Mechanism of HrcA function in heat shock regulation in Mycobacterium tuberculosis

Hakiem, Owais R.; Parijat, Priyanka; Tripathi, Prajna; Batra, Janendra K.

doi:10.1016/j.biochi.2019.11.012

Cited by 8 publications

(7 citation statements)

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“…Instead, we assumed that the observed changes represent downstream effects and hypothesized that the differentially expressed genes had a common regulator. Four of the nine genes ( dnaK , groEL2 , rv0990c , and rv3224 ) are specifically associated with HrcA, which directly regulates transcription of groEL2 , the groES-groEL1 and rv0991c-rv0990c operons, and its own expression, i.e., the hrcA-dnaJ2 operon ( 22 , 24 ). To ensure that expression of groEL2 was restored to wild-type levels in the complemented strain, we performed qRT-PCR on RNA extracted from three biological replicates of wild-type H37Rv, Δ sfdS , and the complemented strain.…”

Section: Resultsmentioning

confidence: 99%

The Mycobacterium tuberculosis sRNA F6 Modifies Expression of Essential Chaperonins, GroEL2 and GroES

et al. 2021

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Section: Resultsmentioning

confidence: 99%

The Mycobacterium tuberculosis sRNA F6 Modifies Expression of Essential Chaperonins, GroEL2 and GroES

et al. 2021

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“…Both dnaK and groEL operons, regulated negatively by hspR and hrcA in M. tuberculosis get upregulated under heat stress. As HrcA is shown to sequester HspR (Hakiem et al, 2020), it will be interesting to know which repressor protein, HrcA or HspR is upregulated first after heat shock. We analysed the change in the transcription levels of the hrcA and hspR in M. tuberculosis CDC1551 after temperature up-shift to 42°C.…”

Section: Early Onset Of Hrca Expression Under Heat Shockmentioning

confidence: 99%

“…A similar inverted repeat was identified upstream of the groE gene of M. tuberculosis and downstream of the transcription start sites of the Clostridium acetobutylicum groE and dnaK operons. In M. tuberculosis, HrcA negatively regulates the groES and groEL2 operons and binds a CIRCE like DNA element present in the upstream region of HrcA gene (Hakiem et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

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Role of HrcA in stress management in Mycobacterium tuberculosis

Hakiem

Batra

2022

Journal of Applied Microbiology

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Aim:The current study aims to understand the role of HrcA in stress response of M.tuberculosis. Methods and Results:In this study, using an hrcA knock out mutant of M. tuberculosis it is demonstrated that the heat shock repressor, HrcA is important for countering environmental stresses pathogen faces within the host during the infection process. Also, with scanning electron microscopy, it has been shown that HrcA plays a role in maintaining the morphology and cell size of the pathogen as disruption of the hrcA gene resulted in significantly elongated bacilli. Furthermore, heat shock proteins like ClpC1, ClpB, DnaK, GroEL2, GroEL1, DnaJ2 and GroES were detected in the secretome of M. tuberculosis by mass spectrometric analysis. The study also demonstrates a strong humoral response against M. tuberculosis heat shock proteins in H 37 R v -infected mice sera. Conclusion:The study establishes that though hrcA is not an essential gene for M. tuberculosis, it regulates the expression of heat shock proteins during infection and disruption of hrcA gives a survival advantage to the pathogen during stress conditions. Significance and Impact of the Study:HrcA plays an important role in maintaining a fine balance of heat shock proteins during infection to give adequate survival advantage and also evade immune detection.

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“…Transcription of groEL2 is controlled by the HrcA heat shock repressor, which also regulates the groES-groEL1 and rv0991c-rv0990c operons as well as its own expression, i.e. the hrcA-dnaJ2 operon (28,29). To determine if the observed changes in groEL2 expression could be associated with transcriptional control by HrcA, we also measured the expression of the first gene in each of these operons i.e.…”

Section: Deletion Of Sfds Leads To Upregulation Of Essential Chaperoninsmentioning

confidence: 99%

TheMycobacterium tuberculosissRNA F6 modifies expression of essential chaperonins, GroEL2 and GroES

Houghton¹,

Rodgers

Rose

et al. 2020

Preprint

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Almost 140 years after the identification of Mycobacterium tuberculosis as the etiological agent of tuberculosis, important aspects of its biology remain poorly described. Little is known about the role of post-transcriptional control of gene expression and RNA biology, including the role of most of the small RNAs (sRNAs) identified to date. We have carried out a detailed investigation of the M. tuberculosis sRNA, F6, and show it to be dependent on SigF for expression and significantly induced during in vitro starvation and in a mouse model of infection. However, we found no evidence of attenuation of a ΔF6 strain within the first 20 weeks of infection. A further exploration of F6 using in vitro models of infection suggests a role for F6 as a highly specific regulator of the heat shock repressor, HrcA. Our results point towards a role for F6 during periods of low metabolic activity similar to cold shock and associated with nutrient starvation such as that found in human granulomas in later stages of infection.

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Mechanism of HrcA function in heat shock regulation in Mycobacterium tuberculosis

Cited by 8 publications

References 53 publications

The Mycobacterium tuberculosis sRNA F6 Modifies Expression of Essential Chaperonins, GroEL2 and GroES

The Mycobacterium tuberculosis sRNA F6 Modifies Expression of Essential Chaperonins, GroEL2 and GroES

Role of HrcA in stress management in Mycobacterium tuberculosis

TheMycobacterium tuberculosissRNA F6 modifies expression of essential chaperonins, GroEL2 and GroES

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