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Z. Hong, M. Ueguchi-Tanaka, S. Shimizu-Sato, Y. Inukai, S. Fujioka, Y. Shimada, S. Takatsuto, M. Agetsuma, S. Yoshida, Y. Watanabe, S. Uozu, H. Kitano, M. Ashikari and M. Matsuoka, “Loss-of-Function of a Rice Brassinosteroid Biosynthetic Enzyme, C-6 Oxidase, Prevents the Organized Arrangement and Polar Elongation of Cells in the Leaves and Stem,” Plant Journal, Vol. 32, No. 4, 2002, pp. 495-508.
doi:10.1046/j.1365-313X.2002.01438.x
has been cited by the following article:
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TITLE:
New Alleles of Rice ebisu dwarf (d2) Mutant Show both Brassinosteroid-Deficient and -Insensitive Phenotypes
AUTHORS:
Tomoaki Sakamoto, Yoichi Morinaka, Hidemi Kitano, Shozo Fujioka
KEYWORDS:
Brassinosteroids; Brassinosteroid Biosynthetic Enzymes; Brassinosteroid Sensitivity;Cytochrome P450 Monooxygenase; Mutant Allele; Rice
JOURNAL NAME:
American Journal of Plant Sciences,
Vol.3 No.12,
December
26,
2012
ABSTRACT: 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. However, the content of endogenous bioactive brassinosteroid, castasterone, and the expression of brassinosteroid-response genes indicated that partial suppression of the brassinosteroid response in addition to a brassinosteroid deficiency has occurred in the Nipponbare-derived d2 mutants. Based on these results, we discuss the possibility that wild-type Nipponbare has some defects in an unknown factor or factors related to the brassinosteroid response in rice.