Shewanella oneidensis arcA Mutation Impairs Aerobic Growth Mainly by Compromising Translation.

Peilu Xie,Haichun Gao,Huihui Liang,Jiahao Wang

doi:10.3390/life11090926

Abstract

Arc (anoxic redox control), one of the most intensely investigated two-component regulatory systems in γ-proteobacteria, plays a major role in mediating the metabolic transition from aerobiosis to anaerobiosis. In Shewanella oneidensis, a research model for respiratory versatility, Arc is crucial for aerobic growth. However, how this occurs remains largely unknown. In this study, we demonstrated that the loss of the response regulator ArcA distorts the correlation between transcription and translation by inhibiting the ribosome biosynthesis. This effect largely underlies the growth defect because it concurs with the effect of chloramphenicol, which impairs translation. Reduced transcription of ArcA-dependent ribosomal protein S1 appears to have a significant impact on ribosome assembly. We further show that the lowered translation efficiency is not accountable for the envelope defect, another major defect resulting from the ArcA loss. Overall, our results suggest that although the arcA mutation impairs growth through multi-fold complex impacts in physiology, the reduced translation efficacy appears to be a major cause for the phenotype, demonstrating that Arc is a primary system that coordinates proteomic resources with metabolism in S. oneidensis.

Highlights

We have previously demonstrated that oligopeptide transport is partially accountable for the defect in aerobic growth of the arcA mutant, but its contribution is minor [26]
We have previously shown that the defect of an S. oneidensis arcA mutant in aerobic growth is dependent on tryptone [40]
As this phenomenon implies that the defect is associated with nutrients, oligopeptides in particular [42], we examined roles of peptide transporters and peptidases in S. oneidensis

Summary

Introduction

Reduced transcription of ArcA-dependent ribosomal protein S1 appears to have a significant impact on ribosome assembly. Our results suggest that the arcA mutation impairs growth through multi-fold complex impacts in physiology, the reduced translation efficacy appears to be a major cause for the phenotype, demonstrating that. In Escherichia coli, the model organism for which our understanding of the physiological impacts and molecular mechanisms of Arc is most well developed, transmembrane sensor kinase ArcB undergoes autophosphorylation by sensing the redox state of quinone pool under anaerobic or microaerobic respiratory conditions, eventually resulting in the phosphorylation of DNA-binding response regulator ArcA (ArcA-P) through a phospho-relay mechanism [6]. In bacteria equipped with Arc, Fnr (a fumarate–nitrate reduction regulator) and Crp (a cyclic–AMP receptor protein) are two other transcriptional regulatory systems profoundly involved in regulation of metabolism.

Objectives

Methods

Results

Conclusion