Reduced TOR signaling sustains hyphal development in Candida albicans by lowering Hog1 basal activity.
Identifieur interne : 001083 ( Main/Corpus ); précédent : 001082; suivant : 001084Reduced TOR signaling sustains hyphal development in Candida albicans by lowering Hog1 basal activity.
Auteurs : Chang Su ; Yang Lu ; Haoping LiuSource :
- Molecular biology of the cell [ 1939-4586 ] ; 2013.
English descriptors
- KwdEn :
- Candida albicans (cytology), Candida albicans (enzymology), Candida albicans (growth & development), Enzyme Induction (MeSH), Fungal Proteins (metabolism), Gene Expression Regulation, Fungal (MeSH), Hyphae (cytology), Hyphae (enzymology), Hyphae (growth & development), Mitogen-Activated Protein Kinases (genetics), Mitogen-Activated Protein Kinases (metabolism), Phenotype (MeSH), Promoter Regions, Genetic (MeSH), Protein Binding (MeSH), Protein Tyrosine Phosphatases (metabolism), Repressor Proteins (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), Stress, Physiological (MeSH), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (metabolism), Up-Regulation (MeSH).
- MESH :
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , genetics : Mitogen-Activated Protein Kinases.
- chemical , metabolism : Fungal Proteins, Mitogen-Activated Protein Kinases, Protein Tyrosine Phosphatases, Repressor Proteins, TOR Serine-Threonine Kinases.
- cytology : Candida albicans, Hyphae.
- enzymology : Candida albicans, Hyphae.
- growth & development : Candida albicans, Hyphae.
- chemical , pharmacology : Sirolimus.
- Enzyme Induction, Gene Expression Regulation, Fungal, Phenotype, Promoter Regions, Genetic, Protein Binding, Signal Transduction, Stress, Physiological, Up-Regulation.
Abstract
Candida albicans is able to undergo reversible morphological changes between yeast and hyphal forms in response to environmental cues. This morphological plasticity is essential for its pathogenesis. Hyphal development requires two temporally linked changes in promoter chromatin, which is sequentially regulated by temporarily clearing the transcription inhibitor Nrg1 upon activation of cAMP/protein kinase A and promoter recruitment of the histone deacetylase Hda1 under reduced target of rapamycin (Tor1) signaling. The GATA family transcription factor Brg1 recruits Hda1 to promoters for sustained hyphal development, and BRG1 expression is a readout of reduced Tor1 signaling. How Tor1 regulates BRG1 expression is not clear. Using a forward genetic screen for mutants that can sustain hyphal elongation in rich media, we found hog1, ssk2, and pbs2 mutants of the HOG mitogen-activated protein kinase pathway to express BRG1 irrespective of rapamycin. Furthermore, rapamycin lowers the basal activity of Hog1 through the functions of the two Hog1 tyrosine phosphatases Ptp2 and Ptp3. Active Hog1 represses the expression of BRG1 via the transcriptional repressor Sko1 as Sko1 disassociates from the promoter of BRG1 in the hog1 mutant or in rapamycin. Our data suggest that reduced Tor1 signaling lowers Hog1 basal activity via Hog1 phosphatases to activate BRG1 expression for hyphal elongation.
DOI: 10.1091/mbc.E12-06-0477
PubMed: 23171549
PubMed Central: PMC3564525
Links to Exploration step
pubmed:23171549Le document en format XML
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<front><div type="abstract" xml:lang="en">Candida albicans is able to undergo reversible morphological changes between yeast and hyphal forms in response to environmental cues. This morphological plasticity is essential for its pathogenesis. Hyphal development requires two temporally linked changes in promoter chromatin, which is sequentially regulated by temporarily clearing the transcription inhibitor Nrg1 upon activation of cAMP/protein kinase A and promoter recruitment of the histone deacetylase Hda1 under reduced target of rapamycin (Tor1) signaling. The GATA family transcription factor Brg1 recruits Hda1 to promoters for sustained hyphal development, and BRG1 expression is a readout of reduced Tor1 signaling. How Tor1 regulates BRG1 expression is not clear. Using a forward genetic screen for mutants that can sustain hyphal elongation in rich media, we found hog1, ssk2, and pbs2 mutants of the HOG mitogen-activated protein kinase pathway to express BRG1 irrespective of rapamycin. Furthermore, rapamycin lowers the basal activity of Hog1 through the functions of the two Hog1 tyrosine phosphatases Ptp2 and Ptp3. Active Hog1 represses the expression of BRG1 via the transcriptional repressor Sko1 as Sko1 disassociates from the promoter of BRG1 in the hog1 mutant or in rapamycin. Our data suggest that reduced Tor1 signaling lowers Hog1 basal activity via Hog1 phosphatases to activate BRG1 expression for hyphal elongation.</div>
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<Abstract><AbstractText>Candida albicans is able to undergo reversible morphological changes between yeast and hyphal forms in response to environmental cues. This morphological plasticity is essential for its pathogenesis. Hyphal development requires two temporally linked changes in promoter chromatin, which is sequentially regulated by temporarily clearing the transcription inhibitor Nrg1 upon activation of cAMP/protein kinase A and promoter recruitment of the histone deacetylase Hda1 under reduced target of rapamycin (Tor1) signaling. The GATA family transcription factor Brg1 recruits Hda1 to promoters for sustained hyphal development, and BRG1 expression is a readout of reduced Tor1 signaling. How Tor1 regulates BRG1 expression is not clear. Using a forward genetic screen for mutants that can sustain hyphal elongation in rich media, we found hog1, ssk2, and pbs2 mutants of the HOG mitogen-activated protein kinase pathway to express BRG1 irrespective of rapamycin. Furthermore, rapamycin lowers the basal activity of Hog1 through the functions of the two Hog1 tyrosine phosphatases Ptp2 and Ptp3. Active Hog1 represses the expression of BRG1 via the transcriptional repressor Sko1 as Sko1 disassociates from the promoter of BRG1 in the hog1 mutant or in rapamycin. Our data suggest that reduced Tor1 signaling lowers Hog1 basal activity via Hog1 phosphatases to activate BRG1 expression for hyphal elongation.</AbstractText>
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