Plant development goes like clockwork

Montaigu, Amaury de; Tóth, Réka; Coupland, George

doi:10.1016/j.tig.2010.04.003

Cited by 169 publications

(133 citation statements)

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“…Timing of the floral transition is coordinated by a clock that controls the progression of development through genetic and epigenetic programming [11][12][13] . The floral transition requires triggering the initiation of flowering 14,15 , and also involves complex redeployment of a variety of metabolic and biochemical processes 16,17 .…”

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confidence: 99%

Release of SOS2 kinase from sequestration with GIGANTEA determines salt tolerance in Arabidopsis

et al. 2013

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Environmental challenges to plants typically entail retardation of vegetative growth and delay or cessation of flowering. Here we report a link between the flowering time regulator, GIGANTEA (GI), and adaptation to salt stress that is mechanistically based on GI degradation under saline conditions, thus retarding flowering. GI, a switch in photoperiodicity and circadian clock control, and the SNF1-related protein kinase SOS2 functionally interact. In the absence of stress, the GI:SOS2 complex prevents SOS2-based activation of SOS1, the major plant Na þ /H þ -antiporter mediating adaptation to salinity. GI overexpressing, rapidly flowering, plants show enhanced salt sensitivity, whereas gi mutants exhibit enhanced salt tolerance and delayed flowering. Salt-induced degradation of GI confers salt tolerance by the release of the SOS2 kinase. The GI-SOS2 interaction introduces a higher order regulatory circuit that can explain in molecular terms, the long observed connection between floral transition and adaptive environmental stress tolerance in Arabidopsis.

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confidence: 99%

Release of SOS2 kinase from sequestration with GIGANTEA determines salt tolerance in Arabidopsis

et al. 2013

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“…The fact that the CE has been shown to be critical for proper temporal expression of MyoD during development and now for the circadian expression of MyoD raises intriguing questions about the possibility that (i) CLOCK and/or BMAL1 have a noncircadian function during myogenesis and (ii) the CE serves as a "timing" module to provide a temporal component to MyoD expression during embryonic development and adulthood. At this time, CLOCK and/or BMAL1 have not been shown to regulate developmental gene expression in mammals, but there are some studies linking their homologs to development in Arabidopsis (27).…”

Section: Discussionmentioning

confidence: 99%

CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

Andrews

Zhang

McCarthy

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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MyoD, a master regulator of myogenesis, exhibits a circadian rhythm in its mRNA and protein levels, suggesting a possible role in the daily maintenance of muscle phenotype and function. We report that MyoD is a direct target of the circadian transcriptional activators CLOCK and BMAL1, which bind in a rhythmic manner to the core enhancer of the MyoD promoter. Skeletal muscle of Clock Δ19 and Bmal1 −/− mutant mice exhibited ∼30% reductions in normalized maximal force. A similar reduction in force was observed at the single-fiber level. Electron microscopy (EM) showed that the myofilament architecture was disrupted in skeletal muscle of Clock Δ19 , Bmal1 −/− , and MyoD −/− mice. The alteration in myofilament organization was associated with decreased expression of actin, myosins, titin, and several MyoD target genes. EM analysis also demonstrated that muscle from both Clock Δ19 and Bmal1 −/− mice had a 40% reduction in mitochondrial volume. The remaining mitochondria in these mutant mice displayed aberrant morphology and increased uncoupling of respiration. This mitochondrial pathology was not seen in muscle of MyoD −/− mice. We suggest that altered expression of both Pgc-1α and Pgc-1β in Clock Δ19 and Bmal1 −/− mice may underlie this pathology. Taken together, our results demonstrate that disruption of CLOCK or BMAL1 leads to structural and functional alterations at the cellular level in skeletal muscle. The identification of MyoD as a clock-controlled gene provides a mechanism by which the circadian clock may generate a muscle-specific circadian transcriptome in an adaptive role for the daily maintenance of adult skeletal muscle.circadian clock | myofilaments | mitochondria A fundamental, evolutionarily conserved property of most organisms, from cyanobacteria to plants and animals, is the daily cycling of their internal physiology as well as certain behaviors in animals, such as sleep and feeding (1). The timing of these circadian rhythms is synchronized to the environment by external cues, with light and nutrient availability being two of the most salient entrainment cues (2). The synchronization of endogenous circadian rhythms with the daily cycles in the environment provides an adaptive mechanism for organisms to anticipate cyclic demands on cellular physiology and behavior (3, 4). At the molecular level, the circadian clock represents a well-defined gene regulatory network composed of transcriptional-translational feedback loops (5). The positive arm of the loop is composed of the transcription factors CLOCK and BMAL1, which heterodimerize and bind to E-box elements on target genes such as Per1 to drive the negative part of the feedback loop (5). More recently, the same molecular clock factors that have been identified in the central clock in the suprachiasmatic nucleus have been found to exist in most peripheral tissues (reviewed in ref. 6).We recently characterized the circadian transcriptome of adult skeletal muscle. These mRNAs exhibit significant oscillation in gene expression with a repeating period len...

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“…Such alleles could confer an advantage by adjusting the activity of temporally regulated processes without severely disrupting the circadian system. diurnal | circadian | rhythms | Arabidopsis | GIGANTEA I n plants, many aspects of physiology and development, including metabolism, growth, flowering, and plant defense, are controlled by genes whose expression pattern oscillates on a daily basis (1,2). These genes usually show peaks of expression around the time at which their function is required to regulate downstream processes.…”

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Natural diversity in daily rhythms of gene expression contributes to phenotypic variation

Montaigu

Giakountis

Rubin

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Daily rhythms of gene expression provide a benefit to most organisms by ensuring that biological processes are activated at the optimal time of day. Although temporal patterns of expression control plant traits of agricultural importance, how natural genetic variation modifies these patterns during the day and how precisely these patterns influence phenotypes is poorly understood. The circadian clock regulates the timing of gene expression, and natural variation in circadian rhythms has been described, but circadian rhythms are measured in artificial continuous conditions that do not reflect the complexity of biologically relevant day/ night cycles. By studying transcriptional rhythms of the eveningexpressed gene GIGANTEA (GI) at high temporal resolution and during day/night cycles, we show that natural variation in the timing of GI expression occurs mostly under long days in 77 Arabidopsis accessions. This variation is explained by natural alleles that alter light sensitivity of GI, specifically in the evening, and that act at least partly independent of circadian rhythms. Natural alleles induce precise changes in the temporal waveform of GI expression, and these changes have detectable effects on PHYTOCHROME INTERACTING FACTOR 4 expression and growth. Our findings provide a paradigm for how natural alleles act within day/night cycles to precisely modify temporal gene expression waveforms and cause phenotypic diversity. Such alleles could confer an advantage by adjusting the activity of temporally regulated processes without severely disrupting the circadian system. diurnal | circadian | rhythms | Arabidopsis | GIGANTEA

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Plant development goes like clockwork

Cited by 169 publications

References 100 publications

Release of SOS2 kinase from sequestration with GIGANTEA determines salt tolerance in Arabidopsis

Release of SOS2 kinase from sequestration with GIGANTEA determines salt tolerance in Arabidopsis

CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function

Natural diversity in daily rhythms of gene expression contributes to phenotypic variation

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