<p>Drought stress triggers abscisic acid (ABA) signaling in plants but underline regulatory mechanisms remains incompletely understood. Recently, HOS15, a CUL4-DDB1-based substrate receptor, was shown to regulate ABA signaling and drought stress responses by targeting the drought-induced protein DIL9 for degradation. We show a novel HOS15-DIL9 regulatory module fine-tuning ABA signaling and drought. HOS15 mediated DIL9 turnover likely modulates downstream stress genes expression. Additionally, DIL9 directly binds to the promoters of <i>ABF</i>s (<i>ABF1-4</i>) and <i>NCED3</i> and activates their expression under drought stress. <i>ABFs</i> and <i>NCED3</i> expression markedly elevated in <i>DIL9-GFP/hos15-2</i> compared to <i>DIL9-GFP</i> plants under stress conditions, indicating that HOS15 restricts DIL9 activation of <i>ABFs</i> and <i>NCED3</i> genes. HOS15 promotes DIL9 degradation, thereby establishing a negative feedback loop that links NCED3-depedent ABA biosynthesis coupled to ABF-mediated ABA signaling. Thus, our findings demonstrate that HOS15 attenuates DIL9 activity <i>via</i> proteasomal degradation, thereby fine-tuning ABA and drought responses in Arabidopsis.</p>

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Arabidopsis E3 Ligase HOS15 Regulates ABA and Drought Responses via DIL9 Degradation

  • Shah Zareen,
  • Akhtar Ali,
  • Min Jae Bae,
  • Nassem Albakri,
  • Kisuk Park,
  • Hyeseon Yun,
  • Dae-Jin Yun,
  • Junghoon Park

摘要

Drought stress triggers abscisic acid (ABA) signaling in plants but underline regulatory mechanisms remains incompletely understood. Recently, HOS15, a CUL4-DDB1-based substrate receptor, was shown to regulate ABA signaling and drought stress responses by targeting the drought-induced protein DIL9 for degradation. We show a novel HOS15-DIL9 regulatory module fine-tuning ABA signaling and drought. HOS15 mediated DIL9 turnover likely modulates downstream stress genes expression. Additionally, DIL9 directly binds to the promoters of ABFs (ABF1-4) and NCED3 and activates their expression under drought stress. ABFs and NCED3 expression markedly elevated in DIL9-GFP/hos15-2 compared to DIL9-GFP plants under stress conditions, indicating that HOS15 restricts DIL9 activation of ABFs and NCED3 genes. HOS15 promotes DIL9 degradation, thereby establishing a negative feedback loop that links NCED3-depedent ABA biosynthesis coupled to ABF-mediated ABA signaling. Thus, our findings demonstrate that HOS15 attenuates DIL9 activity via proteasomal degradation, thereby fine-tuning ABA and drought responses in Arabidopsis.