Affiliation:
1. Department of Plant Pathology and Institute of Plant Breeding, Genetics and Genomics University of Georgia Athens Georgia USA
2. National Center for Supercomputing Applications University of Illinois at Urbana‐Champaign Urbana Illinois USA
3. Carver Biotechnology Center University of Illinois at Urbana‐Champaign Urbana Illinois USA
4. Division of Plant Science and Technology University of Missouri Columbia Missouri USA
5. Department of Crop Sciences University of Illinois at Urbana‐Champaign Urbana Illinois USA
Abstract
AbstractPlant pathogens are constantly under selection pressure for host resistance adaptation. Soybean cyst nematode (SCN, Heterodera glycines) is a major pest of soybean primarily managed through resistant cultivars; however, SCN populations have evolved virulence in response to selection pressures driven by repeated monoculture of the same genetic resistance. Resistance to SCN is mediated by multiple epistatic interactions between Rhg (for resistance to H. glycines) genes. However, the identity of SCN virulence genes that confer the ability to overcome resistance remains unknown. To identify candidate genomic regions showing signatures of selection for increased virulence, we conducted whole genome resequencing of pooled individuals (Pool‐Seq) from two pairs of SCN populations adapted on soybeans with Peking‐type (rhg1‐a, rhg2, and Rhg4) resistance. Population differentiation and principal component analysis‐based approaches identified approximately 0.72–0.79 million SNPs, the frequency of which showed potential selection signatures across multiple genomic regions. Chromosomes 3 and 6 between population pairs showed the greatest density of outlier SNPs with high population differentiation. Conducting multiple outlier detection tests to identify overlapping SNPs resulted in a total of 966 significantly differentiated SNPs, of which 285 exon SNPs were mapped to 97 genes. Of these, six genes encoded members of known stylet‐secreted effector protein families potentially involved in host defence modulation including venom‐allergen‐like, annexin, glutathione synthetase, SPRYSEC, chitinase, and CLE effector proteins. Further functional analysis of identified candidate genes will provide new insights into the genetic mechanisms by which SCN overcomes soybean resistance and inform the development of molecular markers for rapidly screening the virulence profile of an SCN‐infested field.
Funder
North Central Soybean Research Program
Reference114 articles.
1. Soybean Yield Loss Estimates Due to Diseases in the United States and Ontario, Canada, from 2010 to 2014
2. Dissecting the economic impact of soybean diseases in the United States over two decades
3. Epistatic interaction between Rhg1-a and Rhg2 in PI 90763 confers resistance to virulent soybean cyst nematode populations
4. Disease resistance through impairment of α‐SNAP–NSF interaction and vesicular trafficking by soybean Rhg1;Bayless A. M.;Proceedings of the National Academy of Sciences of the United States of America,2016
5. An atypical N‐ethylmaleimide sensitive factor enables the viability of nematode‐resistant Rhg1 soybeans;Bayless A. M.;Proceedings of the National Academy of Sciences of the United States of America,2018