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

• Main Authors: Alberto Elías-Villalobos, Dominique Helmlinger, José I. Ibeas
• Format: Article
• Language: English
• Published: Shared Science Publishers OG 2015-11-01
• Series: Microbial Cell
• Subjects: histone; acetylation; deacetylation; HAT; HDAC; dimorphism; virulence; pathogenic fungi; Ustilago maydis; Hos2; Clr3; plant pathogen
• Online Access: http://microbialcell.com/researcharticles/histone-deacetylases-revealing-the-molecular-base-of-dimorphism-in-pathogenic-fungi/

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.