Os11g0104300
DWARF 53(Os11g0104300) acts as a repressor of strigolactone signalling in rice.[1]
Contents
Annotated Information
Name
DWARF53（D53)
Phenotype
The rice (Oryza sativa) d53 mutant, which displays reduced height and increased tillering, as well as thinner stem and shorter crown root compared to wild-type plants, is caused by a gain-of-function mutation and is insensitive to exogenous SL treatment. Further, measurement of SLs produced in the root exudates showed that d53 accumulated markedly higher levels of 2′-epi-5-deoxystrigol (epi-5DS), a native SL of rice, than the wild-type cultivar Norin 8.[2] [[File:phenotype of d53 mutant.jpg]
Characterization
D53 was mapped to the terminal region of the short arm of rice chromosome 11. A single-nucleotide substitution and 15-nucleotide deletion in the third exon of LOC_Os11g01330 in d53, which resulted in an amino acid substitution (R812T) and deletion of five amino acids (813GKTGI817).[2]
Function
DWARF53（D53) encodes a substrate of the SCF-D3 ubiquitination complex and functions as a repressor of SL signalling, whose hormone-induced degradation represents a key molecular link between SL perception and responses. D53 can interact with transcriptional co-repressors known as TOPLESS-RELATED PROTEINS.[2] In the absence of SLs, D53 is stable and may recruit TPL/TPR proteins and repress downstream responses. In the presence of SLs, perception of SL leads to SCFD3-mediated ubiquitination of D53 and its subsequent degradation by the proteasome system, which in turn releases the repression of downstream responses.[1]
Expression
The D53 gene product shares predicted features with the class I Clp ATPase proteins and can form a complex with thea/bhydrolase protein DWARF 14 (D14) and the F-box protein DWARF 3 (D3), two previously identified signalling components potentially responsible for SL perception. In a D14- and D3-dependent manner, SLs induce D53 degradation by the proteasome and abrogate its activity in promoting axillary bud outgrowth.[2]
Labs working on this gene
- National Key Laboratory for Crop Genetics and Germplasm Enhancement, Jiangsu Plant Gene Engineering Research Center, Nanjing Agricultural University, Nanjing 210095, China
- National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Science, Chinese Academy of Agricultural Sciences, Beijing 100081, China
- Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
- Howard Hughes Medical Institute, Box 357280, University of Washington, Seattle, Washington 98195, USA
- National Centre for Plant Gene Research (Beijing), Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, 1-2 Beichen West Road, Beijing 100101, China
- Department of Applied Biological Chemistry, The University of Tokyo, 1-1-1 Yayoi, Bunkyo, Tokyo 113-8657, Japan
References
- ↑ 1.0 1.1 Liang Jiang, Xue Liu, Guosheng Xiong, Huihui Liu, Fulu Chen, Lei Wang, Xiangbing Meng, Guifu Liu, Hong Yu, Yundong Yuan, Wei Yi, Lihua Zhao, Honglei Ma, Yuanzheng He, Zhongshan Wu, Karsten Melcher, Qian Qian, H. Eric Xu, Yonghong Wang & Jiayang Li[J]. Nature, 2013, 504,:401–405.
- ↑ 2.0 2.1 2.2 2.3 Feng Zhou, Qibing Lin, Lihong Zhu, Yulong Ren, Kunneng Zhou, Nitzan Shabek, Fuqing Wu, Haibin Mao, Wei Dong, Lu Gan, Weiwei Ma, He Gao, Jun Chen, Chao Yang, Dan Wang, Junjie Tan, Xin Zhang, Xiuping Guo, Jiulin Wang, Ling Jiang, Xi Liu, Weiqi Chen, Jinfang Chu, Cunyu Yan, Kotomi Ueno etal.D14–SCFD3-dependent degradation of D53 regulates strigolactone signalling[J]. Nature, 2013, 504:406–410.
