A loss-of-function mutation in the DWARF4/PETANKO5 gene enhances the late-flowering and semi-dwarf phenotypes of the Arabidopsis clock mutant lhy-12;cca1-101 under continuous light without affecting FLC expression

  • Suzuki Syunji
    Gene Research Center, University of Tsukuba
  • Miyata Kana
    Gene Research Center, University of Tsukuba Department of Natural Sciences, International Christian University
  • Hara Miyuki
    Gene Research Center, University of Tsukuba Department of Natural Sciences, International Christian University
  • Niinuma Kanae
    Gene Research Center, University of Tsukuba
  • Tsukaya Hirokazu
    Department of Biological Sciences, Graduate School of Science, The University of Tokyo Bio-Next Project, Okazaki Institute for Integrative Bioscience, National Institutes of Natural Sciences
  • Takase Masahide
    Department of Biological Sciences, Graduate School of Science, The University of Tokyo
  • Hayama Ryosuke
    Department of Natural Sciences, International Christian University
  • Mizoguchi Tsuyoshi
    Gene Research Center, University of Tsukuba Department of Natural Sciences, International Christian University

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  • A loss-of-function mutation in the <i>DWARF4</i>/<i>PETANKO5</i> gene enhances the late-flowering and semi-dwarf phenotypes of the <i>Arabidopsis</i> clock mutant <i>lhy-12;cca1-101</i> under continuous light without affecting <i>FLC</i> expression

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The circadian clock plays important roles in the control of photoperiodic flowering in Arabidopsis. Mutations in the LATE ELONGATED HYPOCOTYL (LHY) and CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) genes (lhy;cca1) accelerate flowering under short days, whereas lhy;cca1 delays flowering under continuous light (LL). The lhy;cca1 mutant also exhibits short hypocotyls and petioles under LL. However, the molecular mechanisms underlying the regulation of both flowering time and organ lengths in the LHY/CCA1-dependent pathway are not fully understood. To address these questions, we performed EMS mutagenesis of the lhy-12;cca1-101 line and screened for mutations that enhance the lhy;cca1 phenotypes under LL. In this screen, we identified a novel allele of dwarf4 (dwf4) and named it petanko 5 (pta5). A similar level of enhancement of the delay in flowering was observed in these two dwf4 mutants when combined with the lhy;cca1 mutations. The lhy;cca1 and dwf4 mutations did not significantly affect the expression level of the floral repressor gene FLC under LL. Our results suggest that a defect in brassinosteroid (BR) signaling delayed flowering independent of the FLC expression level, at least in plants with the lhy;cca1 mutation grown under LL. The dwf4/pta5 mutation did not enhance the late-flowering phenotype of plants overexpressing SVP under LL, suggesting that SVP and BR function in a common pathway that controls flowering time. Our results suggest that the lhy;cca1 mutant exhibits delayed flowering due to both the BR signaling-dependent and -independent pathways under LL.

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