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Fig. 2. Involution of the petrosal-nodose ganglionic complex and carotid body between E13.5 and E16.5 in Phox2b^lacZ/lacZ mutants. (A-F) At E13.5 the petrosal-nodose complex is already markedly atrophic, as assessed by peripherin in situ hybridization (A,B, quantified in I) and has lost expression of lacZ (C,D) and Phox2a (E,F), which was initially expressed in the mutant placodal precursors at E10.5 (Pattyn et al., 1999). (G,H) In situ hybridization with peripherin showing that, at E16.5, the involution is almost complete. (I) Quantification of the ganglionic atrophy at E13.5 and E16.5. Measurements of control ganglia were considered as 100±5.5% at E13.5 (n=6) and 100±3.7% at E16.5 (n=4). The relative measurements of mutant ganglia are 25.8±5.3% at E13.5 (n=4) and 7±2% at E16.5 (n=4). (J-O) The anlage of the carotid body is first detected at E13.5 in a heterozygous mutant (arrowhead in J) by immunohistochemistry against Phox2a (L) or in situ hybridization for lacZ (J) or Tbx20 (N). In a homozygous mutant, lacZ expression is already affected at this stage (arrowhead in K) and neither Phox2a (M) nor Tbx20 (O) expression occurs. (P-S) At E16.5 the carotid body, which still expresses lacZ (P) and has switched on Th (R) in the heterozygote, is no longer detectable in the homozygote (Q,S). ec, external carotid artery; ic, internal carotid artery.

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