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Annotated Information

  • This gene is a rice dwarf mutant, ebisu dwarf (d2), which first was described asebisu dwarf in an article published in 1925. The D2 gene encodes a P450 protein that is classified in the CYP90D group that is highly similar to other BR biosynthesis P450 proteins, such as CPD/CYP90A, DWF4/CYP90B, and DWARF/CYP85. ebisu dwarf (dwarf2 or d2) is a good example of dwarf mutant, although its dwarfism is slightly stronger than the desirable level. In fact, the erect leaves of d2 allow this cultivar to be planted more densely than the original cultivar, which has bent leaves; consequently, a greater volume of crop products can be harvested in the same cultivation area.This dwarf mutant has unusual phenotypic characteristics, such as its erect leaves and the specific inhibition of second internode elongation. Thus, elucidation of the molecular mechanism of the relationship between dwarfism and erect leaves in d2 mutants is important for further molecular breeding for architectural modification.


  • RNAs extracted from the leaf blade and elongating stem produced the strongest bands derived from the D2 mRNA. Bands of intermediate intensity were amplified with RNAs from the shoot apical region and leaf sheath, whereas RNAs from the root, flower, rachis, and elongated stem produced only faint bands. The preferential expression of D2 in the leaf and elongating stem corresponded to the abnormal phenotype of the leaf structure and shortened stem. There also examined the expression pattern of the D2 homologous gene (CYP90D3). The expression level of CYP90D3 was much less than that of D2/CYP90D2, and the PCR product of CYP90D3 was barely detected in any organs under conditions identical to those used for D2/CYP90D2 (25 cycles). However, when the number of cycles was increased to 37, strong bands were observed in the root and faint bands were seen in the stem, leaf sheath, and flower[1].


  • ebisu dwarf (d2) is a mutant caused by mutation in a rice brassinosteroid biosynthetic enzyme gene, CYP90D2/D2, thereby conferring a brassinosteroid-deficient dwarf phenotype. Three newly isolated d2 alleles derived from a Nippon- bare mutant library (d2-3, d2-4, and d2-6) produced more severe dwarf phenotypes than the previously characterized null allele from a Taichung 65 mutant library, d2-1. Linkage analysis and a complementation test clearly indicated that the mutant phenotypes in d2-6 were caused by defects in CYP90D2/D2, and exogenous treatment with brassinolide, a bioactive brassinosteroid, rescued the dwarf phenotype of three Nipponbare-derived d2 mutants.Sequence analysis of CYP90D2/D2 from the three lines revealed that d2-3 had a single nucleotide substitution at the junction of exon 5 and intron 5 (G to C), d2-4 had a single nucleotide sub- stitution (G to T) in exon 2 that induced an amino acid residue change (from Gly to Cys), whereas d2-6 had a 40-bp deletion in exon 4 (Figure 2).The plant heights of the d2-3, d2-4, and d2-6 mutants were about 30 cm, whereas that of Nipponbare, the wild-type that gave rise to d2-3, d2-4, and d2-6, was about 90 cm (Figure 3)[2].


  • We characterized a rice dwarf mutant, ebisu dwarf (d2). It showed the pleiotropic abnormal phenotype similar to that of the rice brassinosteroid (BR)-insensitive mutant, d61. The dwarf phenotype of d2 was rescued by exogenous brassinolide treatment. The accumulation profile of BR intermediates in the d2 mutants confirmed that these plants are deficient in late BR biosynthesis. We cloned the D2 gene by map-based cloning. The D2 gene encoded a novel cytochrome P450 classified in CYP90D that is highly similar to the reported BR synthesis enzymes. Introduction of the wild D2 gene into d2-1 rescued the abnormal phenotype of the mutants. In feeding experiments, 3-dehydro-6-deoxoteasterone, 3-dehydroteasterone, and brassinolide effectively caused the lamina joints of the d2 plants to bend, whereas more upstream compounds did not cause bending. Based on these results, we conclude that D2/CYP90D2 catalyzes the steps from 6-deoxoteasterone to 3-dehydro-6-deoxoteasterone and from teasterone to 3-dehydroteasterone in the late BR biosynthesis pathway[1].

