Soybean cyst nematode-resistance: Gene identification and breeding strategies

Soybean cyst nematode (SCN, Heterodera glycines Ichinohe) is the most economically damaging disease of soybean worldwide, and breeding host plant resistance is the most feasible option for SCN management. In this review, we summarise the progress made so far in identifying nematode-resistance genes, the currently available sources of resistance, possible mechanisms of SCN resistance and strategies for soybean breeding. To date, only two sources of SCN resistance have been widely used, from the accessions PI 88788 and Peking, which has resulted in a shift in SCN resistance and created a narrow genetic base for SCN resistance. These resistant germplasms for SCN are classified into two types according to their copy number variation in a 31-kb genomic region: PI 88788-type resistance requires high copy numbers of a rhg1 resistance allele ( rhg1-b ) and Peking-type resistance requires both low copy numbers of a different rhg1 resistance allele ( rhg1-a ) and a resistant allele at another locus, Rhg4 . Resistance related to rhg1 primarily involves impairment of vesicle trafficking through disruption of soluble NSF-attachment protein receptor (SNARE) complexes. By contrast, resistance via Rhg4 involves disturbance of folate homeostasis at SCN feeding sites due to alteration of the enzymatic activity of serine hydroxymethyltransferase (SHMT). Other potential mechanisms, including plant defences mediated by salicylic acid (SA) and jasmonic acid (JA) signalling modulation, have also been suggested for SCN resistance. Indeed, genome-wide association studies (GWAS) have identified other candidate SCN resistance genes, such as GmSNAP11 . Although gene functional analysis in a transient expression system could increase the efficiency of candidate gene identification, information on novel genes and mechanisms for SCN resistance remains limited. Any beneficial candidate genes identified might, when fully exploited, be valuable for improving the efficiency of marker-assisted breeding and dissecting the molecular mechanisms underlying SCN resistance.