4.8 Article

Teaching an Old Hormone New Tricks: Cytosolic Ca2+ Elevation Involvement in Plant Brassinosteroid Signal Transduction Cascades

Journal

PLANT PHYSIOLOGY
Volume 163, Issue 2, Pages 555-565

Publisher

AMER SOC PLANT BIOLOGISTS
DOI: 10.1104/pp.112.213371

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Funding

  1. National Science Foundation [1146827]
  2. Direct For Biological Sciences
  3. Division Of Integrative Organismal Systems [1146827] Funding Source: National Science Foundation

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Brassinosteroids (BRs) are hormones that control many aspects of plant growth and development, acting at the cell level to promote division and expansion. BR regulation of plant and plant cell function occurs through altered expression of many genes. Transcriptional reprogramming downstream from cell perception of this hormone is currently known to be mediated by a phosphorylation/dephosphorylation (phosphorelay) cascade that alters the stability of two master transcription regulators. Here, we provide evidence that BR perception by their receptor also causes an elevation in cytosolic Ca2+, initiating a Ca2+ signaling cascade in Arabidopsis (Arabidopsis thaliana) cell cytosol. BR-dependent increases in the expression of some genes (INDOLE-3-ACETIC ACID-INDUCIBLE1 and PHYTOCHROME B ACTIVATION-TAGGED SUPPRESSOR1) were impaired in wild-type plants by a Ca2+ channel blocker and also in the defense-no-death (dnd1) mutant, which lacks a functional cyclic GMP-activated cell membrane Ca2+-conducting channel. Alternatively, mutations that impair the BR phosphorelay cascade did not much affect the BR-dependent expression of these genes. Similar effects of the Ca2+ channel blocker and dnd1 mutation were observed on a BR plant growth phenotype, deetiolation of the seedling hypocotyl. Further evidence presented in this report suggests that a BR-dependent elevation in cyclic GMP may be involved in the Ca2+ signaling cascade initiated by this hormone. The work presented here leads to a new model of the molecular steps that mediate some of the cell responses to this plant hormone.

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