ArticleJournal of bacteriology1998
Isolation of Candida glabrata homologs of the Saccharomyces cerevisiae KRE9 and KNH1 genes and their involvement in cell wall beta-1,6-glucan synthesis.
Article in Journal of bacteriology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
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- Lessons on fruiting body morphogenesis from genomes and transcriptomes ofStudies in mycology · 2023Article
- Portrait of Matrix Gene Expression in Candida glabrata Biofilms with Stress Induced by Different Drugs.Genes · 2018Article
- Remodeling of the Candida glabrata cell wall in the gastrointestinal tract affects the gut microbiota and the immune response.Scientific reports · 2018Article
- Generational distribution of a Candida glabrata population: Resilient old cells prevail, while younger cells dominate in the vulnerable host.PLoS pathogens · 2017Article
- Effect of beta-1,6-glucan inhibitors on the invasion process of Candida albicans: potential mechanism of their in vivo efficacy.Antimicrobial agents and chemotherapy · 2009Article
- Cell wall beta-(1,6)-glucan of Saccharomyces cerevisiae: structural characterization and in situ synthesis.The Journal of biological chemistry · 2009Article
- Discovery of a small-molecule inhibitor of {beta}-1,6-glucan synthesis.Antimicrobial agents and chemotherapy · 2009Article
- Borrelia burgdorferi ftsZ plays a role in cell division.Journal of bacteriology · 2006Article
- Inner kinetochore of the pathogenic yeast Candida glabrata.Eukaryotic cell · 2004Article
- Saccharomyces cerevisiae mid2p is a potential cell wall stress sensor and upstream activator of the PKC1-MPK1 cell integrity pathway.Journal of bacteriology · 1999Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Candida glabrata KRE9 (CgKRE9) and KNH1 (CgKNH1) genes have been isolated as multicopy suppressors of the tetracycline-sensitive growth of a Saccharomyces cerevisiae mutant with the disrupted KNH1 locus and the KRE9 gene placed under the control of a tetracycline-responsive promoter. Although a cgknh1Delta mutant showed no phenotype beyond slightly increased sensitivity to the K1 killer toxin, disruption of CgKRE9 resulted in several phenotypes similar to those of the S. cerevisiae kre9Delta null mutant: a severe growth defect on glucose medium, resistance to the K1 killer toxin, a 50% reduction of beta-1,6-glucan, and the presence of aggregates of cells with abnormal morphology on glucose medium. Replacement in C. glabrata of the cognate CgKRE9 promoter with the tetracycline-responsive promoter in a cgknh1Delta background rendered cell growth tetracycline sensitive on media containing glucose or galactose. cgkre9Delta cells were shown to be sensitive to calcofluor white specifically on glucose medium. In cgkre9 mutants grown on glucose medium, cellular chitin levels were massively increased.
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