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Figure 2 | Neural Development

Figure 2

From: Brn3a regulates neuronal subtype specification in the trigeminal ganglion by promoting Runx expression during sensory differentiation

Figure 2

Loss of Brn3a profoundly affects the major sensory subtypes at birth. Expression of markers of known sensory subtypes were examined at P0 in transverse sections of Brn3a knockout and heterozygote control TG. