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In Arabidopsis, although studies have demonstrated that phytochrome A(phyA) and phyB are involved in blue light signaling, how blue light-activated phytochromes modulate the activity of the CONSTITUTIVELY PHOTOMORPHOGENIC1(COP1)-SUPPRESSOR OF PHYA-105(SPA1) E3 complex remains largely unknown. Here, we show that phyA responds to early and weak blue light, whereas phyB responds to sustainable and strong blue light. Activation of both phyA and phyB by blue light inhibits SPA1 activity.Specifically,...  相似文献   

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Plants have evolved light signaling mechanisms to optimally adapt developmental patterns to the ambient light environments. CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) and LONG HYPOCOTYL5 (HY5) are two critical components in the light signaling pathway in Arabidopsis thaliana. COP1 acts as an E3 ubiquitin ligase that targets positive regulators, such as HY5, leading to their degradation in darkness. However, functional analysis of the COP1-HY5 module in maize (Zea mays) has not been reported. Here, we investigated the expression patterns and roles of the COP1 and HY5 orthologs, ZmCOP1 and ZmHY5, in regulating photomorphogenesis. These two genes have high amino acid identities with their Arabidopsis homolog and were both regulated by light. Subcellular localization assay showed that ZmCOP1 was distributed in the cytosol and ZmHY5 localized in the nucleus. Exogenous expression of ZmCOP1 rescued the physiological defects of the cop1-4 mutant, and expression of ZmHY5 complemented the long hypocotyl phenotype of the hy5-215 mutant in Arabidopsis. Yeast two-hybrid and fluorescence resonance energy transfer assays showed that ZmCOP1 interacted with ZmHY5. Our study gains insight into the conserved function and regulatory mechanism of the COP1-HY5 signaling pathway in maize and Arabidopsis.  相似文献   

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Wild-type Arabidopsis seedlings are capable of following two developmental programs: photomorphogenesis in the light and skotomorphogenesis in darkness. Screening of Arabidopsis mutants for constitutive photomorphogenic development in darkness resulted in the identification of three new loci designated COP8, COP10, and COP11. Detailed examination of the temporal morphological and cellular differentiation patterns of wild-type and mutant seedlings revealed that in darkness, seedlings homozygous for recessive mutations in COP8, COP10, and COP11 failed to suppress the photomorphogenic developmental pathway and were unable to initiate skotomorphogenesis. As a consequence, the mutant seedlings grown in the dark had short hypocotyls and open and expanded cotyledons, with characteristic photomorphogenic cellular differentiation patterns and elevated levels of light-inducible gene expression. In addition, plastids of dark-grown mutants were defective in etioplast differentiation. Similar to cop1 and cop9, and in contrast to det1 (deetiolated), these new mutants lacked dark-adaptive change of light-regulated gene expression and retained normal phytochrome control of seed germination. Epistatic analyses with the long hypocotyl hy1, hy2, hy3, hy4, and hy5 mutations suggested that these three loci, similar to COP1 and COP9, act downstream of both phytochromes and a blue light receptor, and probably HY5 as well. Further, cop8-1, cop10-1, and cop11-1 mutants accumulated higher levels of COP1, a feature similar to the cop9-1 mutant. These results suggested that COP8, COP10, and COP11, together with COP1, COP9, and DET1, function to suppress the photomorphogenic developmental program and to promote skotomorphogenesis in darkness. The identical phenotypes resulting from mutations in COP8, COP9, COP10, and COP11 imply that their encoded products function in close proximity, possibly with some of them as a complex, in the same signal transduction pathway.  相似文献   

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COP1 E3泛素连接酶最初是在植物中作为光形态建成的关键抑制因子被发现和广泛研究的,是植物生长发育和环境适应过程中的核心“开关”。光受体接收外界环境信号后传递给COP1,COP1再靶向调控下游核心转录因子,从而完成光形态建成等生命过程。在哺乳动物中,尽管大部分光受体都消失,但COP1仍在代谢调控和肿瘤发生过程中靶向重要的转录因子。通过比较动植物中COP1调控过程的异同发现,哺乳动物中COP1所感知的上游信号几乎是未知的,其中COP1结合CRL4形成的复合体E3泛素连接酶的组装机制调控仍不清楚。植物中光是其主要能量来源和COP1的主要上游信号,而作为动物的主要能量来源,葡萄糖和相关激素很可能也是动物COP1的上游信号。同时,通过总结医学研究中针对蛋白质泛素化相关过程的丰富靶点和相关药物,可以为植物COP1等E3泛素连接酶的研究提供有效工具。COP1在细胞生命过程调控中至关重要,其功能和作用机制随着进化而产生多样性,尚有待继续深入探究。  相似文献   

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In the dark, etiolated seedlings display a long hypocotyl, the growth of which is rapidly inhibited when the seedlings are exposed to light. In contrast, the phytohormone ethylene prevents hypocotyl elongation in the dark but enhances its growth in the light. However, the mechanism by which light and ethylene signalling oppositely affect this process at the protein level is unclear. Here, we report that ethylene enhances the movement of CONSTITUTIVE PHOTOMORPHOGENESIS 1 (COP1) to the nucleus where it mediates the degradation of LONG HYPOCOTYL 5 (HY5), contributing to hypocotyl growth in the light. Our results indicate that HY5 is required for ethylene-promoted hypocotyl growth in the light, but not in the dark. Using genetic and biochemical analyses, we found that HY5 functions downstream of ETHYLENE INSENSITIVE 3 (EIN3) for ethylene-promoted hypocotyl growth. Furthermore, the upstream regulation of HY5 stability by ethylene is COP1-dependent, and COP1 is genetically located downstream of EIN3, indicating that the COP1-HY5 complex integrates light and ethylene signalling downstream of EIN3. Importantly, the ethylene precursor 1-aminocyclopropane-1-carboxylate (ACC) enriched the nuclear localisation of COP1; however, this effect was dependent on EIN3 only in the presence of light, strongly suggesting that ethylene promotes the effects of light on the movement of COP1 from the cytoplasm to the nucleus. Thus, our investigation demonstrates that the COP1-HY5 complex is a novel integrator that plays an essential role in ethylene-promoted hypocotyl growth in the light.  相似文献   

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