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Fig. 3 irx4a inhibition does not significantly alter A/P or D/V patterning. In situ hybridization was carried out on 24 hpf embryos using CNS markers to evaluate potential patterning defects induced by inhibition of irx4a function. (A, B) At 24 hpf the expression patterns of the forebrain marker emx, the midbrain–hindbrain boundary marker pax2.1 and the hindbrain marker krox20 appear unaffected in morphant embryos compared to controls. (C, D) Expression of fgf8 corroborates that the midbrain–hindbrain boundary is correctly established in morphant embryos. (E, F) Expression of shh and c-myc is unchanged in morphant embryos indicating that dorso-ventral patterning is also normally established in the absence of irx4a function. MB-HB, midbrain–hindbrain boundary; os, optic stalk; r3, rhombomere 3; r5, rhombomere 5; t, telencephalon; tc, tectum. The panel shows lateral views; dorsal is up, anterior is towards the left. Scale bar in (F) 50 μm.
Reprinted from Molecular and cellular neurosciences, 40(3), Feijoo, C.G., Saldias, M.P., De la Paz, J.F., Gómez-Skarmeta, J.L., and Allende, M.L., Formation of posterior cranial placode derivatives requires the Iroquois transcription factor irx4a, 328-337, Copyright (2009) with permission from Elsevier. Full text @ Mol. Cell Neurosci.