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阐明铁摄取缺陷的集胞藻 6803 OMP 纯合敲除突变体的应对策略。

Elucidation of the coping strategy in an OMP homozygous knockout mutant of Synechocystis 6803 defective in iron uptake.

机构信息

Applied Genomics Section, Bhabha Atomic Research Centre, Mumbai, 400 085, India.

Homi Bhabha National Institute, Training School Complex, Anushaktinagar, Mumbai, 400 094, India.

出版信息

Arch Microbiol. 2022 Jun 3;204(7):358. doi: 10.1007/s00203-022-02968-w.

Abstract

The TonB-dependent outer membrane (OM) transporters import iron (Fe) under Fe-deficient growth conditions in the unicellular cyanobacterium Synechocystis sp. strain PCC 6803 (S. 6803 or WT). The present study characterises the mechanisms employed by a homozygous Δslr1908 (Slr1908, an OM protein) mutant of S. 6803 to adapt to intracellular iron deficiency imposed due to lack of Slr1908 when grown under Fe sufficient conditions for short (1 week) and long term (3 weeks). Although the homozygous Δslr1908 cells showed symptoms of stress such as slow growth, high ROS and altered ultrastructure, they were transcriptionally as well as translationally modulating their physiology to abrogate the Fe limitation. The mutant displayed only 20% of the Fe content in comparison to the WT after 1 week of growth, which increased to 50% by the end of the third week. The increase in intracellular Fe is ascribed to higher transcripts as well as corresponding protein of slr0042 which is the alternate OM route for Fe uptake. The mutant was also allocating its available Fe pools judiciously among Fe requiring proteins such as catalase, superoxide dismutase and cytochromes. The results elucidate the mechanism employed to tide over the Fe deficiency by Δslr1908 mutant and will be important in explaining the fine-tuning of Fe homeostasis in this model cyanobacterium.

摘要

在单细胞蓝藻集胞藻 6803 中(S. 6803 或 WT),TonB 依赖性外膜(OM)转运蛋白在缺铁生长条件下将铁(Fe)导入细胞内。本研究描述了 S. 6803 的 homozygous Δslr1908(Slr1908,一种 OM 蛋白)突变体在铁充足条件下生长时,由于缺乏 Slr1908 而导致细胞内铁缺乏时适应的机制。尽管 homozygous Δslr1908 细胞表现出应激症状,如生长缓慢、高 ROS 和超微结构改变,但它们在转录和翻译水平上都在调节其生理机能以消除铁限制。与 WT 相比,突变体在生长 1 周后的铁含量仅为 20%,而在第 3 周结束时增加到 50%。细胞内铁的增加归因于 slr0042 的更高转录本和相应蛋白,slr0042 是铁摄取的替代 OM 途径。突变体还明智地在需要铁的蛋白质(如过氧化氢酶、超氧化物歧化酶和细胞色素)之间分配其可用的铁池。这些结果阐明了 Δslr1908 突变体克服铁缺乏的机制,对于解释这种模式蓝藻中铁稳态的精细调节将非常重要。

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