Apoptosis contributes to placode morphogenesis in the posterior placodal area of mice.

In the embryonic head of vertebrates, neurogenic and non-neurogenic ectodermal placodes arise from the panplacodal primordium. Whether and how growth processes of the ectodermal layer, changes in the transcriptional precursor cell profile, or positional changes among precursor cells contribute to interplacodal boundary formation is subject to intense investigation. We demonstrate that large scale apoptosis in the multiplacodal posterior placodal area (PPA) of C57BL/6 mice assists in the segregation of otic and epibranchial placodes. Complex patterns of interplacodal apoptosis precede and parallel the structural individualization of high-grade thickened placodes, with the fundamental separation between otic and epibranchial precursor cells being seemingly prevalent. Interplacodal apoptosis between the emerging epibranchial placodes, which express Neurogenin2 prior to their complete structural individualization, comes out most strongly between the epibranchial placodes 1 and 2. Apoptosis then moves from interplacodal to intraplacodal positions in dorsal and, with a delay, ventral parts of the epibranchial placodes. Intraplacodal apoptosis appears to exert corrective actions among premigratory neuroblasts, and helps to eliminate the epibranchial placodes. The present findings confirm and extend earlier observations in Tupaia belangeri (Washausen et al. in Dev Biol 278:86-102, 2005), regarded as an intermediate between primates and other eutherian orders. Having now available maps of apoptosis in the PPA of embryonic mice, further investigations into the functions of inter- and intraplacodal apoptosis can be carried out in an experimentally and genetically more accessible mammalian model organism.