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Peer-Reviewed Publications

The Candida albicans HIR histone chaperone regulates the yeast-to-hyphae transition by controlling the sensitivity to morphogenesis signals.

Jenull S, Tscherner M, Gulati M, Nobile CJ, Chauhan N, Kuchler K

Sci Rep. 2017 Aug 16;7(1):8308

Abstract Morphological plasticity such as the yeast-to-hyphae transition is a key virulence factor of the human fungal pathogen Candida albicans. Hyphal formation is controlled by a multilayer regulatory network composed of environmental sensing, signaling, transcriptional modulators as well as chromatin modifications. Here, we demonstrate a novel role for the replication-independent HIR histone chaperone complex in fungal morphogenesis. HIR operates as a crucial modulator of hyphal development, since genetic ablation of the HIR complex subunit Hir1 decreases sensitivity to morphogenetic stimuli. Strikingly, HIR1-deficient cells display altered transcriptional amplitudes upon hyphal initiation, suggesting that Hir1 affects transcription by establishing transcriptional thresholds required for driving morphogenetic cell-fate decisions. Furthermore, ectopic expression of the transcription factor Ume6, which facilitates hyphal maintenance, rescues filamentation defects of hir1Δ/Δ cells, suggesting that Hir1 impacts the early phase of hyphal initiation. Hence, chromatin chaperone-mediated fine-tuning of transcription is crucial for driving morphogenetic conversions in the fungal pathogen C. albicans.
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PMID: 28814742 [PubMed - in process]

Peer-Reviewed Publications authored by Karl Kuchler from Pubmed Logo at the NCBI.
 
Karl Kuchler Laboratory, Medical University Vienna, Max F. Perutz Laboratories, Department of Medical Biochemistry,
Dr. Bohr-Gasse 9/2, A-1030 Vienna, AUSTRIA, [T] +43/1/4277-61806, [F] +43/1/4277-9618, [E] karl.kuchler@meduniwien.ac.at