Circadian clocks are believed to confer an advantage to plants, but the nature of that advantage has been unknown. We show that a substantial photosynthetic advantage is conferred by correct matching of the circadian clock period with that of the external light-dark cycle. In wild type and in long– and short–circadian period mutants of Arabidopsis thaliana , plants with a clock period matched to the environment contain more chlorophyll, fix more carbon, grow faster, and survive better than plants with circadian periods differing from their environment. This explains why plants gain advantage from circadian control.

Cellular life emerged ∼3.7 billion years ago. With scant exception, terrestrial organisms have evolved under predictable daily cycles owing to the Earth’s rotation. The advantage conferred on organisms that anticipate such environmental cycles has driven the evolution of endogenous circadian rhythms that tune internal physiology to external conditions. The molecular phylogeny of mechanisms driving these rhythms has been difficult to dissect because identified clock genes and proteins are not conserved across the domains of life: Bacteria, Archaea and Eukaryota. Here we show that oxidation–reduction cycles of peroxiredoxin proteins constitute a universal marker for circadian rhythms in all domains of life, by characterizing their oscillations in a variety of model organisms. Furthermore, we explore the interconnectivity between these metabolic cycles and transcription–translation feedback loops of the clockwork in each system. Our results suggest an intimate co-evolution of cellular timekeeping with redox homeostatic mechanisms after the Great Oxidation Event ∼2.5 billion years ago.

The cycling bioluminescence of Arabidopsis plants carrying a firefly luciferase fusion construct was used to identify mutant individuals with aberrant cycling patterns. Both long- and short-period mutants were recovered. A semidominant short-period mutation, timing of CAB expression ( toc1 ), was mapped to chromosome 5. The toc1 mutation shortens the period of two distinct circadian rhythms, the expression of chlorophyll a/b -binding protein ( CAB ) genes and the movements of primary leaves, although toc1 mutants do not show extensive pleiotropy for other phenotypes.

Tic TOC1 Plant Clock: The molecular clocks intertwined with cellular physiology regulate daily cycles. In plants, these circadian rhythms affect processes as diverse as carbon metabolism and leaf orientation. Huang et al. (p. 75 , published online 8 March) have now analyzed the interactions driven by a key element of the circadian clock in plants, TOC1 (“TIMING OF CAB EXPRESSION 1”). TOC1 helps to coordinate responses of the morning and evening cycles, functioning to repress activity of other clock components.

Spring Into Flower: In spring, plants respond to increasing day length and shifts in the spectrum of solar irradiance by releasing the flowering induction pathway, which includes expression of the FLOWERING LOCUS T (FT) protein. Song et al. (p. 1045 ) have now identified a trio of controls brought to bear on FT gene expression by the FKF1 (FLAVIN-BINDING, KELCH REPEAT, F-BOX 1) protein. FKF1 removes a repressor and also stabilizes the activating CONSTANS (CO) protein in the afternoons through a binding interaction enhanced by blue light—an increasing component of solar irradiation during spring. Then FKF1 itself helps to activate transcription of the CO gene. Thus, by removing the repressor and shoring up the activator, FKF1 sets flowering on its way.

Circadian clocks are critical timing regulators of physiology and behaviour that are ubiquitous in eukaryotes. Most mechanistic models of the clock are based on transcription cycles, but evidence for post-translational regulation has recently surfaced in plants and cyanobacteria. Two groups now demonstrate a role for the oxidation of peroxiredoxin proteins in maintaining an entrainable oscillation in human red blood cells and in the unicellular alga Ostreococcus tauri. These data suggest a role for non-transcriptional mechanisms in clock models and open the door to future work exploring the connections between the transcriptional and non-transcriptional circadian machinery. Circadian clocks are critical timing regulators of physiology and behaviour that are ubiquitous in eukaryotes. Most mechanistic models of the this clock are based on transcription cycles, but some evidence for post-translational regulation has recently surfaced in plants and cyanobacteria. This is one of two groups demonstrating a role for the oxidation of peroxiredoxin proteins in maintaining an entrainable oscillation in human red blood cells and a unicellular alga. These data indicate a role for non-transcriptional mechanisms in clock models and open the door to future work exploring the connections between the transcriptional and non transcriptional circadian machinery. Circadian rhythms are ubiquitous in eukaryotes, and coordinate numerous aspects of behaviour, physiology and metabolism, from sleep/wake cycles in mammals to growth and photosynthesis in plants1,2. This daily timekeeping is thought to be driven by transcriptional–translational feedback loops, whereby rhythmic expression of ‘clock’ gene products regulates the expression of associated genes in approximately 24-hour cycles. The specific transcriptional components differ between phylogenetic kingdoms3. The unicellular pico-eukaryotic alga Ostreococcus tauri possesses a naturally minimized clock, which includes many features that are shared with plants, such as a central negative feedback loop that involves the morning-expressed CCA1 and evening-expressed TOC1 genes4. Given that recent observations in animals and plants have revealed prominent post-translational contributions to timekeeping5, a reappraisal of the transcriptional contribution to oscillator function is overdue. Here we show that non-transcriptional mechanisms are sufficient to sustain circadian timekeeping in the eukaryotic lineage, although they normally function in conjunction with transcriptional components. We identify oxidation of peroxiredoxin proteins as a transcription-independent rhythmic biomarker, which is also rhythmic in mammals6. Moreover we show that pharmacological modulators of the mammalian clock mechanism have the same effects on rhythms in Ostreococcus. Post-translational mechanisms, and at least one rhythmic marker, seem to be better conserved than transcriptional clock regulators. It is plausible that the oldest oscillator components are non-transcriptional in nature, as in cyanobacteria7, and are conserved across kingdoms.