Abstract
The Repeat-Induced Point (RIP) mutation pathway is a fungal-specific genome defense mechanism that counteracts the deleterious effects of transposable elements. This pathway permanently mutates its target sequences by introducing cytosine to thymine transitions. We investigated the genome-wide occurrence of RIP in the pitch canker pathogen, Fusarium circinatum, and its close relatives in the Fusarium fujikuroi species complex (FFSC). Our results showed that the examined fungi all exhibited hallmarks of RIP, but that they differed in terms of the extent to which their genomes were affected by this pathway. RIP mutations constituted a large proportion of all the FFSC genomes, including both core and dispensable chromosomes, although the latter were generally more extensively affected by RIP. Large RIP-affected genomic regions were also much more gene sparse than the rest of the genome. Our data further showed that RIP-directed sequence diversification increased the variability between homologous regions of related species, and that RIP-affected regions can interfere with homologous recombination during meiosis, thereby contributing to post-mating segregation distortion. Taken together, these findings suggest that RIP can drive the independent divergence of chromosomes, alter chromosome architecture, and contribute to the divergence among F. circinatum and other members of this economically important group of fungi.
Highlights
The genus Fusarium includes a diverse assemblage of fungi—many of which are plant, animal and human pathogens [1]
In F. fujikuroi, the genomic location of the majority of H3k9me3 markers coincided with the location of mutations resembling those associated with Repeat-Induced Point (RIP) (Supplementary Figure S2), which is similar to what has been observed for N. crassa [17,37]. These results suggest that, should RIP occur in the Fusarium fujikuroi species complex (FFSC), the process is likely mediated by the RID and the DIM-2/DIM-5 pathways [17,37]
Genomesusing using three of the widely indices. These analyses showed that indices (Table 3 and Supplementary Table S3) [40,41,42,43]. These analyses showed that 3% to almost 10% of of the various FFSC genomes contained RIP mutations for the core chromosomes (Figure 2)
Summary
The genus Fusarium includes a diverse assemblage of fungi—many of which are plant, animal and human pathogens [1] They produce a wide range of highly toxic secondary metabolites that may contaminate food and feed-stocks. The causal agent of pine pitch canker, Fusarium circinatum, represents one of the most important fungal pathogens of wild and planted conifers, pine species [3] and its genome has been sequenced, and assembled into chromosome-sized scaffolds [4,5] This is true for various of the close relatives of the pathogen [6,7,8]. It is not surprising that Fusarium is emerging as a model for research in the field of fungal evolutionary biology [2,8]
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