|DE JONG, RONNIE - Wageningen University|
|KOMBRINK, ANJA - Wageningen University|
|YADETA, KOSTE - Wageningen University|
|VAN DEN BERG, GRARDY - Wageningen University|
|THOMMA, BART - Wageningen University|
Submitted to: Genome Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/14/2013
Publication Date: 8/3/2013
Citation: De Jong, R., Bolton, M.D., Kombrink, A., Yadeta, K.A., Van Den Berg, G.C., Thomma, B.P. 2013. Extensive chromosomal reshuffling drives evolution of virulence in an asexual pathogen. Genome Research. 23:1271-1282.
Interpretive Summary: Plant pathogens that utilize sexual reproduction tend to have populations that are genetically more diverse. This diversity tends to help the population overcome environmental pressures, such as those faced when a crop has genetic resistance to the pathogen. However, many plant pathogens rely on asexual reproduction, which is thought to be more limited in its ability to provide genetic diversity in populations. In this paper, we investigated genetic variation in the asexual pathogen Verticillium dahliae, a pathogen that causes disease in many crops including sugarbeet, potato, and tomato. We discovered that mitotic chromosomal recombination is occurring in this fungus in regions of the genome that harbor effectors, genes that are important for causing disease in the host. This targeted asexual recombination appears to provide a means of genetic variation, enabling rapid development of molecules that contribute to establishment of disease.
Technical Abstract: Pathogen populations that undergo regular sexual reproduction are thought to pose a greater risk to plant breeders than pathogens limited to asexual reproduction because they can recombine alleles that contribute to virulence in the face of dynamic environmental conditions. Despite this, many devastating plant pathogens appear to rely strictly on asexual reproduction. Here, we investigated variation in the asexual plant pathogenic fungus Verticillium dahliae, and discovered that extensive mitotic chromosomal recombinations establish highly dynamic ‘plastic’ regions of the genome to mediate variation. Such plastic regions occur at the flanks of chromosomal breakpoints, enabling rapid development of molecules that contribute to establishment of disease.