GlnR Activation Induces Peroxide Resistance in Mycobacterial Biofilms

Mycobacteria spontaneously form surface-associated multicellular communities, called biofilms, which display resistance to a wide range of exogenous stresses. A causal relationship between biofilm formation and emergence of stress resistance is not known. Here, we report that activation of a nitroge...

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Published inFrontiers in microbiology Vol. 9; p. 1428
Main Authors Yang, Yong, Richards, Jacob P, Gundrum, Jennifer, Ojha, Anil K
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 04.07.2018
Subjects
biofilms
GlnR
Microbiology
mycobacteria
peroxide
starvation
starvation
GlnR
peroxide
biofilms
mycobacteria
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Summary:Mycobacteria spontaneously form surface-associated multicellular communities, called biofilms, which display resistance to a wide range of exogenous stresses. A causal relationship between biofilm formation and emergence of stress resistance is not known. Here, we report that activation of a nitrogen starvation response regulator, GlnR, during the development of biofilms leads to peroxide resistance. The resistance arises from induction of a GlnR-dependent peroxide resistance ( ) gene cluster comprising of 8 ORFs (MSMEG_0565-0572). Expression of increases the NADPH to NADP ratio, suggesting that a reduced cytosolic environment of nitrogen-starved cells in biofilms contributes to peroxide resistance. Increased NADPH levels from activity likely support the activity of enzymes involved in nitrogen assimilation, as suggested by a higher threshold of nitrogen supplement required by a mutant to form biofilms. Together, our study uniquely interlinks a nutrient sensing mechanism with emergence of stress resistance during mycobacterial biofilm development. The gene cluster is conserved in several mycobacteria that can cause nosocomial infections, offering a possible explanation for their resistance to peroxide-based sterilization of medical equipment.
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Reviewed by: John T. Belisle, Colorado State University, United States; Tanya Parish, Infectious Disease Research Institute, United States
Edited by: Thomas Dick, Rutgers, The State University of New Jersey, Newark, United States
This article was submitted to Antimicrobials, Resistance and Chemotherapy, a section of the journal Frontiers in Microbiology
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2018.01428