Department of Microbiology, Cornell University, Ithaca, New York, USA.
Department of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, New York, USA.
J Bacteriol. 2023 Feb 22;205(2):e0037022. doi: 10.1128/jb.00370-22. Epub 2023 Jan 18.
The universally conserved protein elongation factor P (EF-P) facilitates translation at amino acids that form peptide bonds with low efficiency, particularly polyproline tracts. Despite its wide conservation, it is not essential in most bacteria and its physiological role remains unclear. Here, we show that EF-P affects the process of sporulation initiation in the bacterium Bacillus subtilis. We observe that the lack of EF-P delays expression of sporulation-specific genes. Using ribosome profiling, we observe that expression of , encoding a transcription factor that functions as the master regulator of sporulation, is lower in a Δ strain than the wild type. Ectopic expression of Spo0A rescues the sporulation initiation phenotype, indicating that reduced expression explains the sporulation defect in Δ cells. Since Spo0A is the earliest sporulation transcription factor, these data suggest that sporulation initiation can be delayed when protein synthesis is impaired. Elongation factor P (EF-P) is a universally conserved translation factor that prevents ribosome stalling at amino acids that form peptide bonds with low efficiency, particularly polyproline tracts. Phenotypes associated with EF-P deletion are pleiotropic, and the mechanistic basis underlying many of these phenotypes is unclear. Here, we show that the absence of EF-P affects the ability of B. subtilis to initiate sporulation by preventing normal expression of Spo0A, the key transcriptional regulator of this process. These data illustrate a mechanism that accounts for the sporulation delay and further suggest that cells are capable of sensing translation stress before committing to sporulation.
普遍存在的蛋白质延伸因子 P(EF-P)促进与低效率形成肽键的氨基酸的翻译,特别是多脯氨酸链。尽管它广泛存在,但在大多数细菌中并非必需,其生理作用仍不清楚。在这里,我们表明 EF-P 影响细菌枯草芽孢杆菌中孢子形成起始的过程。我们观察到缺乏 EF-P 会延迟孢子形成特异性基因的表达。使用核糖体谱分析,我们观察到编码转录因子的基因的表达低于野生型。该转录因子作为孢子形成的主调控因子,在Δ菌株中表达较低。Spo0A 的异位表达挽救了孢子形成起始表型,表明在Δ细胞中表达减少解释了孢子形成缺陷。由于 Spo0A 是最早的孢子形成转录因子,这些数据表明当蛋白质合成受损时,孢子形成起始可以被延迟。延伸因子 P(EF-P)是一种普遍存在的翻译因子,可防止核糖体在与低效率形成肽键的氨基酸处停滞,特别是多脯氨酸链。与 EF-P 缺失相关的表型是多效的,并且许多这些表型的机制基础尚不清楚。在这里,我们表明 EF-P 的缺失通过阻止 Spo0A 的正常表达来影响枯草芽孢杆菌启动孢子形成的能力,Spo0A 是该过程的关键转录调节剂。这些数据说明了一种机制,该机制解释了孢子形成的延迟,并进一步表明细胞在开始孢子形成之前能够感知翻译应激。