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Driven by cell elongation, hypocotyl growth is tightly controlled by light and responds to external stimuli and endogenous hormonal pathways. Hypocotyls are known to be responsive to the stress signalling hormone abscisic acid (ABA) which effectively inhibits cell elongation, but how this regulation is connected to light responses and other endogenous hormonal pathways has been a subject of limited studies. Here, we show that whereas hypocotyl elongation is sensitive to ABA in light-grown seedlings, the hypocotyl of dark-grown etiolated 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. However, etiolated hypocotyls retain ABA responsiveness, as could be detected by the induction of ABI1 and RD29B transcripts in response to exogenous ABA, suggesting that inhibition of hypocotyl elongation mediated by ABA does not follows the canonical ABA signalling dependent on transcription. Here, using RNA-seq analysis we identified a number of ABA differentially expressed genes (DEGs) that correlate with ABA inhibition of hypocotyl elongation, specifically in dark-grown pifq or light-grown WT plants, and whose expression remains unchanged by ABA treatment in dark-grown WT plants. Among these DEGs we identified a number of genes playing a role in cell elongation directly at the level of the plasma membrane, as SAURs, ion transporters, auxin flux regulators, channels, and cell wall modification enzymes. The use of the auxin transport inhibitor, NPA …