株型是影响水稻产量的重要因素。野生稻具有匍匐生长和分蘖过多的株型特征，不利于密植栽培。在水稻驯化过程中，人类通过对自然变异位点的人工选择逐渐把野生稻的株型驯化成直立生长和分蘖适当的栽培稻株型。我们前期的研究表明，PROG1是决定野生稻匍匐生长的关键基因。为解析PROG1的遗传调控网络，我们用EMS诱变PROG1的近等基因系，获得了一批株型回复直立生长的突变体。我们对其中一个突变体suppresser of PROG1 6 (sop6)进行了图位克隆，发现SOP6编码一个功能未知的类枯草杆菌蛋白酶。在本项目中，我们拟采用分子生物学、生物化学、生物信息学等方法，深入开展SOP6的功能研究，阐明SOP6的分子机制，探讨其与PROG1的关系，发掘有利基因位点，从而拓展水稻株型调控的遗传网络。

Plant architecture is of major agronomic importance as it determines rice yield. Oryza rufipugen shows a prostrate growth habit with more tillers, prohibiting dense plantings. Such undesirable plant architecture was targeted and continuously selected against by ancient humans, which gradually resulted in the more desirable plant architecture of domesticated rice (O. sativa). Domesticated rice shows relatively erect growth (a narrow tiller angle) and fewer tillers, which allows for effective high-yield cultivation. We previously demonstrated that the PROG1 gene controls aspects of wild-rice plant architecture, including tiller angle and number of tillers. To identify other components in the PROG1 pathway, we initiated a genetic screen for modifiers of a near-isogenic line, NIL(PROG1), in plant architecture. From this screen, we identified several suppressors of PROG1 (sop) from ethyl methanesulfonate–treated populations of NIL(PROG1). One of these mutants, sop6, exhibits erect growth habit. We showed that SOP6 is a previously unreported subtilase (subtilisin-like protease). Based on these results, we will study its gene function, molecular mechanism, the relationship between SOP6 and PROG1, and find potentially valuable alleles. This project may shade light on understanding of the regulatory network of plant architecture in rice.

株型是影响水稻产量的重要因素。野生稻具有匍匐生长和分蘖过多的株型特征，不利于密植栽培。在水稻驯化过程中，人类通过对自然变异植株的人工选择逐渐把野生稻的株型驯化成直立生长和分蘖适当的栽培稻株型。我们前期的研究表明，PROG1是决定野生稻匍匐生长的关键基因。为解析PROG1的遗传调控网络，我们用EMS诱变PROG1的近等基因系NIL（PROG1），获得了一批株型回复直立生长的突变体。其中一个突变体suppresser of PROG1 5（sop5）能基本上回复NIL（PROG1）的表型，同时还表现出茎秆粗壮、叶片宽厚、粒型变宽等性状。我们克隆了SOP5基因，发现该基因编码植物特有的转录因子，突变位点造成该基因在翻译时提前终止。将SOP5基因的表达量下调，会使水稻表现出分蘖数减少、叶倾角变小等类似突变体的表型；而过量表达SOP5基因则会出现相反的表型。sop5突变体对BR不敏感。过量表达SOP5基因可以基本互补bri1突变体的表型；而sop5突变体和BIN2 knock-down株系聚合时表现出类似sop5的表型。这暗示SOP5在BR信号通路的下游发挥作用。进一步的实验表明，SOP5蛋白能够与BR信号通路的关键负调控因子BIN2互作，推测BIN2能够通过与SOP5的直接互作对其进行磷酸化修饰。这说明SOP5受到BR信号通路的调控。同时我们的研究还发现，SOP5对株型的调控还受到Striglactone信号通路和GA信号通路的调节。因此，SOP5可以通过整合协调多种发育信号，精细调控水稻的株型建成。