Patterns of senescence and apoptosis during development of branchial arches, epibranchial placodes, and pharyngeal pouches

BackgroundMany developmental processes are coregulated by apoptosis and senescence. However, there is a lack of data on the development of branchial arches, epibranchial placodes, and pharyngeal pouches, which harbor epibranchial signaling centers. ResultsUsing immunohistochemical, histochemical, and 3D reconstruction methods, we show that in mice, senescence and apoptosis together may contribute to the invagination of the branchial clefts and the deepening of the cervical sinus floor, in antagonism to the proliferation acting in the evaginating branchial arches. The concomitant apoptotic elimination of lateral line rudiments occurs in the absence of senescence. In the epibranchial placodes, senescence and apoptosis appear to (1) support invagination or at least indentation by immobilizing the margins of the centrally proliferating pit, (2) coregulate the number and fate of Pax8(+) precursors, (3) progressively narrow neuroblast delamination sites, and (4) contribute to placode regression. Putative epibranchial signaling centers in the pharyngeal pouches are likely deactivated by rostral senescence and caudal apoptosis. ConclusionsOur results reveal a plethora of novel patterns of apoptosis and senescence, some overlapping, some complementary, whose functional contributions to the development of the branchial region, including the epibranchial placodes and their signaling centers, can now be tested experimentally.

Automated summary

Using various methods, this study reveals that senescence and apoptosis contribute to the development of branchial arches, epibranchial placodes, and pharyngeal pouches in mice. These processes play a role in the invagination of branchial clefts, deepening of the cervical sinus floor, induction of pit indentation, regulation of Pax8(+) precursors, narrowing of neuroblast delamination sites, and regression of placodes. The putative signaling centers in the pharyngeal pouches are likely deactivated by senescence and apoptosis.