Gustatory innervation and bax-dependent caspase-2: Participants in the life and death pathways of mouse taste receptor cells

In the adult mouse tongue, an average of 11% of the gustatory receptor cell s are replaced each day. In investigating homeostatic cell death mechanisms in gustatory renewing epithelium, we observed that taste receptor cells we re selectively immunopositive for the bcl-2 family death factor, Bar, and f or the protease Caspase-2(Nedd2/Ich1). We determined that 8-10% of the tast e receptor cells of the vallate papilla were Bar positive and that 11% were Caspase-2 positive. Some of these immunopositive taste cells had apoptotic morphological defects. Within the subset of vallate taste cells immunoposi tive for either Caspase-2 or Bar, up to 79% coexpressed both death factors. Bar and Caspase-2 first appeared in occasional vallate taste receptor cell s on the same postnatal day-the day after birth. bare null mutation markedl y reduced gustatory Caspase-2 immunoexpression. These observations suggest that taste cell death pathways utilize p53, Bar, and Caspase-2 to dispose o f aged receptor cells. Apart from reducing Caspase-2 expression, Bar defici ency also altered taste organ development. bax(-/-) mice had a more profuse ly innervated vallate papilla, which grew to be 25% longer and taller, with the mean taste bud containing more than twice the normal number of taste c ells. This augmentation of taste organ development with increased innervati on is complementary to the well-documented reduction in taste organ develop ment with sparse innervation. We propose that additional taste neurons surv ived programmed cell death in Bax-deficient mice, thereby providing an indu ctive boost to vallate gustatory development. (C) 2000 Wiley-Liss, Inc.