Although the human body appears superficially symmetrical with regard to the left–right (L-R) axis, most visceral organs are asymmetric in terms of their size, shape, or position. Such morphological asymmetries of visceral organs, which are essential for their proper function, are under the control of a genetic pathway that operates in the developing embryo. In many vertebrates including mammals, the breaking of L-R symmetry occurs at a structure known as the L-R organizer (LRO) located at the midline of the developing embryo. This symmetry breaking is followed by transfer of an active form of the signaling molecule Nodal from the LRO to the lateral plate mesoderm (LPM) on the left side, which results in asymmetric expression of Nodal (a left-side determinant) in the left LPM. Finally, L-R asymmetric morphogenesis of visceral organs is induced by Nodal-Pitx2 signaling. This review will describe our current understanding of the mechanisms that underlie the generation of L-R asymmetry in vertebrates, with a focus on mice.

尽管人体在左右（LR）轴上看起来是表面对称的，但大多数内脏器官的大小，形状或位置都不对称。内脏器官的这种形态不对称，对于它们的正常功能是必不可少的，处于发育中的胚胎的遗传途径的控制之下。在包括哺乳动物在内的许多脊椎动物中，LR对称性的破坏发生在位于发育胚胎中线的称为LR组织者（LRO）的结构上。此对称性破坏后，信号分子Nodal的活性形式从LRO转移到左侧的侧板中胚层（LPM），这导致Nodal表达不对称（左侧行列式）在左侧LPM中。最后，内脏器官的LR不对称形态发生是由Nodal-Pitx2信号传导诱导的。这篇综述将描述我们目前对脊椎动物中LR不对称性产生基础的机制的理解，重点是小鼠。