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鉴定淋病奈瑟菌中参与厌氧不饱和脂肪酸合成的保守蛋白:对缺乏 FabA 的兼性和专性厌氧菌的意义。

Identification of a conserved protein involved in anaerobic unsaturated fatty acid synthesis in Neiserria gonorrhoeae: implications for facultative and obligate anaerobes that lack FabA.

机构信息

Department of Microbiology and Immunology, School of Medicine and Dentistry, University of Rochester, Box 672, 601 Elmwood Ave, Rochester, NY 14642, USA.

出版信息

Mol Microbiol. 2011 Oct;82(2):489-501. doi: 10.1111/j.1365-2958.2011.07826.x. Epub 2011 Sep 19.

Abstract

Transcriptome analysis of the facultative anaerobe, Neisseria gonorrhoeae, revealed that many genes of unknown function were induced under anaerobic conditions. Mutation of one such gene, NGO1024, encoding a protein belonging to the 2-nitropropane dioxygenase-like superfamily of proteins, was found to result in an inability of gonococci to grow anaerobically. Anaerobic growth of an NG1024 mutant was restored upon supplementation with unsaturated fatty acids (UFA), but not with the saturated fatty acid palmitate. Gonococcal fatty acid profiles confirmed that NGO1024 was involved in UFA synthesis anaerobically, but not aerobically, demonstrating that gonococci contain two distinct pathways for the production of UFAs, with a yet unidentified aerobic mechanism, and an anaerobic mechanism involving NGO1024. Expression of genes involved in classical anaerobic UFA synthesis, fabA, fabM and fabB, was toxic in gonococci and unable to complement a NGO1024 mutation, suggesting that the chemistry involved in gonococcal anaerobic UFA synthesis is distinct from that of the classical pathway. NGO1024 homologues, which we suggest naming UfaA, form a distinct lineage within the 2-nitropropane dioxygenase-like superfamily, and are found in many facultative and obligate anaerobes that produce UFAs but lack fabA, suggesting that UfaA is part of a widespread pathway involved in UFA synthesis.

摘要

需氧条件下,淋球菌(Neisseria gonorrhoeae)转录组分析显示许多功能未知的基因被诱导。一个这样的基因 NGO1024 发生突变后,淋球菌丧失了在厌氧条件下生长的能力,该基因编码的蛋白属于 2-硝基丙烷双加氧酶超家族蛋白。NG1024 突变株在补充不饱和脂肪酸(UFA)时可以恢复厌氧生长,但补充饱和脂肪酸棕榈酸则不行。淋球菌脂肪酸图谱证实 NGO1024 参与 UFA 的厌氧合成,但不参与有氧合成,这表明淋球菌存在两种不同的 UFA 合成途径,一种是尚未鉴定的有氧机制,另一种是涉及 NGO1024 的厌氧机制。参与经典厌氧 UFA 合成的基因 fabA、fabM 和 fabB 的表达在淋球菌中是有毒的,并且不能弥补 NGO1024 突变,这表明淋球菌厌氧 UFA 合成的化学性质与经典途径不同。我们建议将 NGO1024 的同源物命名为 UfaA,它在 2-硝基丙烷双加氧酶超家族中形成一个独特的分支,存在于许多产生 UFA 但缺乏 fabA 的需氧和严格厌氧菌中,这表明 UfaA 是参与 UFA 合成的广泛途径的一部分。

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