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Fig. 8. Loss of Hoxc8 function phenocopies the molecular defects observed in Raldh2^L–/– spinal cord. Expression of Raldh2 protein (A-C) and selected molecular markers (D-O) on E12.5 flat-mounted spinal cords at brachial level. All the insets represent in-situ hybridization of transverse sections at the middle posterior LMC level (level of the horizontal bars in J-O). (C) In the Hoxc8^–/– posterior LMC region, the distance between the ventral midline (dotted line) and the Raldh2+ cells is increased (compare horizontal bars in A and C). (D-O) Composite images in which Raldh2 protein is shown on the left side only. (D-F) Decreased RARß expression in the posterior medial LMC domain in the Hoxc8^+/– spinal cord (brackets, D,E). (F) In Hoxc8^–/– mutant, RARß expression is absent throughout the LMC. (G-I) Lim1 expression is diminished in the posterior LMC of Hoxc8^+/– and Hoxc8^–/– mutants (brackets). (J-L) The outline of the two Islet1+ motor columns is marked by arrowheads. (L) No segregation of motoneurons into columns is visible in Hoxc8^–/– spinal cord. (M-O) Horizontal bars (white, red in insets) delineate the bigger distance between the ventral midline (dotted line) and the Pea3+ cells in Hoxc8^+/– and Hoxc8^–/– mutants compared with wild type. (O) In Hoxc8^–/– mutant, Pea3 expression is greatly reduced throughout the LMC. (P-R) Gdnf transcripts on transverse sections at thoracic level and brachial plexus level (bp; insets). a, anterior; CM, cutaneous maximus; p, posterior.

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