Disease relevance of TOC1

• Silencing of the TOC1 gene causes arrhythmia in constant darkness and in various intensities of red light, whereas in blue light, the clock runs faster in silenced plants than in wild-type plants [1].
• Our results show that TOC1 RNA interference and toc1-2 mutant plants displayed an important reduction in sensitivity to red and far-red light in the control of hypocotyl elongation, whereas increments in TOC1 gene dosage clearly enhanced light sensitivity [1].

High impact information on TOC1

• Reciprocal regulation between TOC1 and LHY/CCA1 within the Arabidopsis circadian clock [2].
• The toc1 mutation causes shortened circadian rhythms in light-grown Arabidopsis plants [3].
• 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 [4].
• A semidominant short-period mutation, timing of CAB expression (toc1), was mapped to chromosome 5 [4].
• The amplitude and peak levels increase for TOC1 and GI RNA rhythms as the temperature increases (from 17 to 27 degrees C), whereas they decrease for LHY [5].

Biological context of TOC1

• These results suggest that APRR9 (and perhaps other members of the APRR1/TOC1 quintet) must also be taken into consideration for a better understanding of the molecular mechanisms underlying circadian rhythms, and also underlying control of the flowering time through the photoperiodic long-day pathway [6].
• Aberrant expression of the light-inducible and circadian-regulated APRR9 gene belonging to the circadian-associated APRR1/TOC1 quintet results in the phenotype of early flowering in Arabidopsis thaliana [6].
• As demonstrated previously, these APRR1/TOC1 quintet members are crucial for a better understanding of the molecular links between circadian rhythms and photosensory signal transduction [7].
• Increments in TOC1 gene dosage delayed the pace of the clock, whereas TOC1 overexpression abolished rhythmicity in all light conditions tested [1].
• We use these markers together with the short-period mutant, toc1-1, and the clock-controlled cab2::luciferase reporter gene to assess the nature of the circadian clock throughout development and to suggest the position of TOC1 within the circadian clock system [8].

Anatomical context of TOC1

• Cell autonomous circadian waves of the APRR1/TOC1 quintet in an established cell line of Arabidopsis thaliana [9].
• Our data suggest that AIP1 is essential for the normal functioning of the actin cytoskeleton in plant development [10].

Associations of TOC1 with chemical compounds

• The Arabidopsis PSEUDO-RESPONSE REGULATOR (PRR) genes, including the clock component TIMING OF CAB EXPRESSION 1/PRR1, are related to bacterial, fungal, and plant response regulators but lack the conserved Asp that is normally phosphorylated by an upstream sensory kinase [11].

Physical interactions of TOC1

• (iii) The APRR9 protein is capable of interacting with APRR1/TOC1, suggesting a hetrodimer formation between these cognate family members [7].

Regulatory relationships of TOC1

• In particular, the light-inducible expression of APRR9 was severely repressed in APRR1-ox plants, suggesting that there is a negative APRR1-->APRR9 regulation [12].
• Our results show that the TOC1-ZTL interaction is important in the control of TOC1 protein stability, and is probably responsible for the regulation of circadian period by the clock [13].
• PRR3 was temporally coexpressed with TOC1 under different photoperiods, yet its tissue expression was only partially overlapping with that of TOC1, as PRR3 appeared restricted to the vasculature [14].

Other interactions of TOC1

• Transfer to constant red light (Rc) rapidly induces a biphasic pattern of CCA1 and LHY expression, and a reciprocal TOC1 expression pattern over the first 24 h, consistent with initial induction of this synchronous oscillation by the light signal [15].
• The LOV domain of LKP2 was shown to be necessary and sufficient for the interaction with TOC1 [16].
• Furthermore, APRR1/TOC1 was implicated in the L-element-mediated light response of APRR9, directly or indirectly [17].
• The APRR3 component of the clock-associated APRR1/TOC1 quintet is phosphorylated by a novel protein kinase belonging to the WNK family, the gene for which is also transcribed rhythmically in Arabidopsis thaliana [18].
• The light-induced expressions of PIF4 and PIL6 were severely impaired in APRR1-ox transgenic lines [19].

References