Genome sequencing and genomic comparison of the conifer pathogen Heterobasidion parviporum


Zhen Zeng 1 Hui Sun 1,2 Eeva J. Vainio 3 Tommaso Raffaello 1 Andriy Kovalchuk 1 Sebastien Duplessis 4 Emmanuelle Morin 4 Fred Asiegbu 1
1Department of Forest Sciences, University of Helsinki, Helsinki, Finland
2Collaborative Innovation Center of Sustainable Forestry in Southern China, College of Forestry, Nanjing Forestry University, Nanjing, China
3LUKE, Natural Resources Institute Finland, Helsinki, Finland
4Centre INRA Nancy Lorraine, INRA, UMR 1136 Interactions Arbres/Microorganismes, INRA/Universite de Lorraine, Champenoux, France

In this study, 15 isolates of the causative agent of root and butt rot disease Heterobasidion parviporum from all across Finland were screened for pathogenicity and virulence. All isolates were pathogenic and displayed varied virulence. A draft genome assembly of the most virulent isolate as a reference was constructed and described for the rest of 14 isolates, of which whole genomes were also sequenced. Genome-wide alignments and variant callings showed that these isolates exhibited overall high genomic similarity with an average of at least 96% nucleotide identity when compared to the reference, yet had remarkable intra-specific level of polymorphism with a bias for CpG to TpG mutations, probably attributed to repeat-induced point mutation (RIP)-like activity or DNA methylation as one way of epigenetic regulation of gene expression. Reads mapping coverage analysis classified all predicted genes into 5 groups and secreted proteins in each group were more closely explored. Two genomic regions found exclusively in the reference may contribute to its virulence. Genes enriched for copy number variations (deletions and duplications) and nucleotide polymorphisms were found to be involved in oxidation-reduction process and encoding domains relevant to transcription factors. However, gene number variation cannot be directly correlated to varied virulence and not a single gene could be pinpointed as a determinant for the virulence in this fungus. Instead, it is likely the regulatory networks play more important roles in compensation of modification of gene number and genetic variations.