A PIF-SAUR module safeguards hypocotyl elongation from ABA inhibition in the dark
Driven by cell elongation, hypocotyl growth is tightly controlled by light and responds to both external stimuli and endogenous hormonal pathways. Hypocotyls are responsive to the stress signalling hormone abscisic acid (ABA), which effectively inhibits cell elongation. However, how this regulation is connected to light signalling has been a subject of limited studies. Here, we show that, contrary to light-grown seedlings, hypocotyl elongation of dark-grown seedlings is ABA-insensitive. In the dark, hypocotyl sensitivity to ABA is restored in the constitutive photomorphogenic pifq and cop1-4 mutants, suggesting that an active light signalling pathway is necessary for hypocotyl responsiveness to ABA. Surprisingly, etiolated hypocotyls retain an intact ABA signalling pathway, as could be detected by the induction of ABI1 and RD29B transcripts in response to exogenous ABA, suggesting that inhibition of hypocotyl elongation occurs through a divergent path that can be inhibited by PIFs. Here, using RNA-seq analysis we identified a number of ABA differentially expressed genes (DEGs) that correlate with ABA inhibition of hypocotyl elongation. Among these DEGs a number of SMALL AUXIN-UP RNA (SAUR) genes that are known to directly repress D-CLADE TYPE 2C PROTEIN PHOSPHATASES (PP2C.D) were found. The abrogation of PP2CD.D2-SAUR interaction in the pp2c.d2/PP2C.D2M331K -GFP line, restored ABA sensitivity in the dark, suggesting that SAUR proteins, upregulated by PIFs, are sufficient to render hypocotyls insensitive to ABA. This hypocotyl-specific mechanism enables to promote growth towards the light at all costs, overriding ABA inhibition of cell elongation, to ensure subsequent seedling establishment and survival. Overall design: RNA-Seq profiling of wild type and pifq mutant arabidopsis seedlings with or without ABA and in presence or absence of light. Three biological replicates per sample type.