆yeaG mutant and wild-type strains following 24 h of N starvation. Consistent with the results obtained so far, four out of five of the genes (katE, pdhR, bolA and poxB) that are subjected to positive regulation by σ38 showed reduced levels of expression in the ∆yeaG mutant strain; the expression level of rpsV did not significantly differ in the ∆yeaG mutant and wild-type strains following 24 h of N starvation (Fig. 5H). Whereas sdhB is negatively regulated by the σ38 containing RNA polymerase in the stationary phase of growth in rich medium through promoter occlusion21, it seems that reduced σ38 levels in the ∆yeaG strain does not detectably affect the expression levels of sdhB in 24 h N-starved E. coli.

Bottom Line: The mechanism by which yeaG acts, involves the transcriptional repression of two toxin/antitoxin modules, mqsR/mqsA and dinJ/yafQ.This, consequently, has a positive effect on the expression of rpoS, the master regulator of the general bacterial stress response.Overall, results indicate that yeaG is required to fully execute the rpoS-dependent gene expression program to allow E. coli to adapt to sustained N starvation and unravels a novel facet to the regulatory basis that underpins adaptive response to N stress.

View Article: PubMed Central - PubMed

Affiliation: MRC Centre for Molecular Microbiology and Infection, Imperial College London, UK.

ABSTRACT
The Escherichia coli eukaryote-like serine/threonine kinase, encoded by yeaG, is expressed in response to diverse stresses, including nitrogen (N) starvation. A role for yeaG in bacterial stress response is unknown. Here we reveal for the first time that wild-type E. coli displays metabolic heterogeneity following sustained periods of N starvation, with the metabolically active population displaying compromised viability. In contrast, such heterogeneity in metabolic activity is not observed in an E. coli ∆yeaG mutant, which continues to exist as a single and metabolically active population and thus displays an overall compromised ability to survive sustained periods of N starvation. The mechanism by which yeaG acts, involves the transcriptional repression of two toxin/antitoxin modules, mqsR/mqsA and dinJ/yafQ. This, consequently, has a positive effect on the expression of rpoS, the master regulator of the general bacterial stress response. Overall, results indicate that yeaG is required to fully execute the rpoS-dependent gene expression program to allow E. coli to adapt to sustained N starvation and unravels a novel facet to the regulatory basis that underpins adaptive response to N stress.

No MeSH data available.


Related in: MedlinePlus