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PIF4-induced BR synthesis is critical to diurnal and thermomorphogenic growth.

ABSTRACT: The Arabidopsis PIF4 and BES1/BZR1 transcription factors antagonize light signaling by facilitating co-activated expression of a large number of cell wall-loosening and auxin-related genes. While PIF4 directly activates expression of these targets, BES1 and BZR1 activity switch from a repressive to an activator function, depending on interaction with TOPLESS and other families of regulators including PIFs. However, the complexity of this regulation and its role in diurnal control of plant growth and brassinosteroid (BR) levels is little understood. We show by using a protein array that BES1, PIF4, and the BES1-PIF4 complex recognize different DNA elements, thus revealing a distinctive cis-regulatory code beneath BES1-repressive and PIF4 co-activation function. BES1 homodimers bind to conserved BRRE- and G-box elements in the BR biosynthetic promoters and inhibit their expression during the day, while elevated PIF4 competes for BES1 homodimer formation, resulting in de-repressed BR biosynthesis at dawn and in response to warmth. Our findings demonstrate a central role of PIF4 in BR synthesis activation, increased BR levels being essential to thermomorphogenic hypocotyl growth.

SUBMITTER: Martinez C

PROVIDER: S-EPMC6276883 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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PIF4-induced BR synthesis is critical to diurnal and thermomorphogenic growth.

Martínez Cristina C Espinosa-Ruíz Ana A de Lucas Miguel M Bernardo-García Stella S Franco-Zorrilla José M JM Prat Salomé S

The EMBO journal 20181102 23

The <i>Arabidopsis</i> PIF4 and BES1/BZR1 transcription factors antagonize light signaling by facilitating co-activated expression of a large number of cell wall-loosening and auxin-related genes. While PIF4 directly activates expression of these targets, BES1 and BZR1 activity switch from a repressive to an activator function, depending on interaction with TOPLESS and other families of regulators including PIFs. However, the complexity of this regulation and its role in diurnal control of plant ...[more]

PMID: 30389669

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Project description:Objective: Sleep loss has emerged as a risk factor for the development of impaired glucose tolerance. The mechanisms underpinning this observation are unknown; however, both mitochondrial dysfunction and circadian misalignment have been proposed. Because exercise improves glucose tolerance and mitochondrial function, and alters circadian rhythms, we investigated whether exercise may counteract the effects induced by inadequate sleep.Methods: To minimize between-group differences of baseline characteristics, 24 healthy young males were allocated into one of the three experimental groups: a Normal Sleep (NS) group (8 h time in bed (TIB) per night, for five nights), a Sleep Restriction (SR) group (4 h TIB per night, for five nights), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB per night, for five nights and three high-intensity interval exercise (HIIE) sessions). Glucose tolerance, mitochondrial respiratory function, sarcoplasmic protein synthesis (SarcPS), and diurnal measures of peripheral skin temperature were assessed pre- and post-intervention.Results: We report that the SR group had reduced glucose tolerance post-intervention (mean change ± SD, P value, SR glucose AUC: 149 ± 115 A.U., P = 0.002), which was also associated with reduction in mitochondrial respiratory function (SR: -15.9 ± 12.4 pmol O2.s-1.mg-1, P = 0.001), a lower rate of SarcPS (FSR%/day SR: 1.11 ± 0.25%, P < 0.001), and reduced amplitude of diurnal rhythms. These effects were not observed when incorporating three sessions of HIIE during this period (SR+EX: glucose AUC 67 ± 57, P = 0.239, mitochondrial respiratory function: 0.6 ± 11.8 pmol O2.s-1.mg-1, P = 0.997, and SarcPS (FSR%/day): 1.77 ± 0.22%, P = 0.971).Conclusions: A five-night period of sleep restriction leads to reduction in mitochondrial respiratory function, SarcPS, and amplitude of skin temperature diurnal rhythms, with concurrent reduction in glucose tolerance. We provide novel data demonstrating that these same detrimental effects are not observed when HIIE is performed during the period of sleep restriction. These data therefore provide evidence in support of the use of HIIE as an intervention to mitigate the detrimental physiological effects of sleep loss.

Dataset Information

PIF4-induced BR synthesis is critical to diurnal and thermomorphogenic growth.

Publications

PIF4-induced BR synthesis is critical to diurnal and thermomorphogenic growth.

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