Open AccessWhole‐genome re‐sequencing reveals the impact of the interaction of copy number variants of the rhg1 and Rhg4 genes on broad‐based resistance to soybean cyst nematode
Author(s) -
Patil Gunvant B.,
Lakhssassi Naoufal,
Wan Jinrong,
Song Li,
Zhou Zhou,
Klepadlo Mariola,
Vuong Tri D.,
Stec Adrian O.,
Kahil Sondus S.,
Colantonio Vincent,
Valliyodan Babu,
Rice J. Hollis,
Piya Sarbottam,
Hewezi Tarek,
Stupar Robert M.,
Meksem Khalid,
Nguyen Henry T.
Publication year - 2019
Publication title -
plant biotechnology journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.525
H-Index - 115
eISSN - 1467-7652
pISSN - 1467-7644
DOI - 10.1111/pbi.13086
Subject(s) - soybean cyst nematode , biology , genetics , haplotype , locus (genetics) , gene , epistasis , single nucleotide polymorphism , genome , snp , whole genome sequencing , genotype
Summary Soybean cyst nematode ( SCN ) is the most devastating plant‐parasitic nematode. Most commercial soybean varieties with SCN resistance are derived from PI 88788. Resistance derived from PI 88788 is breaking down due to narrow genetic background and SCN population shift. PI 88788 requires mainly the rhg1‐b locus, while ‘Peking’ requires rhg1‐a and Rhg4 for SCN resistance. In the present study, whole genome re‐sequencing of 106 soybean lines was used to define the Rhg haplotypes and investigate their responses to the SCN HG ‐Types. The analysis showed a comprehensive profile of SNP s and copy number variations ( CNV ) at these loci. CNV of rhg1 (Gm SNAP 18) only contributed towards resistance in lines derived from PI 88788 and ‘Cloud’. At least 5.6 copies of the PI 88788‐type rhg1 were required to confer SCN resistance, regardless of the Rhg4 ( Gm SHMT 08 ) haplotype. However, when the Gm SNAP 18 copies dropped below 5.6, a ‘Peking’‐type Gm SHMT 08 haplotype was required to ensure SCN resistance. This points to a novel mechanism of epistasis between Gm SNAP 18 and Gm SHMT 08 involving minimum requirements for copy number. The presence of more Rhg4 copies confers resistance to multiple SCN races. Moreover, transcript abundance of the Gm SHMT 08 in root tissue correlates with more copies of the Rhg4 locus, reinforcing SCN resistance. Finally, haplotype analysis of the Gm SHMT 08 and Gm SNAP 18 promoters inferred additional levels of the resistance mechanism. This is the first report revealing the genetic basis of broad‐based resistance to SCN and providing new insight into epistasis, haplotype‐compatibility, CNV , promoter variation and its impact on broad‐based disease resistance in plants.