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. Author manuscript; available in PMC: 2011 Mar 9.
Published in final edited form as: Neuron. 2010 Sep 9;67(5):781–796. doi: 10.1016/j.neuron.2010.08.008

Figure 3. Cell Autonomous Role of Hoxc9 in MN Fate and Hox Gene Expression.

Figure 3

(A–L) Analysis of Hoxc9 knockdown at thoracic levels after dsRNA electroporations in chick neural tube. Bolt indicates electroporated side. (A) Hoxc9 dsRNA reduces Hoxc9 protein expression. (B) Nuclear LacZ expression plasmid was coelectroporated to mark electroporated cells. Note that the LacZ plasmid labels only a fraction of cells that incorporate the dsRNA. (C) Hoxc9 dsRNA does not affect Isl1/2 expression. (D) Ectopic RALDH2 is detected after thoracic Hoxc9 RNAi. (E) Loss of pSmad expression. (F) The number of Hb9+Isl1/2+ HMC neurons is reduced after Hoxc9 removal. (G–L) Hoxc6, Hoxa4, Hoxc4, Hoxa5, Hoxa7, and Hoxc8 are ectopically expressed or upregulated in cells that have lost Hoxc9. (M–V) Derepression of Hoxc4, Hoxc5, Hoxa5, Hoxa7, and Hoxc8 expression at thoracic levels in Hoxc9 mutants. The normal brachial patterns of Hox genes were intact in Hoxc9 mutants (Figure S4A–S4H). Ectopic Hox5 expression was relatively weak at thoracic levels, possibly due to the presence of Hoxc8 which normally restricts Hox5 genes to rostral brachial MNs (Dasen et al., 2005). (W–X) Loss of Hoxd9 expression in MNs that ectopically express Hoxc6. (Y) Summary indicating brachially-restricted Hox genes that are ectopically expressed or upregulated in Hoxc9 mutants. Light-gray bars indicated reduced protein expression levels.