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      An overview of floral regulatory genes in annual and perennial plants

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      Gene
      Elsevier BV

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          Regulation of flowering time: all roads lead to Rome.

          Plants undergo a major physiological change as they transition from vegetative growth to reproductive development. This transition is a result of responses to various endogenous and exogenous signals that later integrate to result in flowering. Five genetically defined pathways have been identified that control flowering. The vernalization pathway refers to the acceleration of flowering on exposure to a long period of cold. The photoperiod pathway refers to regulation of flowering in response to day length and quality of light perceived. The gibberellin pathway refers to the requirement of gibberellic acid for normal flowering patterns. The autonomous pathway refers to endogenous regulators that are independent of the photoperiod and gibberellin pathways. Most recently, an endogenous pathway that adds plant age to the control of flowering time has been described. The molecular mechanisms of these pathways have been studied extensively in Arabidopsis thaliana and several other flowering plants.
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            Coordinated regulation of Arabidopsis thaliana development by light and gibberellins.

            Light and gibberellins (GAs) mediate many essential and partially overlapping plant developmental processes. DELLA proteins are GA-signalling repressors that block GA-induced development. GA induces degradation of DELLA proteins via the ubiquitin/proteasome pathway, but light promotes accumulation of DELLA proteins by reducing GA levels. It was proposed that DELLA proteins restrain plant growth largely through their effect on gene expression. However, the precise mechanism of their function in coordinating GA signalling and gene expression remains unknown. Here we characterize a nuclear protein interaction cascade mediating transduction of GA signals to the activity regulation of a light-responsive transcription factor. In the absence of GA, nuclear-localized DELLA proteins accumulate to higher levels, interact with phytochrome-interacting factor 3 (PIF3, a bHLH-type transcription factor) and prevent PIF3 from binding to its target gene promoters and regulating gene expression, and therefore abrogate PIF3-mediated light control of hypocotyl elongation. In the presence of GA, GID1 proteins (GA receptors) elevate their direct interaction with DELLA proteins in the nucleus, trigger DELLA protein's ubiquitination and proteasome-mediated degradation, and thus release PIF3 from the negative effect of DELLA proteins.
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              FKF1 and GIGANTEA complex formation is required for day-length measurement in Arabidopsis.

              Precise timing of CONSTANS (CO) gene expression is necessary for day-length discrimination for photoperiodic flowering. The FLAVIN-BINDING, KELCH REPEAT, F-BOX 1 (FKF1), and GIGANTEA (GI) proteins regulate CO transcription in Arabidopsis. We demonstrate that FKF1 and GI proteins form a complex in a blue-light-dependent manner. The timing of this interaction regulates the timing of daytime CO expression. FKF1 function is dependent on GI, which interacts with a CO repressor, CYCLING DOF FACTOR 1 (CDF1), and controls CDF1 stability. GI, FKF1, and CDF1 proteins associate with CO chromatin. Thus, the FKF1-GI complex forms on the CO promoter in late afternoon to regulate CO expression, providing a mechanistic view of how the coincidence of light with circadian timing regulates photoperiodic flowering.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Gene
                Gene
                Elsevier BV
                03781119
                November 2023
                November 2023
                : 885
                : 147699
                Article
                10.1016/j.gene.2023.147699
                37567454
                f72c5f23-60c9-49e4-8ed2-497e4ec5447d
                © 2023

                https://www.elsevier.com/tdm/userlicense/1.0/

                https://doi.org/10.15223/policy-017

                https://doi.org/10.15223/policy-037

                https://doi.org/10.15223/policy-012

                https://doi.org/10.15223/policy-029

                https://doi.org/10.15223/policy-004

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