PMID- 21525334
OWN - NLM
STAT- MEDLINE
DCOM- 20110926
LR  - 20211020
IS  - 1532-2548 (Electronic)
IS  - 0032-0889 (Print)
IS  - 0032-0889 (Linking)
VI  - 156
IP  - 2
DP  - 2011 Jun
TI  - FAR-RED INSENSITIVE219 modulates CONSTITUTIVE PHOTOMORPHOGENIC1 activity via 
      physical interaction to regulate hypocotyl elongation in Arabidopsis.
PG  - 631-46
LID - 10.1104/pp.111.177667 [doi]
AB  - FAR-RED INSENSITIVE219 (FIN219) in Arabidopsis (Arabidopsis thaliana) is involved 
      in phytochrome A-mediated far-red (FR) light signaling. Previous genetic studies 
      revealed that FIN219 acts as an extragenic suppressor of CONSTITUTIVE 
      PHOTOMORPHOGENIC1 (COP1). However, the molecular mechanism underlying the 
      suppression of COP1 remains unknown. Here, we used a transgenic approach to study 
      the regulation of COP1 by FIN219. Transgenic seedlings containing ectopic 
      expression of the FIN219 amino (N)-terminal domain in wild-type Columbia (named 
      NCox for the expression of the N-terminal coiled-coil domain and NTox for the 
      N-terminal 300-amino acid region) exhibited a dominant-negative long-hypocotyl 
      phenotype under FR light, reflected as reduced photomorphogenic responses and 
      altered levels of COP1 and ELONGATED HYPOCOTYL5 (HY5). Yeast two-hybrid, 
      pull-down, and bimolecular fluorescence complementation assays revealed that 
      FIN219 could interact with the WD-40 domain of COP1 and with its N-terminal 
      coiled-coil domain through its carboxyl-terminal domain. Further in vivo 
      coimmunoprecipitation study confirms that FIN219 interacts with COP1 under 
      continuous FR light. Studies of the double mutant fin219-2/cop1-6 indicated that 
      HY5 stability requires FIN219 under darkness and FR light. Moreover, FIN219 
      levels positively regulated by phytochrome A can modulate the subcellular 
      location of COP1 and are differentially regulated by various fluence rates of FR 
      light. We conclude that the dominant-negative long-hypocotyl phenotype conferred 
      by NCox and NTox in a wild-type background was caused by the misregulation of 
      COP1 binding with the carboxyl terminus of FIN219. Our data provide a critical 
      mechanism controlling the key repressor COP1 in response to FR light.
FAU - Wang, Jhy-Gong
AU  - Wang JG
AD  - Institute of Plant Biology, College of Life Science, National Taiwan University, 
      Taipei 106, Taiwan.
FAU - Chen, Chih-Hao
AU  - Chen CH
FAU - Chien, Ching-Te
AU  - Chien CT
FAU - Hsieh, Hsu-Liang
AU  - Hsieh HL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110427
PL  - United States
TA  - Plant Physiol
JT  - Plant physiology
JID - 0401224
RN  - 0 (Arabidopsis Proteins)
RN  - 0 (Basic-Leucine Zipper Transcription Factors)
RN  - 0 (FIN219 protein, Arabidopsis)
RN  - 0 (HY5 protein, Arabidopsis)
RN  - 0 (Nuclear Proteins)
RN  - EC 2.3.2.27 (AT2G32950 protein, Arabidopsis)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
SB  - IM
MH  - Arabidopsis/genetics/*growth & development/*metabolism/radiation effects
MH  - Arabidopsis Proteins/chemistry/genetics/*metabolism
MH  - Basic-Leucine Zipper Transcription Factors/metabolism
MH  - Cytoplasm/metabolism/radiation effects
MH  - Gene Expression Regulation, Plant/radiation effects
MH  - Genes, Dominant/genetics
MH  - Hypocotyl/*growth & development/metabolism/radiation effects
MH  - Light
MH  - Light Signal Transduction/radiation effects
MH  - Morphogenesis/radiation effects
MH  - Mutation/genetics
MH  - Nuclear Proteins/metabolism
MH  - Phenotype
MH  - Plants, Genetically Modified
MH  - Protein Binding/radiation effects
MH  - Protein Multimerization/radiation effects
MH  - Protein Stability/radiation effects
MH  - Protein Structure, Tertiary
MH  - Seedlings/genetics/radiation effects
MH  - Ubiquitin-Protein Ligases/genetics/*metabolism
PMC - PMC3177264
EDAT- 2011/04/29 06:00
MHDA- 2011/09/29 06:00
PMCR- 2011/04/27
CRDT- 2011/04/29 06:00
PHST- 2011/04/29 06:00 [entrez]
PHST- 2011/04/29 06:00 [pubmed]
PHST- 2011/09/29 06:00 [medline]
PHST- 2011/04/27 00:00 [pmc-release]
AID - pp.111.177667 [pii]
AID - 177667 [pii]
AID - 10.1104/pp.111.177667 [doi]
PST - ppublish
SO  - Plant Physiol. 2011 Jun;156(2):631-46. doi: 10.1104/pp.111.177667. Epub 2011 Apr 
      27.