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 Nipponbare 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.
Highlights
Brassinosteroids are endogenous phytohormones that are involved in the regulation of various growth and developmental processes in higher plants, including cell and stem elongation, dark-adapted morphogenesis, environmental stress responses, and the differentiation of tracheary elements [1,2,3]
Because the gross morphology of newly isolated three mutants were ranged between group-2 and group-3, we hypothesized that these mutants had defects in one or (a) more novel brassinosteroid biosynthetic enzymes or had novel defects in one or more previously identified brassinosteroid biosynthetic enzymes
The expression of CYP90D3 in Taichung 65 seemed to be regulated normally by the homeostatic system that controls the levels of bioactive brassinosteroids, these results indicate that the magnitude of the mutant phenotype caused by the mutations in CYP90D2/D2 could not be explained by the insertion of miniature Ping (mPing) in the Taichung 65 CYP90D3 gene or by the genetic redundancy of the CYP90D2/D2 and CYP90D3 genes in rice
Summary
Brassinosteroids are endogenous phytohormones that are involved in the regulation of various growth and developmental processes in higher plants, including cell and stem elongation, dark-adapted morphogenesis (skotomorphogenesis), environmental stress responses, and the differentiation of tracheary elements [1,2,3]. Overproduction and deficiency of brassinosteroids both increased grain and biomass yield, they did this by different mechanisms [6,7,8]. Brassinosteroid-deficient dwarf (brd2) is caused by mutations in the sterol biosynthetic enzyme gene DIMINUTO/ DWARF1, which functions in the conversion of 24-methylenecholesterol to campesterol [16]. Characterization of these brassinosteroid-deficient mutants has helped us to understand the regulation of brassinosteroid biosynthesis in rice and the functions of brassinosteroids in rice growth and development. There are several enzymes involved in rice brassinosteroid biosynthesis for which mutants have not yet been isolated
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