Mds3 Regulates Morphogenesis in Candida albicans through the TOR Pathway

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Published inMolecular and Cellular Biology Vol. 30; no. 14; pp. 3695 - 3710
Main Authors Zacchi, Lucia F., Gomez-Raja, Jonatan, Davis, Dana A.
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.07.2010
Taylor & Francis
American Society for Microbiology (ASM)
Subjects
Base Sequence
Candida albicans
Candida albicans - genetics
Candida albicans - growth & development
Candida albicans - metabolism
Candida albicans - pathogenicity
DNA Primers - genetics
DNA, Fungal - genetics
Fungal Proteins - genetics
Fungal Proteins - metabolism
Gene Expression Regulation, Developmental - drug effects
Gene Expression Regulation, Fungal - drug effects
Genes, Fungal
Humans
Morphogenesis - drug effects
Morphogenesis - genetics
Morphogenesis - physiology
Mutation
Oligonucleotide Array Sequence Analysis
Signal Transduction - drug effects
Sirolimus - pharmacology
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The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3 Δ/Δ cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3 Δ/Δ mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1 - 1 allele or an rbp1 Δ/Δ deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4 Δ/Δ and mds3 Δ/Δ mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.
The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3 Delta/Delta cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3 Delta/Delta mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1 Delta/Delta deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4 Delta/Delta and mds3 Delta/Delta mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.
The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3/ cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3/ mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1/ deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4/ and mds3/ mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.
The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3Δ/Δ cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3Δ/Δ mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1Δ/Δ deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4Δ/Δ and mds3Δ/Δ mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.
Author Dana A. Davis
Lucia F. Zacchi
Jonatan Gomez-Raja
AuthorAffiliation Department of Microbiology, University of Minnesota, Minneapolis, Minnesota 55455
AuthorAffiliation_xml – name: Department of Microbiology, University of Minnesota, Minneapolis, Minnesota 55455
Author_xml – sequence: 1
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/20457806$$D View this record in MEDLINE/PubMed
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Snippet Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal...
The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal...
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SourceType Open Access Repository
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StartPage 3695
SubjectTerms Base Sequence
Candida albicans
Candida albicans - genetics
Candida albicans - growth & development
Candida albicans - metabolism
Candida albicans - pathogenicity
DNA Primers - genetics
DNA, Fungal - genetics
Fungal Proteins - genetics
Fungal Proteins - metabolism
Gene Expression Regulation, Developmental - drug effects
Gene Expression Regulation, Fungal - drug effects
Genes, Fungal
Humans
Morphogenesis - drug effects
Morphogenesis - genetics
Morphogenesis - physiology
Mutation
Oligonucleotide Array Sequence Analysis
Signal Transduction - drug effects
Sirolimus - pharmacology
Title Mds3 Regulates Morphogenesis in Candida albicans through the TOR Pathway
URI http://mcb.asm.org/content/30/14/3695.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.01540-09
https://www.ncbi.nlm.nih.gov/pubmed/20457806
https://search.proquest.com/docview/754534818
https://search.proquest.com/docview/754868748
https://pubmed.ncbi.nlm.nih.gov/PMC2897559
Volume 30
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