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Mutations in  ZIC3  cause human X-linked heterotaxy and isolated cardiovascular malformations. A mouse model with targeted deletion of  Zic3  demonstrates an early role for  Zic3  in gastrulation, CNS, cardiac and left–right axial development. The observation of multiple malformations in  Zic3  null  mice and the relatively broad expression pattern of  Zic3  suggest its important roles in multiple developmental processes. Here, we report that Zic3 is primarily required in epiblast derivatives to affect left–right patterning and its expression in epiblast is necessary for proper transcriptional control of embryonic cardiac development. However, cardiac malformations in  Zic3  deficiency occur not because  Zic3  is intrinsically required in the heart but rather because it functions early in the establishment of left–right body axis. In addition, we provide evidence supporting a role for  Zic3  specifically in the perinodal region of the posterior lateral plate mesoderm for the establishment of laterality. These data delineate the spatial requirement of  Zic3  during left–right patterning in the mammalian embryo, and provide basis for further understanding the molecular mechanisms underlying the complex interaction of Zic3 with signaling pathways involved in the early establishment of laterality.

Zic3 is required in the extra-cardiac perinodal region of the lateral plate mesoderm for left–right patterning and heart development