Data from: Dynamic antagonism between phytochromes and PIF-family bHLHs induces selective reciprocal responses to light and shade in a rapidly responsive transcriptional network in Arabidopsis

Abstract

Plants respond to shade-modulated light-signals, via the phytochrome (phy) system, by adaptive changes, collectively termed the shade avoidance syndrome (SAS). To examine the roles of the Phy-Interacting bHLH Factors, PIF1, 3, 4 and 5, in relaying this information to the transcriptional network, we compared the genome-wide expression profiles of wild-type and quadruple pif (pifq) mutants in response to shade. The data identify a subset of genes, enriched in transcription-factor-encoding loci, that respond rapidly (within 1 h), in a PIF-dependent manner, to the shade signal, and that contain promoter-located G-box-sequence motifs (CACGTG), known to be preferred PIF binding sites. These genes are thus potential direct targets of phy-PIF signaling that function in the primary transcriptional circuitry controlling downstream response-elaboration. A second subset of PIF-dependent, early-response genes, lacking G-box motifs, are enriched for auxin-responsive loci, suggestive of being indirect targets of phy-PIF signaling involved in the rapid cell-expansion known to be induced by shade. A meta-analysis comparing deetiolation- and shade-responsive transcriptomes identifies a further subset of G-box-containing genes that reciprocally display rapid repression and induction in response to light and shade signals at the inception of deetiolation and shade-avoidance, respectively. Collectively, these data define a core set of transcriptional and hormonal (auxin, cytokinin) processes that appear to be dynamically poised to react rapidly to changes in the light environment via perturbations in the mutually antagonistic actions of the phys and PIFs. Data from comparative analysis of the quadruple pifq and all triple pif-mutant combinations in response to light and shade, confirm that the PIF-quartet members act with overlapping redundancy on seedling morphogenesis and transcriptional regulation, but that the individual PIFs contribute differentially to these responses.