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Doctoral dissertation: "Heterobasidion annosum sensu stricto Pathogenesis: Bioinformatic and Functional Study of Cerato-platanin Family Proteins"

 Hongxin Chen will defend the doctoral dissertation entitled "Heterobasidion annosum sensu stricto Pathogenesis: Bioinformatic and Functional Study of Cerato-platanin Family Proteins" in Lecture Hall B2, Forest Sciences building, Viikki (Latokartanonkaari 7), on November 6th 2015, at 12 noon. Professor Michael Thon, University of Salamanca, Spain, will serve as the opponent, and Professor Fred O. Asiegbu as the custos.


The basidiomycete white-rot fungus Heterobasidion annosum sensu stricto (s.s.) is one of the most severe conifer pathogens in the Northern Hemisphere. It can live as a saprotroph on dead wood tissues or a necrotroph on living trees. Taking advantage of a sequenced genome from a closely related species, Heterobasidion irregulare, we performed an in-depth transcriptomic analysis of this fungus under various abiotic stresses (temperature stress, osmotic stress, oxidative stress, and nutrient starvation) and during saprotrophic growth on pine bark, sapwood, and heartwood. The results unraveled potential regulatory mechanisms to overcome these conditions.

Based on the specific induction in the microarray, cerato-platanins were selected for further study in the interactions between H. annosum s.s. and Pinus sylvestris. As the first step, a genome-wide bioinformatic study of the cerato-platanin family in Dikarya was therefore conducted. The results suggested that they exist in both Ascomycota and Basidiomycota, but were lost in early branches of jelly fungi as well as in some groups with yeast or yeast-like forms in their life cycles. The ancestor of the Dikarya possessed multiple copies of cerato-platanins, which sorted differently in Ascomycota and Basidiomycota, and this gene family might have expanded in Basidiomycota.

To gain insight into the role of cerato-platanins as potential virulence factors in H. annosum s.s., we performed the functional study of HaCPL2 by using a recombinant protein produced in Pichia pastoris. Interestingly, HaCPL2 was able to induce cell death in both host (P. sylvestris) and non-host (Nicotiana tabacum) plants. Besides cell death symptoms, HaCPL2 retarded apical root growth of P. sylvestris seedlings and induced phytoalexin production in N. tabacum. Defense-related gene expression was also upregulated in both plants after HaCPL2 treatment.

This study has provided valuable information about potential gene regulatory mechanisms in H. annosum s.s. that mediate stress adaptation and growth in different pine wood compartments. Moreover, we propose that HaCPL2, a cerato-platanin protein, could act as an effector and contribute to the virulence in the H. annosum s.s.–P. sylvestris pathosystem. This furthers our understanding of Heterobasidion pathogenesis and provides a future target for disease control.