ArticlePloS one2017
Whole genome re-sequencing to identify suppressor mutations of mutant and foreign Escherichia coli FtsZ.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Construction of a multicopy genomic DNA library and its application for suppression analysis.Journal of microbiology (Seoul, Korea) · 2019Article
- Gain-of-function variants of FtsA form diverse oligomeric structures on lipids and enhance FtsZ protofilament bundling.Molecular microbiology · 2018Article
- Unite to divide: Oligomerization of tubulin and actin homologs regulates initiation of bacterial cell division.F1000Research · 2018Review
- Comparative genomic analysis of multidrug-resistantInfection and drug resistance · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
FtsZ is an essential protein for bacterial cell division, where it forms the cytoskeletal scaffold and may generate the constriction force. We have found previously that some mutant and foreign FtsZ that do not complement an ftsZ null can function for cell division in E. coli upon acquisition of a suppressor mutation somewhere in the genome. We have now identified, via whole genome re-sequencing, single nucleotide polymorphisms in 11 different suppressor strains. Most of the mutations are in genes of various metabolic pathways, which may modulate cell division indirectly. Mutations in three genes, ispA, accD and nlpI, may be more directly involved in cell division. In addition to the genomic suppressor mutations, we identified intragenic suppressors of three FtsZ point mutants (R174A, E250K and L272V).
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Registered trials
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