16
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Arabidopsis transcription factor ELONGATED HYPOCOTYL5 plays a role in the feedback regulation of phytochrome A signaling.

      The Plant cell
      Arabidopsis, genetics, metabolism, Arabidopsis Proteins, Base Sequence, Basic-Leucine Zipper Transcription Factors, Feedback, Physiological, Gene Expression Regulation, Plant, Molecular Sequence Data, Nuclear Proteins, Phytochrome, Phytochrome A, Promoter Regions, Genetic, Sequence Alignment, Signal Transduction, physiology, Two-Hybrid System Techniques

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Phytochrome A (phyA) is the primary photoreceptor responsible for perceiving and mediating various responses to far-red light in Arabidopsis thaliana. FAR-RED ELONGATED HYPOCOTYL1 (FHY1) and its homolog FHY1-LIKE (FHL) are two small plant-specific proteins essential for light-regulated phyA nuclear accumulation and subsequent phyA signaling processes. FHY3 and its homolog FAR-RED IMPAIRED RESPONSE1 (FAR1) are two transposase-derived transcription factors that directly activate FHY1/FHL transcription and thus mediate subsequent phyA nuclear accumulation and responses. Here, we report that ELONGATED HYPOCOTYL5 (HY5), a well-characterized bZIP transcription factor involved in promoting photomorphogenesis, directly binds ACGT-containing elements a few base pairs away from the FHY3/FAR1 binding sites in the FHY1/FHL promoters. We demonstrate that HY5 physically interacts with FHY3/FAR1 through their respective DNA binding domains and negatively regulates FHY3/FAR1-activated FHY1/FHL expression under far-red light. Together, our data show that HY5 plays a role in negative feedback regulation of phyA signaling by attenuating FHY3/FAR1-activated FHY1/FHL expression, providing a mechanism for fine-tuning phyA signaling homeostasis.

          Related collections

          Author and article information

          Comments

          Comment on this article