Center for Systems Biology, School of Mathematical Sciences, Soochow University, Suzhou, People's Republic of China.
Unité de Chronobiologie Théorique, Faculté des Sciences, Université Libre de Bruxelles (ULB), 1050 Brussels, Belgium.
J R Soc Interface. 2019 Sep 27;16(158):20190376. doi: 10.1098/rsif.2019.0376. Epub 2019 Sep 11.
The cell cycle and the circadian clock represent major cellular rhythms, which appear to be coupled. Thus the circadian factor BMAL1 controls the level of cell cycle proteins such as Cyclin E and WEE1, the latter of which inhibits the kinase CDK1 that governs the G2/M transition. In reverse the cell cycle impinges on the circadian clock through direct control by CDK1 of REV-ERBα, which negatively regulates BMAL1. These observations provide evidence for bidirectional coupling of the cell cycle and the circadian clock. By merging detailed models for the two networks in mammalian cells, we previously showed that unidirectional coupling to the circadian clock can entrain the cell cycle to 24 or 48 h, depending on the cell cycle autonomous period, while complex oscillations occur when entrainment fails. Here we show that the reverse unidirectional coupling via phosphorylation of REV-ERBα or via mitotic inhibition of transcription, both controlled by CDK1, can elicit entrainment of the circadian clock by the cell cycle. We then determine the effect of bidirectional coupling of the cell cycle and circadian clock as a function of their relative coupling strengths. In contrast to unidirectional coupling, bidirectional coupling markedly reduces the likelihood of complex oscillations. While the two rhythms oscillate independently as long as both couplings are weak, one rhythm entrains the other if one of the couplings dominates. If the couplings in both directions become stronger and of comparable magnitude, the two rhythms synchronize, generally at an intermediate period within the range defined by the two autonomous periods prior to coupling. More surprisingly, synchronization may also occur at a period slightly below or above this range, while in some conditions the synchronization period can even be much longer. Two or even three modes of synchronization may sometimes coexist, yielding examples of birhythmicity or trirhythmicity. Because synchronization readily occurs in the form of simple periodic oscillations over a wide range of coupling strengths and in the presence of multiple connections between the two oscillatory networks, the results indicate that bidirectional coupling favours the robust synchronization of the cell cycle and the circadian clock.
细胞周期和生物钟代表主要的细胞节律,它们似乎是耦合的。因此,生物钟因子 BMAL1 控制细胞周期蛋白的水平,如细胞周期蛋白 E 和 WEE1,后者抑制控制 G2/M 转换的激酶 CDK1。相反,细胞周期通过 CDK1 对 REV-ERBα 的直接控制作用影响生物钟,REV-ERBα 负调节 BMAL1。这些观察结果为细胞周期和生物钟的双向耦合提供了证据。通过在哺乳动物细胞中合并这两个网络的详细模型,我们之前表明,单向耦合到生物钟可以将细胞周期调整到 24 或 48 小时,具体取决于细胞周期自主周期,而当同步失败时会发生复杂的振荡。在这里,我们表明通过 CDK1 控制的 REV-ERBα 的磷酸化或通过有丝分裂抑制转录的反向单向耦合都可以通过细胞周期引发生物钟的同步。然后,我们确定了细胞周期和生物钟的双向耦合作为它们相对耦合强度的函数的效果。与单向耦合相反,双向耦合显著降低了复杂振荡发生的可能性。只要两个耦合都很弱,两个节律就会独立振荡,但是如果一个耦合占主导地位,则一个节律会使另一个节律同步。如果两个方向的耦合都变得更强且大小相当,则两个节律会同步,通常在耦合之前两个自主周期定义的范围内的中间周期。更令人惊讶的是,在某些条件下,同步周期甚至可能长得多,同步也可能在该范围略低于或高于该范围的周期处发生。在某些情况下,甚至可能同时存在两个或三个同步模式,从而产生双节奏或三节奏的例子。由于同步很容易以简单周期性振荡的形式在广泛的耦合强度范围内发生,并且在两个振荡网络之间存在多个连接,因此结果表明双向耦合有利于细胞周期和生物钟的稳健同步。