数字农科院2.0

Rice DWARF AND LOW-TILLERING and the homeodomain protein OSH15 interact to regulate internode elongation via orchestrating brassinosteroid signaling and metabolism

文献类型： 外文期刊

作者： Niu, Mei;Wang, Hongru;Yin, Wenchao;Meng, Wenjing;Xiao, Yunhua;Liu, Dapu;Zhang, Xiaoxing;Dong, Nana;Liu, Jihong;Yang, Yanzhao;Zhang, Fan;Chu, Chengcai;Tong, Hongning

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期刊名称： PLANT CELL

ISSN： 1040-4651

年卷期： 2022 年

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收录情况： SCIE（2022版）

摘要： DWARF AND LOW-TILLERING interacts with the homeodomain protein OSH15, which directly targets the brassinosteroid receptor gene OsBRI1 and is expressed in lower internodes, to regulate the internode elongation via modulating brassinosteroid signaling and metabolism. Brassinosteroid (BR) phytohormones play crucial roles in regulating internode elongation in rice (Oryza sativa). However, the underlying mechanism remains largely unclear. The dwarf and low-tillering (dlt) mutant is a mild BR-signaling-defective mutant. Here, we identify two dlt enhancers that show more severe shortening of the lower internodes compared to the uppermost internode (IN1). Both mutants carry alleles of ORYZA SATIVA HOMEOBOX 15 (OSH15), the founding gene for dwarf6-type mutants, which have shortened lower internodes but not IN1. Consistent with the mutant phenotype, OSH15 expression is much stronger in lower internodes, particularly in IN2, than IN1. The osh15 single mutants have impaired BR sensitivity accompanied by enhanced BR synthesis in seedlings. DLT physically interacts with OSH15 to co-regulate many genes in seedlings and internodes. OSH15 targets and promotes the expression of the BR receptor gene BR INSENSITIVE1 (OsBRI1), and DLT facilitates this regulation in a dosage-dependent manner. In osh15, dlt, and osh15 dlt, BR levels are higher in seedlings and panicles, but unexpectedly lower in internodes compared with the wild-type. Taken together, our results suggest that DLT interacts with OSH15, which functions in the lower internodes, to modulate rice internode elongation via orchestrating BR signaling and metabolism.

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