FERONIA is a key modulator of brassinosteroid and ethylene responsiveness in arabidopsis hypocotyls

Stephen Deslauriers, Paul B. Larsen

Research output: Contribution to journalArticle

95 Scopus citations

Abstract

Ethylene signaling is a complex pathway that has been intensively analyzed partly due to its importance to the manifestation of horticultural phenomena, including fruit ripening and tissue senescence. In order to further our understanding of how this pathway is regulated, a screen for Arabidopsis mutants with increased ethylene response was conducted. From this, a mutant was identified as having a dark-grown hypocotyl that is indistinguishable from Col-0 wt in the presence of the ethylene perception inhibitor AgNO3, yet has extreme responsiveness to even low levels of ethylene. Map-based cloning of the mutation revealed a T-DNA insertion in the coding sequence of the receptor-like kinase FERONIA, which is required for normal pollen tube reception and cell elongation in a currently unknown capacity. In contrast to a previous report, analysis of our feronia knockout mutant shows it also has altered responsiveness to brassinosteroids, with etiolated fer-2 seedlings being partially brassinosteroid insensitive with regard to promotion of hypocotyl elongation. Our results indicate that FERONIA-dependent brassinosteroid response serves to antagonize the effect of ethylene on hypocotyl growth of etiolated seedlings, with loss of proper brassinosteroid signaling disrupting this balance and leading to a greater impact of ethylene on hypocotyl shortening.

Original languageEnglish (US)
Pages (from-to)626-640
Number of pages15
JournalMolecular Plant
Volume3
Issue number3
DOIs
StatePublished - May 2010
Externally publishedYes

Keywords

  • Arabidopsis
  • Brassinosteroid
  • Ethylene
  • FERONIA
  • Hypocotyl
  • Triple response

Fingerprint Dive into the research topics of 'FERONIA is a key modulator of brassinosteroid and ethylene responsiveness in arabidopsis hypocotyls'. Together they form a unique fingerprint.

  • Cite this