ArticleJournal of bacteriology2001
Overexpression of yccL (gnsA) and ydfY (gnsB) increases levels of unsaturated fatty acids and suppresses both the temperature-sensitive fabA6 mutation and cold-sensitive secG null mutation of Escherichia coli.
Article in Journal of bacteriology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 16 citations in OpenAlex.
- Suppressors ofInternational journal of molecular sciences · 2023Article
- Comparative Proteomics Enables Identification of Nonannotated Cold Shock Proteins in E. coli.Journal of proteome research · 2017Article
- Unsaturated Fatty Acid Synthesis in the Gastric Pathogen Helicobacter pylori Proceeds via a Backtracking Mechanism.Cell chemical biology · 2016Article
- Roles of the protruding loop of factor B essential for the localization of lipoproteins (LolB) in the anchoring of bacterial triacylated proteins to the outer membrane.The Journal of biological chemistry · 2014Article
- Genomic library screens for genes involved in n-butanol tolerance in Escherichia coli.PloS one · 2011Article
- Interactive visualization of clusters in microarray data: an efficient tool for improved metabolic analysis of E. coli.Microbial cell factories · 2009Article
- Overexpression of gnsA, a multicopy suppressor of the secG null mutation, increases acidic phospholipid contents by inhibiting phosphatidylethanolamine synthesis at low temperatures.Journal of bacteriology · 2004Article
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
A multicopy suppressor of the cold-sensitive secG null mutation was isolated. The suppressor contained sfa and yccL, the former of which has been reported to be a multicopy suppressor of the fabA6 mutation carried by a temperature-sensitive unsaturated fatty acid auxotroph. Subcloning of the suppressor gene revealed that yccL, renamed gnsA (secG null mutant suppressor), was responsible for the suppression of both the secG null mutation and the fabA6 mutation. In contrast, the sfa gene did not suppress the fabA6 mutation. The ydfY (gnsB) gene, encoding a protein which is highly similar to GnsA, also suppressed both the secG null mutation and the fabA6 mutation. Although both gnsA and gnsB are linked to cold shock genes, the levels of GnsA and GnsB did not exhibit a cold shock response. A gnsA-gnsB double null mutant grew normally under all conditions examined; thus, the in vivo functions of gnsA and gnsB remain unresolved. However, overexpression of gnsA and gnsB stimulated proOmpA translocation of the secG null mutant at low temperature and caused a significant increase in the unsaturated fatty acid content of phospholipids. Taken together, these results suggest that an increase in membrane fluidity due to the increase in unsaturated fatty acids compensates for the absence of the SecG function, especially at low temperature.
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