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Fig. 5. Loss of spinal interneurons in Pcdh- null mutant mice is due to apoptosis, not aberrant specification. (A-C) P0 hemicords from control, Pcdh- ^del/del and Pcdh- ^del/del;Bax^-/- mice immunostained as indicated. The reductions in ventral populations observed in Pcdh- ^del/del mutants are rescued in the Pcdh- ^del/del; Bax^-/- double mutants, confirming that they are due to increased apoptosis. (D-F) Fragmented ventral interneurons in P0 Pcdh- ^del/del spinal cord can be double-labeled (insets) with antibodies against cleaved caspase 3, a marker of apoptotic cells. (G) Quantitative analysis of ventral interneuron populations at E14, E17 and P0 demonstrates that a normal number of postmitotic interneurons are produced in Pcdh- ^del/del embryos, but that many are lost between E14 and E17, coincident with the initial period of synaptogenesis; further loss is apparent by P0. Scale bar: 100 µm.

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