Cilia in most vertebrate left-right organizers are involved in the original break in left-right (L-R) symmetry, however, less is known about their roles in subsequent steps of the cascade - relaying the signaling and maintaining the established asymmetry. Here we describe the L-R patterning cascades in two mutants of a ciliary transition zone protein TMEM107, revealing that near-complete loss of cilia in Tmem107null leads to left pulmonary isomerism due to the failure of the midline barrier. Contrary, partially retained cilia in the node and the midline of a hypomorphic Tmem107schlei mutant appear sufficient for the formation of the midline barrier and establishment and maintenance of the L-R asymmetry. Despite misregulation of Shh signaling in both mutants, the presence of normal Lefty1 expression and midline barrier formation in Tmem107schlei mutants, suggests a requirement for cilia, but not necessarily Shh signaling for Lefty1 expression and midline barrier formation.

中文翻译：

---

睫状过渡区蛋白TMEM107的缺失导致小鼠异源性。

大多数脊椎动物左右组织者中的纤毛都参与了左右对称（LR）的原始断裂，但是，它们在级联反应的后续步骤中的作用鲜为人知-传递信号并维持既定的不对称性。在这里，我们描述了纤毛过渡区蛋白TMEM107的两个突变体中的LR模式级联，揭示了Tmem107null中纤毛的几乎完全丧失会由于中线屏障的衰竭而导致左肺异构。相反，亚型的Tmem107schlei突变体的结点和中线部分保留了纤毛，足以形成中线屏障，并建立和维持LR不对称性。尽管两个突变体中的Shh信号均调控不当，