To create an organism, it is vital to assemble enough cells of the various differentiated types with the correct spatial arrangement within the embryo. Circadian clocks development is closely correlated with all cellular differentiation. However, the expression of its emergence during mammalian development are not fully understood. To determine whether embryonic development is influenced by circadian rhythm, it is necessary to observe the ontogeny of the circadian clock gene. We first measured the expression of key circadian genes in whole embryos and maternal major tissues of 25 female mice using RT-PCR and immunohistochemical analysis. Our results indicated that mouse embryos begin to express key circadian genes and have the capacity to express active circadian regulatory cycles during development. But circadian molecular rhythms can’t be built in embryo. At E15, the expression of Bmal1, Clock and Per1 mRNA in whole embryo were increased, especially Per1. In the meanwhile, immunohistochemical analysis shows a small number of PER1 positive cells were observed in the bottom of right atrium. From E16 to E17, CLOCK and PER1 positive cells were observed in the airway smooth muscle, the wall of left atrium and skeletal muscle of body wall. It is interesting that CLOCK and PER1 positive cells could not be detected in the liver. By using RT-PCR, we continue to observe the expression of myogenic regulatory factor in embryos and also analyse the relationship of embryo development and maternal rhythms. From E12, the expression of myogenin increased quickly. The expression of Tcap at E15 significantly increased. myogenin may play a direct role in contributing Tcap expression. The expression of MAZ is always the highest than myogenin and Tcap in embryos. MAZ may concern with the development of skeletal muscle. The clock gene is a positive regulator of myogenesis and the development of organ. In contrast to embryonic tissues, circadian variation was present for Bmal1, Clock and Per1 at maternal tissues. Our results indicate that circadian clock genes seem to function differently in different tissues of embryo and maternal mice. Synchrony does not occur during embryo development despite exposure to maternal rhythms. But development of embryo may be affected by maternal tissues of mice.

为了创造一个有机体，在胚胎内以正确的空间排列组装足够多的各种分化类型的细胞是至关重要的。生物钟发育与所有细胞分化密切相关。然而，它在哺乳动物发育过程中出现的表达尚不完全清楚。为了确定胚胎发育是否受昼夜节律的影响，有必要观察生物钟基因的个体发育。我们首先使用 RT-PCR 和免疫组织化学分析测量了 25 只雌性小鼠的整个胚胎和母体主要组织中关键昼夜节律基因的表达。我们的研究结果表明，小鼠胚胎开始表达关键的昼夜节律基因，并具有在发育过程中表达活跃的昼夜节律调节周期的能力。但是昼夜节律不能在胚胎中建立。在 E15，表达式整个胚胎中的Bmal1、Clock和Per1 mRNA增加，尤其是Per1。同时，免疫组化分析显示右心房底部可见少量PER1阳性细胞。从E16到E17，在气道平滑肌、左心房壁和体壁骨骼肌中观察到CLOCK和PER1阳性细胞。有趣的是，在肝脏中无法检测到 CLOCK 和 PER1 阳性细胞。通过使用RT-PCR，我们继续观察胚胎中肌源性调节因子的表达，并分析胚胎发育与母体节律的关系。从E12开始，肌细胞生成素的表达迅速增加。Tcap的表达在 E15 显着增加。肌细胞生成素可能在促进Tcap表达中起直接作用。MAZ在胚胎中的表达量始终高于myogenin和Tcap。MAZ 可能与骨骼肌的发育有关。时钟基因是肌生成和器官发育的正向调节因子。与胚胎组织相比，Bmal1、Clock和Per1存在昼夜节律变化在母体组织。我们的研究结果表明，生物钟基因似乎在胚胎和母鼠的不同组织中发挥不同的作用。尽管暴露于母体节律，但在胚胎发育过程中不会发生同步。但胚胎的发育可能会受到小鼠母体组织的影响。