Knowledge Extension

A proposed model of Strigolactone(SL) signalling patyway [3]).
  • Strigolactones (SLs) are a group of newly identified plant hormones that control plant shoot branching[3]. SL signaling requires the hormone-dependent interaction of DWARF14 (D14) which is regulated by the interaction of OsMADS57 with OsTB1[4].
  • In this study[3], they have identified theD53gene that encodes a substrate of the SCF(D3) ubiquitination complex, and revealed that D53 functions as a repressor ofSL signalling. These results allow to establish a model of SL signalling that is centred around a D14–D3–D53 signalling axis . In the presence of SLs, perception of SL by D14 and the SCF(D3) complex leads to ubiquitination of D53 and its subsequent degradation by the ubiquitin proteasome system, which in turn releases the repression of downstream target genes . In the d53 plant, the mutated D53 protein is resistant to ubiquitination and degradation, leading to the accumulation of d53, which blocks SL signalling and results in dwarf and high tillering phenotypes. The signalling paradigm of SLs is still emerging as SLs are a relatively new class of plant hormone for which many knowledge gaps still exist. Identification of D53 as a repressor of SL signalling adds a critical piece of information that helps to paint the whole picture of the SL signalling pathways.

Moreover, the work has also provided an important paradigm for understanding signalling pathways of other plant hormones, for example, karrikins, a class of plant growth regulators found in the smoke of burning plants. Karrikin signalling involves MAX2 and KAI2, a D14-like α / β-hydrolase. It is probable that a similar protein to D53 could serve as the repressor of karrikin signalling. Indeed, multiple D53-like proteins are found in rice and inArabidopsis. We propose that these proteins could serve as repressors of signalling by karrikin and other plant hormones, in a similar way to D53 in SL signalling.[3]

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Labs working on this gene

  • BioScience and Biotechnology Center, Nagoya University, Chikusa, Nagoya 464-8601, Japan
  • Graduate School of Bioagricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan
  • RIKEN (The Institute of Physical and Chemical Research), Wako-shi, Saitama 351-0198, Japan
  • Department of Chemistry, Joetsu University of Education, Joetsu-shi, Niigata 943-8512, Japan
  • Faculty of Bioresources and Environmental Sciences, Ishikawa Prefectural University, Nonoichi, Japan
  • State Key Laboratory for Crop Genetics and Germplasm Enhancement, Jiangsu Plant Gene Engineering Research Center, Nanjing Agricultural University, Nanjing, China
  • National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Science, Chinese Academy of Agricultural Sciences, Beijing, China
  • Department of Life Science, Chung-Ang University, Seoul, Korea


  1. 1.0 1.1 Zhi Hong;Miyako Ueguchi-Tanaka;Kazuto Umemura;Sakurako Uozu;Shozo Fujioka;Suguru Takatsuto;Shigeo Yoshida;Motoyuki Ashikari;Hidemi Kitano and Makoto Matsuok. A Rice Brassinosteroid-Deficient Mutant, ebisu dwarf (d2), Is Caused by a Loss of Function of a New Member of Cytochrome P450.The Plant Cell, 2003, 15(12):2900-2910
  2. Sakamoto, Tomoaki; Morinaka, Yoichi; Kitano, Hidemi; Fujioka, Shozo.New Alleles of Rice ebisu dwarf (d2) Mutant Show Both Brassinosteroid-Deficient and -Insensitive Phenotypes,American Journal of Plant Sciences . Dec2012, Vol. 3 Issue 12, p1699-1707. 9p.
  3. 3.0 3.1 3.2 3.3 Jiang L, Liu X, Xiong G, et al. DWARF 53 acts as a repressor of strigolactone signalling in rice[J]. Nature 2013.
  4. Guo S, Xu Y, Liu H, et al. The interaction between OsMADS57 and OsTB1 modulates rice tillering via DWARF14[J]. Nature communications 2013; 4: 1566.

Structured Information