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The functional diversification of the RING-finger constitutive photomorphogenesis 1 (COP1) enzyme highly depends on its (in)direct interaction with regulatory proteins involved in the Arabidopsis photomorphogenesis signaling pathways. In last decade, only a few AtCOP1-ligand complexes have been investigated using functional analysis and proved by biochemical interaction analysis, despite much more have been remaining unclear. Identifying the functions of COP1 will undoubtedly provide an opportunity for the discovery of novel COP1 targets either triggered on COP1 or targeted by COP1, which their characteristics have not been reported so far. Here, we have focused on the tertiary structure analysis of COP1 protein and characterization of its potent ligands based on the protein–protein interaction characteristics of the known AtCOP1-based protein complexes, which their interaction with COP1 were biochemically approved. Based on motif analysis and molecular docking results, a total of 88 regulatory proteins with different confidence were identified to be interactive and co-regulated with AtCOP1 E3 ligase. The correlation regulatory network analysis reveals that COP1 functions as a master switch in controlling the Arabidopsis growth and development. The up/down regulations of the potent COP1-ligands gene expression levels in cop1 knockdown T0 plants indicate the COP1 expanded roles in a wide diversity of biological processes. These characteristics consist of the photomorphogenesis signaling pathway, cell cycle regulation, cell division, histone H3-K27 methylation, stomata formation, and iron starvation. Meanwhile, the VPS11 transporter probably transports the COP1 into the endosome, lysosome, and vacuole between the nucleus and cytoplasm during the photomorphogenesis signaling pathway in darkness condition.

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Arsbidopsis COP1 (Constitutive Photomorphogenic 1) defines a key repressor of photomorphogenesis in darkness by acting as an E3 ubiquitin Iigase in the nucleus, and is responsible for the targeted degradation of a number of photomorphogenesis-promoting factors, including phyA, HY5, LAF1, and HFR1. Light activation of multiple classes of photoreceptors (including both phytochromes and cryptochromes) inactivates COP1 and reduces its nuclear abundance, allowing the accumulation of these positively acting light signaling intermediates to promote photomorphogenic development. Recent studies suggest that Arabidopsis COP1 teams up with a family of SPA proteins (SPA1-SPA4) to form the physiologically active COP1-SPA E3 ubiquitin ligase complexes. These COP1-SPA complexes play overlapping and distinct functions in regulating seedling photomorphogenesis under different light conditions and adult plant growth. Further, the COP1-SPA complexes act In concert at a biochemical level with the CDD (COP10, DET1, and DDB1) complex and COP9 signalosome (CSN) to orchestrate the repression of photomorphogenesis.  相似文献   

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植物光形态建成调控因子COP1黑暗中积累在细胞核内,直接与碱性亮氨酸拉链(bZIP)类转录因子HY5相互作用,并被蛋白酶降解,负调控下游基因的表达;而在光下COP1从细胞核内转移到细胞核外,HY5得以在细胞核内积累,可特异结合于查尔酮合成酶基因CHS等光诱导基因启动子上,正调控相关基因的表达。  相似文献   

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Cao D  Lin Y  Cheng CL 《The Plant cell》2000,12(2):199-211
The chlorate-resistant mutant cr88 is defective in photomorphogenesis, as shown by the phenotypes of long hypocotyls in red light and yellow cotyledons under all light conditions. A subset of light-regulated genes is expressed at subnormal levels in cr88. To analyze further the role that CR88 plays in photomorphogenesis, we investigated the genetic interactions between cr88 and mutants of two other loci affecting photomorphogenesis, CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) and LONG HYPOCOTYL5 (HY5). COP1 represses the expression of light-regulated genes in the dark, and HY5 inhibits hypocotyl elongation in the light. Using morphological, cellular, and gene expression criteria for epistasis analyses to position CR88 in the genetic hierarchy of the photomorphogenesis pathway, we determined that CR88 acts downstream of COP1 but in a branch separate from HY5. In the course of our analysis, we discovered that light causes extensive destruction of plastids in dark-grown cop1 seedlings and that cr88 prevents this destruction.  相似文献   

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