Molecular convergence of clock and photosensory pathways through PIF3-TOC1 interaction and co-occupancy of target promoters

SOY J; LEIVAR P; GONZALEZ SCHAIN N; MARTÍN G; DIAZ C; SENTANDREU M; AL-SADY B; QUAIL PH; MONTE E

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

NATL ACAD SCIENCES

Lugar: Washington DC, USA; Año: 2016

0027-8424

A mechanism for integrating light perception andthe endogenouscircadian clock is central to a plant?s capacity to coordinate itsgrowth and development with the prevailing dailylight/darkcycles. Under short-day (SD) photocycles,hypocotylelongation ismaximal at dawn, being promoted by thecollective activity of aquartet of transcription factors, called PIF1,PIF3, PIF4, and PIF5(Phytochrome (phy)-Interacting Factors). PIFprotein abundance inSDs oscillates as a balance between synthesisand photoactivatedphy-imposed degradation, with maximum levelsaccumulating atthe end of the long night. Previous evidenceshows that elongationunder diurnal conditions (as well as in shade)is also subjectedto circadian gating. However, the mechanismunderlying thesephenomena is incompletely understood. Here, weshow that thePIFs and the core-clock component, TOC1, displaycoincident cobindingto the promoters of pre-dawn-phased,growth-relatedgenes under SD conditions. TOC1 interacts withthe PIFs andrepresses their transcriptional activationactivity, antagonizing PIFinducedgrowth. Given the dynamics of TOC1 abundance(displayinghigh post-dusk levels that progressively declineduring thelong night), our data suggest that TOC1functions to provide adirect output from the core clock thattransiently constrains thegrowth-promoting activity of the accumulatingPIFs, early postdusk,thereby gating growth to pre-dawn, whenconditions forcell elongation are optimal. These findingsunveil a previouslyunrecognizedmechanism whereby a core-circadian-clockoutputsignalconverges immediately with the phy-photosensorypathwayto directly co-regulate the activity of the PIFtranscriptionfactors, positioned at the apex of a transcriptionalnetwork thatregulates a diversity of downstream morphogenicresponses.