The Arabidopsis Pseudo-response Regulators, PRR5 and PRR7, Coordinately Play Essential Roles for Circadian Clock Function

Abstract

In Arabidopsis thaliana, a number of clock-associated protein factors have been identified. Among them, TOC1 (TIMING OF CAB EXPRESSION 1) is believed to be a component of the central oscillator. TOC1 is a member of a small family of proteins, designated as ARABIDOPSIS PSEUDO-RESPONSE REGULATOR, including PRR1/TOC1, PRR3, PRR5, PRR7 and PRR9. It has not been certain whether or not other PRR family members are also implicated in clock function per se. To clarify this problem, here we constructed a double mutant line, which is assumed to have severe lesions in both the PRR5 and PRR7 genes. Resulting homozygous prr5-11 prr7-11 young seedlings showed a marked phenotype of hyposensitivity to red light during de-etiolation. In addition, they displayed a phenotype of extremely late flowering under long-day photoperiod conditions, but not short-day conditions. The rhythms at the level of transcription of certain clock-controlled genes were severely perturbed in the double mutant plants when they were released into continuous light (LL) and darkness (DD). The observed phenotype was best interpreted as 'arrhythmic in both LL and DD' and/or 'very short period with markedly reduced amplitude'. Even under the light entrainment (LD) conditions, the mutant plants showed anomalous diurnal oscillation profiles with altered amplitude and/or phase with regard to certain clock-controlled genes, including the clock component CCA1 (CIRCADIAN CLOCK-ASSOCIATED 1) gene. Such events were observed even under temperature entrainment conditions, suggesting that the prr5-11 prr7-11 lesions cannot simply be attributed to a defect in the light signal input pathway. These pleiotropic circadian-associated phenotypes of the double mutant were very remarkable, as compared with those observed previously for each single mutant. Taking these results together, we propose for the first time that PRR5 and PRR7 coordinately (or synergistically) play essential clock-associated roles close to the central oscillator.

Arabidopsis CRY2 and ZTL mediate blue-light regulation of the transcription factor CIB1 by distinct mechanisms

“…Nuclear GI promotes flowering (34), and GI nuclear levels are higher in ztl mutants than in WT, whereas overexpressed ZTL sequesters GI in the cytosol (32). In addition to GI and CIB1, ZTL regulates other proteins that play important roles in the control of the circadian clock and photoperiodic flowering, such as PRR5 and TOC1 (18,35,36). Further studies are needed to elucidate both the individual and the combined effects of ZTL and ZTL-regulated proteins, including CIB1, in the control of flowering time.…”

Plant Circadian Rhythms

“…The circadian phenotypes of the single prr mutants are small (period changes of 1 to 1.5 h) compared with the period shortening (3 to 4 h) seen in toc1-2 mutants, but redundancy among the PRRs may partially account for this. The phenotype of the prr7 prr9 double mutant is more than additive; the period lengthening is dramatically increased, and the double mutant is arrhythmic in the dark (Farré et al, 2005;Nakamichi et al, 2005a;Salomé and McClung, 2005a). Emphasizing the centrality of the PRRs to clock function, the triple prr5 prr7 prr9 mutant is essentially arrhythmic under all conditions tested (Nakamichi et al, 2005b).…”

PRR3 Is a Vascular Regulator of TOC1 Stability in theArabidopsisCircadian Clock

“…PRR single mutants were found to cause a mild effect on period length, whereas some double and triple mutant combinations result in a severe clock phenotype: the double mutant prr9 prr7 displayed a longer period than either of the single mutants, and the prr5 prr7 double mutant phenotype was reported to exhibit very short to arrhythmic oscillations that became further compromised in the prr9 prr7 prr5 triple mutant (Farre et al, 2005;Fujimori et al, 2005;Nakamichi et al, 2005aNakamichi et al, , 2005bSalome and McClung, 2005). Interestingly, combining the clock phenotype of the short-period prr5 mutation with the long-period prr9 mutation resulted in a wild-type period (Eriksson et al, 2003).…”