Role of FHY3 and FAR1 in transcriptional regulation of circadian clock resetting by red light

生物体内的许多生物过程是由大约24小时的节律调节的，与外部昼夜周期相协调。这些节律不仅仅是对黎明和黄昏等外部信号的反应，而是由内部的“昼夜节律”时钟产生的，即使在恒定的环境条件下，它也会继续驱动这些节律。内部节律在预测白天发生的变化以及与昼夜周期协调一致的同步过程中具有优势。然而，生物钟并不是与外界隔绝的，它每天都会根据光信号进行轻微的重置，以确保它被设定为正确的时间。时差现象就是一个经典的例子，我们体内的生物钟必须通过光线来重置，这个过程在几天的时间里逐渐发生。同样地，植物也必须能够控制它们的生物钟，因为黎明和黄昏的时间随着季节的变化而变化。植物体内的时钟调节着叶片运动的节奏和光合作用机制在其他过程中的生产时间，但时钟对于确定开花时间的日长测量也至关重要。红色和蓝色波长都是有效的时钟复位。我们的目的是了解红光重置植物生物钟的机制。我们之前已经证明了一种名为FHY3的蛋白质的参与，这种蛋白质对红光重置生物钟的作用至关重要。我们现在已经确定了一种潜在的机制，通过这种机制，它在植物细胞核中启动了一个名为CCA1的基因，该基因参与了生物钟机制。在CCA1通常不活动的时候打开它会导致重置时钟。在新证据的基础上，我们提出了FHY3与另外两种蛋白质FAR1和ELF4对光的反应方式的模型。我们将通过实验来证实这一模型，并将对该机制的其他组成部分进行研究，以合成一个全面的红光输入时钟的模型。对时钟重置的理解可能对农业特别有益，因为开花时间是许多作物产量的关键决定因素，甚至还调节着某些作物可能生长的纬度。此外，植物和动物产生内部昼夜节律的方式的重叠可能意味着这项研究可能对人类昼夜节律缺陷的研究有启示。

A host of biological process in organisms are regulated with an approximately 24 hour rhythm in tune with the external day / night cycle. These rhythms are not merely a response to external signals like dawn and dusk but are generated by an internal 'circadian' clock that continues to drive these rhythms even in constant environmental conditions. An internal rhythm allows an advantage in anticipating changes occurring over the day and in synchronising processes to occur in harmony with the day / night cycle. However, the circadian clock does not operate in isolation from the world / it is reset slightly every day in response to light signals in order to ensure that it is set to the correct time. The phenomenon of jetlag is a classical example where our internal clock must be reset by light, a process that occurs gradually over the course of a few days. Plants must, likewise, be able to entrain their circadian clock as the timing of dawn and dusk varies over the seasons. The clock in plants regulates a rhythm of leaf movement and the timing of production of the photosynthetic machinery amongst other processes, but the clock is also vital to the measurement of daylength in determining time of flowering. Both red and blue wavelengths are effective in clock resetting. Our aim here is to understand the mechanism by which red light resets the plant clock. We have previously demonstrated the involvement of a protein called FHY3 that is essential for the action of red light in resetting the clock. We have now identified a potential mechanism by which this acts in the nucleus of the plant cell to switch on a gene called CCA1, involved in the clock mechanism. Switching on CCA1 at a time when it is normally inactive has the result of resetting the clock. On the basis of new evidence, we propose a model for the way in which FHY3 acts in response to light along with two other proteins, FAR1 and ELF4. We will confirm this model experimentally and will carry out a search for other components also predicted to be part of this mechanism in order to synthesise a comprehensive model of red light input to the clock. An understanding of clock resetting may be particularly beneficial to agriculture where the timing of flowering is a critical determination of yield in many crops and even regulates the possible latitudes at which some crops can grow. In addition, overlap in the ways in which plant and animals generate their internal circadian rhythm may mean that this research could have implications in the study of human circadian defects.