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延伸因子 P 在大肠杆菌和铜绿假单胞菌中是可有可无的。

Elongation factor P is dispensable in Escherichia coli and Pseudomonas aeruginosa.

机构信息

Infectious Diseases Area, Novartis Institutes for BioMedical Research, 4560 Horton St., Emeryville, CA 94608, USA.

出版信息

Curr Microbiol. 2013 Sep;67(3):293-9. doi: 10.1007/s00284-013-0363-0. Epub 2013 Apr 17.

Abstract

Elongation factor P (EF-P) is a highly conserved ribosomal initiation factor responsible for stimulating formation of the first peptide bond. Its essentiality has been debated and may differ depending on the organism. Here, we demonstrate that EF-P is dispensable in Escherichia coli and Pseudomonas aeruginosa under laboratory growth conditions. Although knockouts are viable, growth rates are diminished compared with wild-type strains. Despite this cost in fitness, these mutants are not more susceptible to a wide range of antibiotics; including ribosome targeting antibiotics, such as lincomycin, chloramphenicol, and streptomycin, which have been shown previously to disrupt EF-P function in vitro. In Pseudomonas, knockout of efp leads to an upregulation of mexX, a phenotype previously observed with other genetic lesions affecting ribosome function and that can be induced by the treatment with antibiotics affecting protein synthesis.

摘要

延伸因子 P(EF-P)是一种高度保守的核糖体起始因子,负责刺激第一个肽键的形成。其必要性一直存在争议,并且可能因生物体而异。在这里,我们证明在实验室生长条件下,EF-P 在大肠杆菌和铜绿假单胞菌中是可有可无的。尽管敲除是可行的,但与野生型菌株相比,生长速度降低。尽管在适应性方面存在这种代价,但这些突变体对广泛的抗生素不更敏感;包括核糖体靶向抗生素,如林可霉素、氯霉素和链霉素,这些抗生素以前已被证明在体外破坏 EF-P 功能。在铜绿假单胞菌中,efp 的敲除导致 mexX 的上调,这是以前观察到的其他影响核糖体功能的遗传损伤的表型,并且可以通过用影响蛋白质合成的抗生素处理来诱导。

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