| Authors: | Lakhssassi, N., Piya, S., Bekal, S., Liu, S., Zhou, Z., Bergounioux, C., Miao, L., Meksem, J., Lakhssassi, A., Jones, K., Kassem, M., Benhamed, , Bendahmane, A., Lambert, K., Boualem, A., Hewezi, T., Meksem, K. |
| Abstract: | Soybean cyst nematode (SCN, Heterodera glycines) is the most devastating pest affecting soybean production worldwide. SCN resistance requires both theGmSHMT08and theGmSNAP18in Peking-type resistance.Here, we describe the molecular interaction between GmSHMT08 and GmSNAP18, which is potentiated by a pathogenesis-related protein GmPR08-Bet VI. LikeGmSNAP18andGmSHMT08,GmPR08-Bet VIexpression was induced in response to SCN and its overexpression decreased SCN cysts by 65% in infected transgenic soybean roots. Overexpression of GmPR08-Bet VI did not have an effect on SCN resistance when the two cytokinin-binding sites in GmPR08-Bet VI were mutated, indicating a new role of GmPR08-Bet VI in SCN resistance. GmPR08-Bet VI was mapped to a QTL for resistance to SCN using different mapping populations. GmSHMT08, GmSNAP18 and GmPR08-Bet VI localize to the cytosol and plasma membrane.GmSNAP18expression and localization hyper-accumulated at the plasma membrane and was specific to the root cells surrounding the nematode in SCN-resistant soybeans. Genes encoding key components of the salicylic acid signalling pathway were induced under SCN infection.GmSNAP18andGmPR08-Bet VIwere also induced under salicylic acid and cytokinin exogenous treatments, whileGmSHMT08was induced only when the resistantGmSNAP18was present, pointing to the presence of a molecular crosstalk between SCN-resistant genes and defence genes. Expression analysis ofGmSHMT08andGmSNAP18identified the need of a minimum expression requirement to trigger the SCN resistance reaction. These results provide insight into a new response mechanism towards plant nematode resistance involving haplotype compatibility, gene dosage and hormone signalling. |
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