The role of the transcriptional repressor CssR in Corynebacterium glutamicum in response to phenolic compounds
Ju Zhang,
Yuying Zhao,
Zhaoxin Peng,
MingFei Yang,
Wenyu Zou,
Xinyu Wu,
Chenghui Wang,
Meiru Si,
Can Chen
Affiliations
Ju Zhang
Key Laboratory of Plant Genetics and Molecular Breeding, Henan Key Laboratory of Crop Molecular Breeding & Bioreactor, College of Life Science and Agronomy, Zhoukou Normal University, Zhoukou, 466001, Henan, China; College of Horticulture, Agricultural University of Hebei/Key Laboratory for Vegetable Germplasm Enhancement and Utilization of Hebei/Collaborative Innovation Center of Vegetable Industry in Hebei, Baoding, 071001, China
Yuying Zhao
College of Life Sciences, Qufu Normal University, Qufu, 273165, Shandong, China
Zhaoxin Peng
College of Life Sciences, Qufu Normal University, Qufu, 273165, Shandong, China
MingFei Yang
College of Life Sciences, Qufu Normal University, Qufu, 273165, Shandong, China
Wenyu Zou
College of Life Sciences, Qufu Normal University, Qufu, 273165, Shandong, China
Xinyu Wu
College of Life Sciences, Qufu Normal University, Qufu, 273165, Shandong, China
Chenghui Wang
College of Life Sciences, Qufu Normal University, Qufu, 273165, Shandong, China
Meiru Si
College of Life Sciences, Qufu Normal University, Qufu, 273165, Shandong, China; Corresponding author.
Can Chen
Key Laboratory of Plant Genetics and Molecular Breeding, Henan Key Laboratory of Crop Molecular Breeding & Bioreactor, College of Life Science and Agronomy, Zhoukou Normal University, Zhoukou, 466001, Henan, China; Corresponding author.
The cssR gene (ncgl1578) of Corynebacterium glutamicum encodes a repressor of the TetR (tetracycline regulator) family. Its role in the stress response to antibiotics/heavy metals has been investigated, but how CssR functions in response to phenolic compounds in C. glutamicum has been rarely studied. In this study, we applied transcriptomic analysis, β-galactosidase analysis, qRT-PCR, and EMSAs to analyze the target genes and functions of CssR in response to phenolic compounds. Consistent with the upregulation of genes involved in the degradation of phenolic compounds, the ΔcssR mutant was more resistant to various phenolic compounds than was the wild-type strain. Furthermore, the addition of phenolic compounds induced the expression of corresponding genes (ncgl0283, ncgl1032, ncgl1111, ncgl2920, ncgl2923, and ncgl2952) in vivo. However, the DNA binding activity of CssR to the promoter of phenolic compound-degrading genes was undetected in vitro. Additionally, we also found that CssR indirectly negatively regulates the expression of cell wall/membrane/envelope biogenesis-related genes, which may enhance resistance to stress caused by phenolic compounds. Together, our findings demonstrate that CssR is a key regulator that copes with stress conditions induced by phenolic compounds, thus greatly expanding our understanding of the functions of TetR family transcription factors.
