A transthyretin-like protein acts downstream of miR397 and LACCASE to regulate grain yield in rice
文献类型： 外文期刊
作者： Yu, Yang 1 ; He, Rui-Rui 1 ; Yang, Lu 1 ; Feng, Yan-Zhao 1 ; Xue, Jiao 2 ; Liu, Qing 3 ; Zhou, Yan-Fei 1 ; Lei, Meng-Qi 1 ; Zhang, Yu-Chan 1 ; Lian, Jian-Ping 1 ; Chen, Yue-Qin 1 ;
作者机构： 1.Sun Yat Sen Univ, Sch Life Sci, Guangdong Prov Key Lab Plant Resources, State Key Lab Biocontrol, Guangzhou 510275, Peoples R China
2.Guangdong Acad Agr Sci, Agrobiol Gene Res Ctr, Guangdong Key Lab Crop Germplasm Resources Preserv, Minist Agr & Rural Affairs,Key Lab South China Mod, Guangzhou 510640, Peoples R China
3.Guangdong Acad Agr Sci, Guangdong Key Lab New Technol Rice Breeding, Guangdong Rice Engn Lab, Rice Res Inst, Guangzhou 510640, Peoples R China
期刊名称：PLANT CELL （ 影响因子：11.6； 五年影响因子：12.9 ）
ISSN： 1040-4651
年卷期： 2024 年
页码：
收录情况： SCI
摘要： Increasing grain yield is a major goal of breeders due to the rising global demand for food. We previously reported that the miR397-LACCASE (OsLAC) module regulates brassinosteroid (BR) signaling and grain yield in rice (Oryza sativa). However, the precise roles of laccase enzymes in the BR pathway remain unclear. Here, we report that OsLAC controls grain yield by preventing the turnover of TRANSTHYRETIN-LIKE (OsTTL), a negative regulator of BR signaling. Overexpressing OsTTL decreased BR sensitivity in rice, while loss-of-function of OsTTL led to enhanced BR signaling and increased grain yield. OsLAC directly binds to OsTTL and regulates its phosphorylation-mediated turnover. The phosphorylation site Ser226 of OsTTL is essential for its ubiquitination and degradation. Overexpressing the dephosphorylation-mimic form of OsTTL (OsTTLS226A) resulted in more severe defects than did overexpressing OsTTL. These findings provide insight into the role of an ancient laccase in BR signaling and suggest that the OsLAC-OsTTL module could serve as a target for improving grain yield. Laccase controls grain size and yield in rice by preventing the turnover of a negative regulator of brassinosteroid signaling.
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