Abstract
SUMMARYMutants defective in brassinosteroid (BR) biosynthesis or signaling pathways often display semi-dwarfism, as do the highly productive gibberellin mutants that enabled the Green Revolution. However, reduced vegetative growth in BR mutants does not necessarily correspond to increased seed yields. To better understand the mode of action of BR, we isolated a rice propiconazole resistant1-D (pzr1-D) mutant by screening an activation-tagging mutant population in the presence of the BR biosynthesis inhibitor propiconazole (Pcz). The expression of a putative transcription factor gene homologous to Arabidopsis Dimerization Partner (DPb) was activated in pzr1-D. pzr1-D exhibited characteristic phenotypes such as reduced height, and increased seed yields and tiller numbers. Like Arabidopsis DPb, rice PZR1 is expressed differentially in the tissues examined. Furthermore, pzr1-D displayed altered cell division phenotypes, including the production of small calli. In addition, the cell number and size in mutant roots and leaves differed from those in wild-type plants of the same age. RNA sequencing revealed that the promoters of differentially expressed genes are enriched with cognate sequences for both BZR1 and EF-DPb transcription factors, suggesting that PZR1 functions in BR-mediated cell division in rice. PZR1 expression may thus be manipulated to increase seed yield in economically important rice varieties.SIGNIFICANCE STATEMENTMutants defective in brassinosteroid biosynthesis or signaling pathways often display semi-dwarfism. However, in many cases these mutants do not necessarily produce increased seed yields. We show a rice propiconazole resistant1-D (pzr1-D) mutant which exhibits reduced height phenotypes along with increase tiller number and seed yields. pzr1-D shows activation of a putative homologous to Arabidopsis Dimerization Partner (DPb) with functions in cell division, pointing that PZR1 may function in BR-mediated cell division in rice.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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