Glyceollin isomers I, II, and III are the major pathogen-elicited secondary metabolites (i.e. phytoalexins) of soybean (Glycine max) that, collectively with other 5-deoxyisoflavonoids, provide race-specific resistance to Phytophthora sojae. The NAC-family transcription factor (TF) GmNAC42-1 is an essential regulator of some but not all glyceollin biosynthesis genes, indicating other essential TF(s) of the glyceollin gene regulatory network remain to be identified. Here, we conducted comparative transcriptomics on soybean hairy roots of the variety Williams 82 and imbibing seeds of Harosoy 63 upon treatment with wall glucan elicitor from P. sojae and identified two homologous R2R3-type MYB TF genes, GmMYB29A1 and GmMYB29A2, up-regulated during the times of peak glyceollin biosynthesis. Overexpression and RNA interference silencing of GmMYB29A2 increased and decreased expression of GmNAC42-1, GmMYB29A1, and glyceollin biosynthesis genes and metabolites, respectively, in response to wall glucan elicitor. By contrast, overexpressing or silencing GmMYB29A1 decreased glyceollin I accumulation with marginal or no effects on the expressions of glyceollin synthesis genes, suggesting a preferential role in promoting glyceollin turnover and/or competing biosynthetic pathways. GmMYB29A2 interacted with the promoters of two glyceollin I biosynthesis genes in vitro and in vivo. Silencing GmMYB29A2 in Williams 82, a soybean variety that encodes the resistance gene Rps1k, rendered it compatible with race 1 P. sojae, whereas overexpressing GmMYB29A2 rendered the susceptible Williams variety incompatible. Compatibility and incompatibility coincided with reduced and enhanced accumulations of glyceollin I but not other 5-deoxyisoflavonoids. Thus, GmMYB29A2 is essential for accumulation of glyceollin I and expression of Phytophthora resistance.

甘油三醇异构体I，II和III是大豆（Glycine max）的主要病原体诱发的次级代谢产物（即phyalealexins），与其他5-deoxyisoflavonoids共同提供对大豆疫霉菌的种族特异性抗性。NAC家族转录因子（TF）GmNAC42-1是某些但不是全部甘油生物合成基因的必需调节剂，表明该甘氨酸基因调节网络的其他必需TF有待确定。在这里，我们在治疗与壁葡聚糖引发子进行了的各种威廉姆斯82大豆发根比较转录和Harosoy 63的吸液种子大豆疫霉，并确定两个同源R2R3-MYB型TF的基因，GmMYB29A1和GmMYB29A2在糖醇生物合成峰值期间被上调。响应于壁葡聚糖激发子，GmMYB29A2的过表达和RNA干扰沉默分别增加和减少了GmNAC42-1，GmMYB29A1和glyceollin生物合成基因和代谢产物的表达。相比之下，过表达或沉默GmMYB29A1减少了糖精蛋白I的积累，对糖精蛋白合成基因的表达几乎没有影响，暗示了在促进糖精蛋白更新和/或竞争生物合成途径方面的优先作用。GmMYB29A2在体外和体内与两个糖精I的生物合成基因的启动子相互作用。沉默GmMYB29A2在Williams 82中，编码抗性基因Rps1k的大豆变种使其与1 P. sojae种相容，而过表达GmMYB29A2使易感威廉斯变种不相容。相容性和不相容性与甘油糖醇I的积累减少和增强相吻合，而其他5-deoxyisoflavonoids则没有。因此，GmMYB29A2对于甘油I的积累和疫霉菌抗性的表达至关重要。