Coordination of non-professional efferocytosis and actomyosin contractility during epithelial tissue morphogenesis

In developing embryos, specific cell populations are often removed to remodel tissue architecture for organogenesis. During urinary tract development, an epithelial duct called the common nephric duct (CND) gets shortened and eventually eliminated to remodel the entry point of the ureter into the bladder. Here we show that non-professional efferocytosis (the process in which epithelial cells engulf apoptotic bodies) is the main mechanism that contributes to CND shortening. Combining biological metrics and computational modeling, we show that efferocytosis with actomyosin contractility are essential factors that drive the CND shortening without compromising the ureter-bladder structural connection. The disruption of either apoptosis, non-professional efferocytosis, or actomyosin results in contractile tension reduction and deficient CND shortening. Actomyosin activity helps to maintain tissue architecture while non-professional efferocytosis removes cellular volume. Together our results demonstrate that non-professional efferocytosis with actomyosin contractility are important morphogenetic factors controlling CND morphogenesis. [Display omitted] •Non-professional efferocytosis is the main mechanism for tissue morphogenesis•Mathematical modeling is designed to estimate non-professional efferocytosis timing•Non-professional efferocytosis and actomyosin are essential factors in morphogenetic force Tang et al. show that non-professional efferocytosis is the main mechanism for epithelial duct shortening morphogenesis. Biological metrics and computational modeling suggest the essential roles of non-professional efferocytosis with actomyosin activity to drive duct shortening. Apoptosis, non-professional efferocytosis, and actomyosin all contribute to tension accumulation as crucial morphogenetic factors.