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ARS Home » Pacific West Area » Albany, California » Plant Gene Expression Center » Research » Publications at this Location » Publication #311103

Research Project: Identification and Analysis of Plant Architectural Genes in Maize

Location: Plant Gene Expression Center

Title: Genome-wide study of KNOX regulatory network reveals brassinosteroid catabolic genes important for shoot meristem function in rice

item Tsuda, Katsutoshi - University Of California
item Kurata, Nori - Shizuoka University
item Ohyanagi, Hajime - National Institute Of Genetics
item Hake, Sarah

Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/15/2014
Publication Date: 9/5/2014
Citation: Tsuda, K., Kurata, N., Ohyanagi, H., Hake, S.C. 2014. Genome-wide study of KNOX regulatory network reveals brassinosteroid catabolic genes important for shoot meristem function in rice. The Plant Cell. 26(9):3488-3500.

Interpretive Summary: Homeobox transcription factors regulate many aspects of development in plants and animals. The KNOTTED1-like homeobox (KNOX) plant transcription factors are essential for organ initiation. Previous data suggested that KNOX proteins regulate the hormones auxin and gibberellin. Here, gain and loss of function studies revealed that the rice KNOX protein, OSH1, negatively regulates the brassinosteroid (BR) phytohormone pathway. Genomics approaches identified BR catabolism genes as direct targets of OSH1 in the shoot meristems. RNAi knockdown studies suggested that BR catabolism is important for shoot meristem function and for regulation of panicle branch angle.

Technical Abstract: In flowering plants, knotted1-like homeobox (KNOX) transcription factors play crucial roles in establishment and maintenance of the shoot apical meristem (SAM), from which aerial organs such as leaves, stems, and flowers initiate. We report that a rice (Oryza sativa) KNOX gene Oryza sativa homeobox1 (OSH1) represses the brassinosteroid (BR) phytohormone pathway through activation of BR catabolism genes. Inducible overexpression of OSH1 caused BR insensitivity, whereas loss of function showed a BR-overproduction phenotype. Genome-wide identification of loci bound and regulated by OSH1 revealed hormonal and transcriptional regulation as the major function of OSH1. Among these targets, BR catabolism genes CYP734A2, CYP734A4, and CYP734A6 were rapidly upregulated by OSH1 induction. Furthermore, RNA interference knockdown plants of CYP734A genes arrested growth of the SAM and mimicked some osh1 phenotypes. Thus, we suggest that local control of BR levels by KNOX genes is a key regulatory step in SAM function.