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C. Yamamuro, Y. Ihara, X. Wu, T. Noguchi, S. Fujioka, S. Takatsuto, M. Ashikari, H. Kitano and M. Matsuoka, “Loss of Function of a Rice brassinosteroid insensitive1 Homolog Prevents Internode Elongation and Bending of the Lamina Joint,” Plant Cell, Vol. 12, No. 9, 2000, pp. 1591-1606.

has been cited by the following article:

• 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.