These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: FIN219, an auxin-regulated gene, defines a link between phytochrome A and the downstream regulator COP1 in light control of Arabidopsis development.
    Author: Hsieh HL, Okamoto H, Wang M, Ang LH, Matsui M, Goodman H, Deng XW.
    Journal: Genes Dev; 2000 Aug 01; 14(15):1958-70. PubMed ID: 10921909.
    Abstract:
    Light signals perceived by photoreceptors are transduced to negatively regulate COP1, a key repressor of photomorphogenic development. To identify genes involved in light inactivation of COP1, a genetic screen was employed to identify extragenic modifier mutations of a temperature-sensitive cop1 allele. One suppressor mutation isolated also exhibited a far-red-specific long hypocotyl phenotype in a wild-type background. Further phenotypic analyses of this new mutation, named fin219, suggested that it defines a novel phytochrome A signaling component. Genetic analysis indicated that FIN219 interacts closely with another phytochrome A signaling component, FHY1. Molecular characterization of FIN219 indicated that it encodes a cytoplasmic localized protein highly similar to the GH3 family of proteins and its expression is rapidly induced by auxin. In contrast to its loss-of-function mutant phenotype, overexpression of FIN219 results in a far-red-specific hyperphotomorphogenic response. Our data suggest that FIN219 may define a critical link for phytochrome A-mediated far-red inactivation of COP1 and a possible cross-talk juncture between auxin regulation and phytochrome signaling.
    [Abstract] [Full Text] [Related] [New Search]