Antitoxin DinJ influences the general stress response through transcript stabilizer CspE.

Area of Science:

• Microbiology
• Molecular Biology
• Bacterial Stress Response

Background:

• Toxin/antitoxin (TA) systems are crucial for bacterial survival and regulation.
• Antitoxins are increasingly recognized for roles beyond self-regulation, impacting broader cellular processes.
• Previous work showed antitoxin MqsA represses the stationary-phase sigma factor RpoS.

Purpose of the Study:

• To investigate the physiological role of antitoxin DinJ from the YafQ/DinJ TA pair.
• To determine how DinJ influences the general stress response in Escherichia coli.
• To elucidate the molecular mechanism by which DinJ affects RpoS levels.

Main Methods:

• Investigated physiological roles of DinJ by measuring RpoS levels and related phenotypes.
• Utilized transcriptome analysis to identify potential DinJ targets.
• Performed DNA-binding assays to confirm direct repression.
• Assessed the impact of CspE inactivation on DinJ's effect on RpoS.

Main Results:

• DinJ production led to decreased RpoS levels, affecting phenotypes like catalase activity and cell adhesion.
• DinJ was found to directly repress the expression of cspE at the LexA palindrome.
• Cold-shock protein CspE enhances the translation of rpoS mRNA.
• Inactivation of CspE abolished DinJ's ability to modulate RpoS levels.

Conclusions:

• Antitoxin DinJ indirectly regulates the general stress response by repressing cspE.
• The mechanism involves DinJ's control over CspE, which in turn affects RpoS translation.
• This study reveals a novel regulatory pathway linking TA systems to bacterial stress adaptation.