Atypical Protein Kinase C-Dependent Polarized Cell Division Is Required for Myocardial Trabeculation

作者：Passer Derek; van de Vrugt Annebel; Atmanli Ayhan; Domian Ibrahim J^*

来源：Cell Reports, 2016, 14(7): 1662-1672.

DOI：10.1016/j.celrep.2016.01.030

A hallmark of cardiac development is the formation of myocardial trabeculations exclusively from the luminal surface of the primitive heart tube. Although a number of genetic defects in the endocardium and cardiac jelly disrupt myocardial trabeculation, the role of cell polarization remains unclear. Here, we demonstrate that atypical protein kinase C iota (Prkci) and its interacting partners are localized primarily to the luminal side of myocardial cells of early murine embryonic hearts. A subset of these cells undergoes polarized cell division with the cell division plane perpendicular to the heart's lumen. Disruption of the cell polarity complex by targeted gene mutations results in aberrant mitotic spindle alignment, loss of polarized cardiomyocyte division, and loss of normal myocardial trabeculation. Collectively, these results suggest that, in response to inductive signals, Prkci and its downstream partners direct polarized cell division of luminal myocardial cells to drive trabeculation in the nascent heart.

• 出版日期2016-2-23