期刊论文详细信息
BMC Microbiology
Activation of gab cluster transcription in Bacillus thuringiensis by γ-aminobutyric acid or succinic semialdehyde is mediated by the Sigma 54-dependent transcriptional activator GabR
Fuping Song1  Jie Zhang1  Pengyue Wang2  Guannan Wang2  Lili Han1  Wei Wang2  Min Yang1  Qi Peng1 
[1] State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, China;College of Life Sciences, Northeast Agriculture University, Harbin, China
关键词: PAS domain;    SSA;    GABA;    Sigma 54;    GabR;   
Others  :  1090494
DOI  :  10.1186/s12866-014-0306-3
 received in 2014-06-30, accepted in 2014-11-24,  发布年份 2014
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【 摘 要 】

Background

Bacillus thuringiensis GabR is a Sigma 54-dependent transcriptional activator containing three typical domains, an N-terminal regulatory domain Per-ARNT-Sim (PAS), a central AAA+ (ATPases associated with different cellular activities) domain and a C-terminal helix-turn-helix (HTH) DNA binding domain. GabR positively regulates the expression of the gabT gene of the gab gene cluster, which is responsible for the γ-aminobutyric acid (GABA) shunt.

Results

Purified GabR was shown to specifically bind to a repeat region that mapped 58 bp upstream of the gabT start codon. The specific signal factors GABA and succinic semialdehyde (SSA) activated gabT expression, whereas GABA- and SSA-inducible gabT transcription was abolished in sigL and gabR mutants. GABA and SSA did not induce the expression of either SigL or GabR. Deletion of the PAS domain of GabR resulted in increased gabT transcriptional activity, both in the presence and absence of GABA.

Conclusions

This study identified the GabR-binding site on the gabT promoter; however, GabR does not bind to its own promoter. gabT transcription is induced by GABA and SSA, and inducible expression is dependent on SigL and activated by GabR. The PAS domain in GabR is repressing its enhancer transcriptional activity on the gabT promoter. Repression is released upon GABA addition, whereupon transcription is induced.

【 授权许可】

   
2014 Peng et al.; licensee BioMed Central.

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