<p>Plants integrate light signals to regulate development and produce protective compounds such as flavonoids under excessive light stress. While these metabolites protect against light damage, their roles in modulating photoreceptor responses remain unclear. Here, we show that naringenin chalcone (NGC), a flavonoid precursor that accumulates in the <i>Arabidopsis chalcone isomerase</i> mutant <i>tt5</i> but which is also present in wild type plants under solar light, promotes UVR8 monomer accumulation beyond its canonical UV-B response. A genetic suppressor screen reveals that loss of <i>UVR8</i> restores normal growth of <i>tt5</i> mutants grown under high light, irrespective of the presence of UV-B. Biochemical and transcriptomic analyses show that NGC binds to monomeric UVR8, stabilizing its active form and triggering gene expression changes, even in the absence of UV-B. This work identifies a mechanism for stabilizing activated UVR8 and reveals crosstalk between light-induced metabolic intermediates and photoreceptor-mediated developmental regulation.</p>

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Flavonoid pathway intermediates implicate UVR8 in functions beyond canonical UV-B signaling

  • Nan Jiang,
  • Tatiana García Navarrete,
  • Yun Sun Lee,
  • Emily G. Pawlowski,
  • Sunyoung Park,
  • Erich Grotewold

摘要

Plants integrate light signals to regulate development and produce protective compounds such as flavonoids under excessive light stress. While these metabolites protect against light damage, their roles in modulating photoreceptor responses remain unclear. Here, we show that naringenin chalcone (NGC), a flavonoid precursor that accumulates in the Arabidopsis chalcone isomerase mutant tt5 but which is also present in wild type plants under solar light, promotes UVR8 monomer accumulation beyond its canonical UV-B response. A genetic suppressor screen reveals that loss of UVR8 restores normal growth of tt5 mutants grown under high light, irrespective of the presence of UV-B. Biochemical and transcriptomic analyses show that NGC binds to monomeric UVR8, stabilizing its active form and triggering gene expression changes, even in the absence of UV-B. This work identifies a mechanism for stabilizing activated UVR8 and reveals crosstalk between light-induced metabolic intermediates and photoreceptor-mediated developmental regulation.