Premature endocycling ofDrosophilafollicle cells causes pleiotropic defects in oogenesis

Abstract

Endocycling cells grow and repeatedly duplicate their genome without dividing. Cells switch from mitotic cycles to endocycles in response to developmental signals during the growth of specific tissues in a wide range of organisms. The purpose of switching to endocycles, however, remains unclear in many tissues. Additionally, cells can switch to endocycles in response to conditional signals, which can have beneficial or pathological effects on tissues. However, the impact of these unscheduled endocycles on development is underexplored. Here, we useDrosophilaovarian somatic follicle cells as a model to examine the impact of unscheduled endocycles on tissue growth and function. Follicle cells normally switch to endocycles at mid-oogenesis. Inducing follicle cells to prematurely switch to endocycles resulted in lethality of the resulting embryos. Analysis of ovaries with precocious follicle cell endocycles revealed aberrant follicular epithelial structure and pleiotropic defects in oocyte growth, developmental gene amplification, and the migration of a special set of follicle cells known as border cells. Overall, these findings reveal how unscheduled endocycles can disrupt tissue growth and function to cause aberrant development.Summary StatementA premature switch to polyploid endocycles inDrosophilaovarian follicle cells caused pleiotropic defects in oogenesis and compromised female fertility, revealing new ways in which unscheduled endocycles cause developmental defects.

An unscheduled switch to endocycles induces a reversible senescent arrest that impairs growth of theDrosophilawing disc

“…6,40,41 We recently found that unscheduled endocycles perturb the morphology of the somatic follicular epithelium that surrounds developing oocytes and result in pleiotropic defects in oogenesis. 42 These findings in Drosophila have contributed to current models for how transient endoreplication cycles of human PGCCs contribute to cancer therapy resistance and progression. 2,19 In this study, we address the impact of unscheduled endocycles on tissue growth using the Drosophila larval wing disc as a model, the anlage of the adult wing and thorax.…”