Mol Plant| 徐云远/张启发/傅向东合作揭示RING E3连接酶CLG1靶向GS3通过核内体途径降解水稻粒大小

G 蛋白信号和泛素依赖性降解都参与了水稻的籽粒发育，但是这些途径在调节这一过程中如何协调尚不清楚。结果表明，编码 E3连接酶的长力更1(CLG1)通过靶向谷粒长度负调节因子 gγ 蛋白 GS3的降解来调节谷粒大小。CLG1过表达导致籽粒长度增加，突变的 CLG1过表达导致三个保守氨基酸的变化导致籽粒长度减少。CLG1与 GS3物理相互作用并泛素化，GS3随后通过内生体降解途径降解，导致籽粒尺寸增大。我们还在 CLG1的第3外显子中发现了一个关键的 SNP，该 SNP 与栽培稻核心种质的粒度变异有关。这种 SNP 使 CLG1的 E3连接酶活性在163位点由 Arg 变为 Ser，从而使粒径增大。CLG1表达水平和 SNP 可能是控制籽粒大小的有效靶点。

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. CLG1 overexpression led to increased grain length, and overexpression of mutated CLG1 with changes in three conserved amino acids decreased grain length. CLG1 physically interacted with and ubiquitinated GS3; the latter was subsequently degraded through the endosome degradation pathway, leading to increased grain size. We also identified a critical SNP in exon 3 of CLG1 that was significantly associated with grain-size variation in a core collection of cultivated rice. This SNP resulted in an amino acid substitution from Arg to Ser at position 163, which enhancing the E3 ligase activity of CLG1, thus increasing grain size. Both the CLG1 expression level and the SNP may be useful targets for manipulating grain size.

https://doi.org/10.1016/j.molp.2021.06.027

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