G-protein signaling and ubiquitin-dependent degradation are both involved in grain development in rice, but how these pathways are coordinated in regulating this process is unknown. Here, we show that Chang Li Geng 1 (CLG1), which encodes an E3 ligase, regulates grain size by targeting the Gγ protein GS3, a negative regulator of grain length, for degradation. Overexpression of CLG1 led to increased grain length, while overexpression of mutated CLG1 with changes in three conserved amino acids decreased grain length. We found that CLG1 physically interacts with and ubiquitinats GS3which is subsequently degraded through the endosome degradation pathway, leading to increased grain size. Furthermore, we identified a critical SNP in the exon 3 of CLG1 that is significantly associated with grain size variation in a core collection of cultivated rice. This SNP results in an amino acid substitution from Arg to Ser at position 163 of CLG1 that enhances the E3 ligase activity of CLG1 and thus increases rice grain size. Both the expression level of CLG1 and the SNP CLG1^163S may be useful variations for manipulating grain size in rice.

G 蛋白信号传导和泛素依赖性降解都参与了水稻的籽粒发育，但这些途径如何协调调节这一过程尚不清楚。在这里，我们展示了编码 E3 连接酶的Chang Li Gen 1 ( CLG1 ) 通过靶向 Gγ 蛋白 GS3（一种谷粒长度的负调控因子）来调节谷粒大小以进行降解。CLG1 的过表达导致粒长增加，而突变的 CLG1 的过表达随着三个保守氨基酸的变化而降低了粒长。我们发现 CLG1 与 GS3 物理相互作用并泛素化，GS3 随后通过内体降解途径降解，导致晶粒尺寸增加。此外，我们在CLG1的外显子 3 中发现了一个关键的 SNP这与栽培稻核心种质的粒度变化显着相关。该 SNP 导致 CLG1 的第 163 位氨基酸从 Arg 替换为 Ser，从而增强了 CLG1 的 E3 连接酶活性，从而增加了水稻的颗粒大小。CLG1 和 SNP CLG1 ^163S的表达水平都可能是控制水稻颗粒大小的有用变异。