Open AccessPlanar cell polarity signaling regulates polarized second heart field morphogenesis to promote both arterial and venous pole septation
Author(s) -
Ding Li,
Allyson Angermeier,
Jianbo Wang
Publication year - 2019
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.181719
Subject(s) - biology , lateral plate mesoderm , morphogenesis , microbiology and biotechnology , mesoderm , anatomy , heart development , population , polarity (international relations) , mesenchyme , progenitor cell , cell polarity , mesenchymal stem cell , stem cell , embryonic stem cell , cell , genetics , medicine , gene , environmental health
Second heart field (SHF) harbors progenitors important for heart formation, but little is known about its morphogenesis. We show that SHF population in the splanchnic mesoderm (SpM-SHF) undergoes polarized morphogenesis to preferentially elongate anteroposteriorly. Loss of Wnt5, a putative ligand of the planar cell polarity (PCP) pathway, cause the SpM-SHF to expand isotropically. Temporal tracking reveals that Wnt5a lineage is a unique subpopulation specified as early as E7.5, and undergoes bi-directional deployment to form specifically the pulmonary trunk and the dorsal mesenchymal protrusion (DMP). In Wnt5a-/- mutants, Wnt5a lineage fails to extend into the arterial and venous poles, leading to both outflow tract and atrial septation defects that can be rescued by an activated form of PCP effector Daam1. We identify oriented actomyosin cable in the medial SpM-SHF as a potential Wnt5a-mediated mechanism to promote SpM-SHF lengthening and restrict its widening. Finally, Wnt5a lineage also contributes to the pulmonary mesenchyme, suggesting that Wnt5a/ PCP is a molecular circuit recruited by the recently identified cardiopulmonary progenitors to coordinate morphogenesis of the pulmonary airways and the cardiac septations necessary for pulmonary circulation.