99 research outputs found

    UVR8-mediated inhibition of shade avoidance involves HFR1 stabilization in Arabidopsis.

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    Sun-loving plants perceive the proximity of potential light-competing neighboring plants as a reduction in the red:far-red ratio (R:FR), which elicits a suite of responses called the "shade avoidance syndrome" (SAS). Changes in R:FR are primarily perceived by phytochrome B (phyB), whereas UV-B perceived by UV RESISTANCE LOCUS 8 (UVR8) elicits opposing responses to provide a counterbalance to SAS, including reduced shade-induced hypocotyl and petiole elongation. Here we show at the genome-wide level that UVR8 broadly suppresses shade-induced gene expression. A subset of this gene regulation is dependent on the UVR8-stabilized atypical bHLH transcription regulator LONG HYPOCOTYL IN FAR-RED 1 (HFR1), which functions in part redundantly with PHYTOCHROME INTERACTING FACTOR 3-LIKE 1 (PIL1). In parallel, UVR8 signaling decreases protein levels of the key positive regulators of SAS, namely the bHLH transcription factors PHYTOCHROME INTERACTING FACTOR 4 (PIF4) and PIF5, in a COP1-dependent but HFR1-independent manner. We propose that UV-B antagonizes SAS via two mechanisms: degradation of PIF4 and PIF5, and HFR1- and PIL1-mediated inhibition of PIF4 and PIF5 function. This work highlights the importance of typical and atypical bHLH transcription regulators for the integration of light signals from different photoreceptors and provides further mechanistic insight into the crosstalk of UVR8 signaling and SAS

    UV-B perceived by the UVR8 photoreceptor inhibits plant thermomorphogenesis

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    Small increases in ambient temperature can elicit striking effects on plant architecture, collectively termed thermomorphogenesis [1]. In Arabidopsis thaliana, these include marked stem elongation and leaf elevation, responses that have been predicted to enhance leaf cooling [ 2, 3, 4 and 5]. Thermomorphogenesis requires increased auxin biosynthesis, mediated by the bHLH transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) [ 6, 7 and 8], and enhanced stability of the auxin co-receptor TIR1, involving HEAT SHOCK PROTEIN 90 (HSP90) [9]. High-temperature-mediated hypocotyl elongation additionally involves localized changes in auxin metabolism, mediated by the indole-3-acetic acid (IAA)-amido synthetase Gretchen Hagen 3 (GH3).17 [10]. Here we show that ultraviolet-B light (UV-B) perceived by the photoreceptor UV RESISTANCE LOCUS 8 (UVR8) [11] strongly attenuates thermomorphogenesis via multiple mechanisms inhibiting PIF4 activity. Suppression of thermomorphogenesis involves UVR8 and CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1)-mediated repression of PIF4 transcript accumulation, reducing PIF4 abundance. UV-B also stabilizes the bHLH protein LONG HYPOCOTYL IN FAR RED (HFR1), which can bind to and inhibit PIF4 function. Collectively, our results demonstrate complex crosstalk between UV-B and high-temperature signaling. As plants grown in sunlight would most likely experience concomitant elevations in UV-B and ambient temperature, elucidating how these pathways are integrated is of key importance to the understanding of plant development in natural environments

    The importance and direction of current and future plant-UV research : break-out session discussions at the UV4Plants Network Meeting in Bled (April 15th -18th , 2018)

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    During the 2nd Network Meeting of UV4Plants at Bled (14th–18th April, 2018) the delegates engaged in a group discussion of prescient questions concerning the future of in plant-UV research. The discussion group was tasked to identify the most valuable directions for plant UV research to take, and to create a coherent framework for how to move the field forward. Here, the outcome of these discussions is summarised in sections that follow the composition of discussion groups as ideas taken from a molecular, biochemical and physiological perspective followed by those from an ecological and plant production perspective. In each case, first basic research questions are considered and then applications and methodological considerations are put forward. Finally, some common ground bringing the two perspectives together is discussed, with the aim of solving scaling problems and ways in which the UV4Plants network might be put to good use.Peer reviewe

    Retinoid Metabolism and Diabetes Mellitus

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    Retinoid acid is a metabolite of vitamin A and functions as an important factor in cell survival, differentiation and death. Most previous studies on retinoid metabolism have focused on its association with cancer, hematologic and dermatologic disorders. Given the special concern over the recent increase in the prevalence of diabetes worldwide, the role of retinoid metabolism on glucose metabolism and insulin resistance in the human body is of marked importance. Therefore, in this issue, we review the literature on the association of retinoid metabolism with glucose tolerance, with regard to insulin secretion, pancreatic autoimmunity, insulin sensitivity and lipid metabolism. Further, we tried to assess the possibility of using retinoids as a novel therapeutic strategy for diabetes

    Lipoprotein (a) in population-based samples of South Asian and European adults in Newcastle upon Tyne

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    SIGLEAvailable from British Library Document Supply Centre-DSC:DXN028211 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

    UV-B photoreceptor-mediated regulation of typical and atypical bHLH transcription regulators

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    The UVR8 photoreceptor perceives UV-B and initiates a signalling cascade that leads to UV-B acclimation. Although the initial steps of the UV-B signalling pathway have been identified and characterized, our understanding of how UVR8 regulates transcription is limited. Moreover, how UVR8 interacts with other light signalling pathways to fine-tune plant development remains elusive. In this work, I aimed to better understand the role of typical and atypical bHLH transcription regulators in UVR8-mediated UV-B signalling and antagonism with plant shade avoidance

    Field inversion gel electrophoresis for apolipoprotein(a) genotyping

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