Histone deacetylases: revealing the molecular base of dimorphism in pathogenic fungi

Microb Cell. 2015 Nov 4;2(12):491-493. doi: 10.15698/mic2015.11.240.

Abstract

Fungi, as every living organism, interact with the external world and have to adapt to its fluctuations. For pathogenic fungi, such interaction involves adapting to the hostile environment of their host. Survival depends on the capacity of fungi to detect and respond to external stimuli, which is achieved through a tight and efficient genetic control. Chromatin modifications represent a well-known layer of regulation that controls gene expression in response to environmental signals. However, less is known about the chromatin modifications that are involved in fungal virulence and the specific cues and signalling pathways that target chromatin modifications to specific genes. In a recently published study, our research group identified one such regulatory pathway. We demonstrated that the histone deacetylase (HDAC) Hos2 is involved in yeast-to-hyphal transition (dimorphism) and it is associated with the virulence of the maize pathogen Ustilago maydis, the causative agent of smut disease in corn. Hos2 activates mating-type genes by directly binding to their gene bodies. Furthermore, Hos2 acts downstream of the nutrient-sensing cyclic AMP-Protein Kinase A pathway. We also found that another HDAC, Clr3, contributes to this regulation, possibly in cooperation with Hos2. As a whole, our data suggest that there is a direct link between changes in the environment and acetylation of nucleosomes within certain genes. We propose that histone acetylation is critical to the proper timing and induction of transcription of the genes encoding factors that coordinate changes in morphology with pathogenesis.

Keywords: Clr3; HAT; HDAC; Hos2; Ustilago maydis; acetylation; deacetylation; dimorphism; histone; pathogenic fungi; plant pathogen; virulence.

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Grants and funding

This work was funded by BIO2010-16787 and BIO2013-48858—P from MICIN and MEC from Spain co-funded by FEDER, by an ATIP-Avenir Grant from the CNRS, a Marie Curie Actions Career Integration Grants (FP7-PEOPLE-2012-CIG/COACTIVATOR), and the Centre National de la Recherche Scientifique (CNRS) to DH. AEV was partly supported by a Postdoctoral Fellowship from the Fondation pour la Recherche Médicale (SPF20130526854). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.