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Fig. 8. Cell type-restricted Pcdh-
mutation reveals a
non-cell-autonomous requirement of -Pcdh function for neuronal
survival. (A,B) FoxP2-positive Pax2-negative dI2
interneurons were quantified in both Wnt1-Cre; Pcdh-
fcon3/fcon3 mice, in which they are mutant, and in
Pax2-Cre; Pcdh- fcon3/fcon3 mice, in which
they are not, at P0. There is no reduction in this population in Wnt1-Cre;
Pcdh- fcon3/fcon3 mice (A, see C), but a loss
of 
30% is observed in Pax2-Cre; Pcdh-
fcon3/fcon3 mice compared with controls (B, see C).
(C) Quantitative analysis of ventral interneuron populations in
Wnt1-Cre; Pcdh- fcon3/fcon3, Pax2-Cre;
Pcdh- fcon3/fcon3 and Hb9-Cre;
Pcdh- fcon3/fcon3 spinal cord at P0. Data for
mutants are expressed as a percentage of control values.
*P<0.05; **P<0.01. Scale bar:
100 µm.
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