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Free Content The rice SPINDLY gene functions as a negative regulator of gibberellin signaling by controlling the suppressive function of the DELLA protein, SLR1, and modulating brassinosteroid synthesis

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SPINDLY (SPY) encodes an O-linked N-acetylglucosamine transferase that is considered to be a negative regulator of gibberellin (GA) signaling through an unknown mechanism. To understand the function of SPY in GA signaling in rice, we isolated a rice SPINDLY homolog (OsSPY) and produced knockdown transgenic plants in which OsSPY expression was reduced by introducing its antisense or RNAi construct. In knockdown plants, the enhanced elongation of lower internodes was correlated with decreased levels of OsSPY expression, similar to the spindly phenotype of Arabidopsis spy mutants, suggesting that OsSPY also functions as a negative factor in GA signaling in rice. The suppressive function of OsSPY in GA signaling was supported by the findings that the dwarfism was partially rescued and OsGA20ox2 (GA20 oxidase) expression was reduced in GA-deficient and GA-insensitive mutants by the knockdown of OsSPY function. The suppression of OsSPY function in a GA-insensitive mutant, gid2, also caused an increase in the phosphorylation of a rice DELLA protein, SLR1, but did not change the amount of SLR1. This indicates that the function of OsSPY in GA signaling is not via changes in the amount or stability of SLR1, but probably involves control of the suppressive function of SLR1. In addition to the GA-related phenotypes, OsSPY antisense and RNAi plants showed increased lamina joint bending, which is a brassinosteroid-related phenotype, indicating that OsSPY may play roles both in GA signaling and in the brassinosteroid pathway.
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Keywords: DELLA protein; SPINDLY gene; brassinosteroid; gibberellin signaling; rice genomics

Document Type: Research Article

Affiliations: 1: Bioscience and Biotechnology Center, Nagoya University, Chikusa, Nagoya, Aichi 464-8601, Japan, 2: Field Production Science Center, University of Tokyo, Nishi-Tokyo, Tokyo 188-0002, Japan, 3: RIKEN (The Institute of Physical and Chemical Research), Wako-shi, Saitama 351-0198, Japan, and 4: Department of Chemistry, Joetsu University of Education, Joetsu-shi, Niigata 943-8512, Japan

Publication date: November 1, 2006

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