Although chronobiologists commonly study rhythms in constant conditions, organisms live in the cycling world of day and night. The two chief entraining stimuli that synchronize the endogenous clock with the exogenous temporal environment are light and temperature (Millar, 2004; Salomé and McClung, 2005b). Both phytochromes and cryptochromes provide light input to the clock, although the signal transduction pathways are incompletely defined. Interestingly, photoreceptor expression is itself rhythmic, indicating that the clock gates its sensitivity to light (e.g., Tóth et al., 2001), although bulk phytochrome protein levels do not oscillate (Sharrock and Clack, 2002). Light input is negatively regulated by ELF3; loss-of-function alleles of elf3 yield conditional arrhythmicity in continuous light but remain rhythmic in the dark (Hicks et al., 1996, 2001; McWatters et al., 2000; Covington et al., 2001; Liu et al., 2001). TIME FOR COFFEE (TIC) may have a similar effect on gating light input, although during a distinct phase; the tic elf3 double mutant is fully arrhythmic in light or dark (Hall et al., 2003). The period alteration of ztl mutants shows fluence rate dependence, suggesting a role for ZTL in light input (Somers et al., 2000).

It seems reasonable that both dawn and dusk provide important entraining cues. Possibly, the dusk signal involves relief from light repression of TOC1 degradation mediated by SCFZTL. The dawn cue likely involves induction of CCA1and LHY and other clock components, although we lack a detailed mechanistic understanding of this signaling. Light input is positively regulated by SENSITIVITY TO RED LIGHT REDUCED1 (SRR1), which also plays an as yet undefined role in the core oscillator (Staiger et al., 2003). The basic helix-loop-helix transcription regulator, PHYTOCHROME-INTERACTING FACTOR3 (PIF3) induces CCA1 and LHYexpression via binding to the G-box (Martínez-García et al., 2000). Phytochrome B (PHYB) in its active form binds specifically and reversibly to DNA-bound PIF3, suggesting a direct link from light perception to modification of the negative limb of the circadian clock (Martínez-García et al., 2000). However, loss of function of PIF3 does not affect period length of rhythmic gene expression (Monte et al., 2004). It is also important to note that the conclusive resetting of the clock by transient expression of CCA1 or LHY has not been demonstrated nor has it been definitively shown that levels of CCA1 or LHY set phase (Salomé and McClung, 2005b).

Temperature signaling to the clock is much less well defined. Abundant evidence supports the importance of temperature cycles in clock entrainment. Temperature steps as small as 0.5°C can entrain the Kalanchoë clock, showing the exquisite sensitivity of the system (Rensing and Ruoff, 2002). In Arabidopsis, gene expression and cotyledon movement can be entrained by temperature cycles (Michael and McClung, 2002; Salomé et al., 2002; Salomé and McClung, 2005a), but the mechanism of action is currently unknown. It has been established that PRR7 and PRR9 are important as the prr7 prr9 double mutant fails to entrain to temperature cycles that effectively entrain the wild type (Salomé and McClung, 2005a).

Considerable natural variation in temperature compensation has been described, and GI has been identified as a quantitative trait locus responsible for a substantial portion of that variation (Edwards et al., 2005
). It seems likely that this clock property will prove amenable to forward and reverse genetic approaches.