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The conserved transcriptional regulator CdnL is required for metabolic homeostasis and morphogenesis in Caulobacter
Author(s) -
Selamawit Abi Woldemeskel,
Allison K. Daitch,
Laura Álvarez,
Gaël Panis,
Rilee Zeinert,
Diego González,
Erika Smith,
Justine Collier,
Peter Chien,
Felipe Cava,
Patrick H. Viollier,
Erin D. Goley
Publication year - 2020
Publication title -
plos genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.587
H-Index - 233
eISSN - 1553-7404
pISSN - 1553-7390
DOI - 10.1371/journal.pgen.1008591
Subject(s) - caulobacter crescentus , biology , regulator , transcriptional regulation , microbiology and biotechnology , morphogenesis , nad+ kinase , transcription factor , homeostasis , regulation of gene expression , biochemistry , gene , cell cycle , enzyme
Bacterial growth and division require regulated synthesis of the macromolecules used to expand and replicate components of the cell. Transcription of housekeeping genes required for metabolic homeostasis and cell proliferation is guided by the sigma factor σ 70 . The conserved CarD-like transcriptional regulator, CdnL, associates with promoter regions where σ 70 localizes and stabilizes the open promoter complex. However, the contributions of CdnL to metabolic homeostasis and bacterial physiology are not well understood. Here, we show that Caulobacter crescentus cells lacking CdnL have severe morphological and growth defects. Specifically, ΔcdnL cells grow slowly in both rich and defined media, and are wider, more curved, and have shorter stalks than WT cells. These defects arise from transcriptional downregulation of most major classes of biosynthetic genes, leading to significant decreases in the levels of critical metabolites, including pyruvate, α-ketoglutarate, ATP, NAD + , UDP-N-acetyl-glucosamine, lipid II, and purine and pyrimidine precursors. Notably, we find that ΔcdnL cells are glutamate auxotrophs, and Δ cdnL is synthetic lethal with other genetic perturbations that limit glutamate synthesis and lipid II production. Our findings implicate CdnL as a direct and indirect regulator of genes required for metabolic homeostasis that impacts morphogenesis through availability of lipid II and other metabolites.

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