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      Molecular mechanisms at the core of the plant circadian oscillator

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      Nature structural & molecular biology

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          Abstract

          Circadian clocks are endogenous timekeeping networks that allow organisms to align their physiology with their changing environment and to perform biological processes at the most relevant times of the day and year. Initial feedback-loop models of the oscillator have been enriched by emerging evidence highlighting the increasing variety of factors and mechanisms that contribute to the generation of rhythms. In this Review, we consider the two major input pathways that connect the circadian clock of the model plant Arabidopsis thaliana to its environment and discuss recent advances in understanding of how transcriptional, post-translational and post-transcriptional mechanisms contribute to clock function.

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          Reciprocal regulation between TOC1 and LHY/CCA1 within the Arabidopsis circadian clock.

          The interactive regulation between clock genes is central for oscillator function. Here, we show interactions between the Arabidopsis clock genes LATE ELONGATED HYPOCOTYL (LHY), CIRCADIAN CLOCK ASSOCIATED 1 (CCA1), and TIMING OF CAB EXPRESSION 1 (TOC1). The MYB transcription factors LHY and CCA1 negatively regulate TOC1 expression. We show that both proteins bind to a region in the TOC1 promoter that is critical for its clock regulation. Conversely, TOC1 appears to participate in the positive regulation of LHY and CCA1 expression. Our results indicate that these interactions form a loop critical for clock function in Arabidopsis.
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            Orchestrated Transcription of Key Pathways in Arabidopsis by the Circadian Clock

            Like most organisms, plants have endogenous biological clocks that coordinate internal events with the external environment. We used high-density oligonucleotide microarrays to examine gene expression in Arabidopsis and found that 6% of the more than 8000 genes on the array exhibited circadian changes in steady-state messenger RNA levels. Clusters of circadian-regulated genes were found in pathways involved in plant responses to light and other key metabolic pathways. Computational analysis of cycling genes allowed the identification of a highly conserved promoter motif that we found to be required for circadian control of gene expression. Our study presents a comprehensive view of the temporal compartmentalization of physiological pathways by the circadian clock in a eukaryote.
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              Constitutive expression of the CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) gene disrupts circadian rhythms and suppresses its own expression.

              The CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) gene encodes a MYB-related transcription factor involved in the phytochrome induction of a light-harvesting chlorophyll a/b-protein (Lhcb) gene. Expression of the CCA1 gene is transiently induced by phytochrome and oscillates with a circadian rhythm. Constitutive expression of CCA1 protein in transgenic plants abolished the circadian rhythm of several genes with dramatically different phases. These plants also had longer hypocotyls and delayed flowering, developmental processes regulated by light and the circadian clock. Furthermore, the expression of both endogenous CCA1 and the related LHY gene was suppressed. Our results suggest that CCA1 is a part of a feedback loop that is closely associated with the circadian clock in Arabidopsis.
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                Author and article information

                Journal
                101186374
                31761
                Nat Struct Mol Biol
                Nat Struct Mol Biol
                Nature structural & molecular biology
                1545-9993
                1545-9985
                13 December 2020
                06 December 2016
                December 2016
                21 December 2020
                : 23
                : 12
                : 1061-1069
                Affiliations
                Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles, Los Angeles, California, USA.
                Author notes
                Correspondence should be addressed to S.A.K. ( stevekay@ 123456usc.edu ).
                Article
                PMC7750160 PMC7750160 7750160 nihpa1646282
                10.1038/nsmb.3327
                7750160
                27922614
                81ea71b7-f8a4-4394-9c18-31f30263ad3c
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