ArticleRNA biology2015
A bacterial homolog YciH of eukaryotic translation initiation factor eIF1 regulates stress-related gene expression and is unlikely to be involved in translation initiation fidelity.
Article in RNA biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- The origins and evolution of translation factors.Trends in genetics : TIG · 2025Review
- Raiding nature's genetic toolbox for UV-C resistance by functional metagenomics.Scientific reports · 2025Article
- The Rcs System Contributes to the Motility Defects of the Twin-Arginine Translocation System Mutant of Extraintestinal Pathogenic Escherichia coli.Journal of bacteriology · 2022Article
- CRISPR interference of nucleotide biosynthesis improves production of a single-domain antibody in Escherichia coli.Biotechnology and bioengineering · 2020Article
- Comprehensive Functional Analysis ofFrontiers in genetics · 2020Article
- Large scale analysis of amino acid substitutions in bacterial proteomics.BMC bioinformatics · 2016Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
YciH is a bacterial protein, homologous to eukaryotic translation initiation factor eIF1. Preceding evidence obtained with the aid of in vitro translation initiation system suggested that it may play a role of a translation initiation factor, ensuring selection against suboptimal initiation complexes. Here we studied the effect of Escherichia coli yciH gene inactivation on translation of model mRNAs. Neither the translation efficiency of leaderless mRNAs, nor mRNAs with non AUG start codons, was found to be affected by YciH in vivo. Comparative proteome analysis revealed that yciH gene knockout leads to a more than fold2- increase in expression of 66 genes and a more than fold2- decrease in the expression of 20 genes. Analysis of these gene sets allowed us to suggest a role of YciH as an inhibitor of translation in a stress response rather than the role of a translation initiation factor.
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