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Redox-dependent condensation of the mycobacterial nucleoid by WhiB4.

Abstract：

:Oxidative stress response in bacteria is mediated through coordination between the regulators of oxidant-remediation systems (e.g. OxyR, SoxR) and nucleoid condensation (e.g. Dps, Fis). However, these genetic factors are either absent or rendered non-functional in the human pathogen Mycobacterium tuberculosis (Mtb). Therefore, how Mtb organizes genome architecture and regulates gene expression to counterbalance oxidative imbalance is unknown. Here, we report that an intracellular redox-sensor, WhiB4, dynamically links genome condensation and oxidative stress response in Mtb. Disruption of WhiB4 affects the expression of genes involved in maintaining redox homeostasis, central metabolism, and respiration under oxidative stress. Notably, disulfide-linked oligomerization of WhiB4 in response to oxidative stress activates the protein's ability to condense DNA. Further, overexpression of WhiB4 led to hypercondensation of nucleoids, redox imbalance and increased susceptibility to oxidative stress, whereas WhiB4 disruption reversed this effect. In accordance with the findings in vitro, ChIP-Seq data demonstrated non-specific binding of WhiB4 to GC-rich regions of the Mtb genome. Lastly, data indicate that WhiB4 deletion affected the expression of ~ 30% of genes preferentially bound by the protein, suggesting both direct and indirect effects on gene expression. We propose that WhiB4 structurally couples Mtb's response to oxidative stress with genome organization and transcription.

journal_name

Redox Biol

journal_title

Redox biology

authors

Chawla M,Mishra S,Anand K,Parikh P,Mehta M,Vij M,Verma T,Singh P,Jakkala K,Verma HN,AjitKumar P,Ganguli M,Narain Seshasayee AS,Singh A

doi

10.1016/j.redox.2018.08.006

subject

Has Abstract

pub_date

2018-10-01 00:00:00

pages

116-133

issn

2213-2317

pii

S2213-2317(18)30642-6

journal_volume

19

pub_type

杂志文章

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