Abstract
(i)SummaryTherhg1-aandrhg1-bhaplotypes of the soybeanRhg1locus are economically effective tools for the control of soybean cyst nematode (SCN;Heterodera glycines), but ongoing SCN evolution requires improved sources of resistance. BothRhg1haplotypes carry multiple tandem repeat copies of a four-gene block encoding four disparate proteins; resistance efficacy scales with copy number. The haplotypes encode different variants of an unusual α-SNAP protein whose abundance increases in the nematode-reprogrammed plant cells that form the syncytium (nematode feeding site), which subsequently collapses. Simultaneous presence of the two α-SNAPRhg1protein types, or substantially elevated expression of either type, was hypothesized to improve SCN resistance but has not been achievable by conventional plant breeding methods. We accomplished both, by transgenic additions to anrhg1-a Rhg4soybean line. Existing resistance to HG type 0 and HG type 2.5.7 SCN was strengthened, but resistance was not improved against an HG type 1.3.6.7 SCN population that was already highly virulent on the parent line. No significant yield penalties from constitutive overexpression of transgenic α-SNAP genes were observed in greenhouse or initial field studies. Cisgenic combination or elevated expression of the different α-SNAP genes may extend the efficacy and/or durability ofRhg1-mediated resistance. We also observed differential protein abundances for some α-SNAPRhg1isoforms after inoculation with different HG type populations of SCN. These approaches provide opportunities to understand the different mechanisms of the twoRhg1haplotypes and to possibly fine-tune them for better management of SCN.
Publisher
Cold Spring Harbor Laboratory