Light signals from the environment are perceived by specific regulatory photoreceptors in the cytoplasmic compartment and transduced by largely unknown mechanisms to the nuclear compartment to control gene expression and cellular development. The long term goal of this research is to dissect the molecular and cellular basis of how light signals are integrated and relayed into the nucleus to achieve the control of the development mode switch, employing the light-regulated seedling development of Arabidopsis thaliana as an experimental system. Both genetic and molecular evidence have suggested-that COP1 (constitutively photomorphogenic 1) encodes a protein which acts inside the nucleus to suppress the photomorphogenic development in darkness, and that light abrogates this repressive action possibly through a cell-specific regulation of its nucleocytoplasmic partitioning. Thus COP1 not only acts as a molecular switch mediating light control of cellular development, it may also directly participate in light signalling crossing the nuclear envelope. Here I propose to extend our current investigation through a combination of genetic, molecular, cell biological, and biochemical approaches. To investigate the cellular basis of COP1 action and its light regulation, we will confirm the proposed light regulation of COP1 nucleocytoplasmic partitioning based on studies with GUS-COP1 fusion by direct immunological examination of native COP1 in light or dark-grown seedlings, and critical evaluation of its role in light control of cellular development. To reveal the biochemical basis of COP1 action in the nucleus, we will use a combination of in vitro and in vivo assays to examine the capability of COP1 to interact with DNA/RNA and activate or repress promoter activity. To identify other cellular components involved this COP1-mediated light control of development mode switch, we will take complementary genetic and molecular approaches. Genetically, we will identify and characterize Arabidopsis mutations which either mimic the COP1 mutant phenotype or modify the phenotype of a temperature sensitive COP1 mutant allele. Molecularly, we will clone and characterize Arabidopsis genes which encode COP1-interactive proteins. Further, the specific roles of other defined cellular components in the COP1-mediated light control of developmental switch will be examined using similar combinatory approaches. Those studies will provide novel insights into the mechanism of light signaling and its control of cellular development. Since many types of human cancers and diseases are caused by the malfunction of cellular signaling processes, it is hoped that the ability to combat those human health problems will be enhanced through improving our general understanding of cellular signaling mechanisms in a model multicellular organism.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM047850-07
Application #
2654970
Study Section
Molecular Cytology Study Section (CTY)
Project Start
1992-08-01
Project End
2000-01-31
Budget Start
1998-02-01
Budget End
1999-01-31
Support Year
7
Fiscal Year
1998
Total Cost
Indirect Cost
Name
Yale University
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
082359691
City
New Haven
State
CT
Country
United States
Zip Code
06520
Zhou, Yangyang; Yang, Li; Duan, Jie et al. (2018) Hinge region of Arabidopsis phyA plays an important role in regulating phyA function. Proc Natl Acad Sci U S A 115:E11864-E11873
Zhao, Xianhai; Jiang, Yan; Li, Jian et al. (2018) COP1 SUPPRESSOR 4 promotes seedling photomorphogenesis by repressing CCA1 and PIF4 expression in Arabidopsis. Proc Natl Acad Sci U S A 115:11631-11636
Shi, Hui; Lyu, Mohan; Luo, Yiwen et al. (2018) Genome-wide regulation of light-controlled seedling morphogenesis by three families of transcription factors. Proc Natl Acad Sci U S A 115:6482-6487
Lin, Fang; Jiang, Yan; Li, Jian et al. (2018) B-BOX DOMAIN PROTEIN28 Negatively Regulates Photomorphogenesis by Repressing the Activity of Transcription Factor HY5 and Undergoes COP1-Mediated Degradation. Plant Cell 30:2006-2019
Dong, Jie; Ni, Weimin; Yu, Renbo et al. (2017) Light-Dependent Degradation of PIF3 by SCFEBF1/2 Promotes a Photomorphogenic Response in Arabidopsis. Curr Biol 27:2420-2430.e6
Ling, Jun-Jie; Li, Jian; Zhu, Danmeng et al. (2017) Noncanonical role of Arabidopsis COP1/SPA complex in repressing BIN2-mediated PIF3 phosphorylation and degradation in darkness. Proc Natl Acad Sci U S A 114:3539-3544
Lin, Fang; Xu, Dongqing; Jiang, Yan et al. (2017) Phosphorylation and negative regulation of CONSTITUTIVELY PHOTOMORPHOGENIC 1 by PINOID in Arabidopsis. Proc Natl Acad Sci U S A 114:6617-6622
Shi, Hui; Liu, Renlu; Xue, Chang et al. (2016) Seedlings Transduce the Depth and Mechanical Pressure of Covering Soil Using COP1 and Ethylene to Regulate EBF1/EBF2 for Soil Emergence. Curr Biol 26:139-149
Shi, Hui; Shen, Xing; Liu, Renlu et al. (2016) The Red Light Receptor Phytochrome B Directly Enhances Substrate-E3 Ligase Interactions to Attenuate Ethylene Responses. Dev Cell 39:597-610
Li, Kunlun; Yu, Renbo; Fan, Liu-Min et al. (2016) DELLA-mediated PIF degradation contributes to coordination of light and gibberellin signalling in Arabidopsis. Nat Commun 7:11868

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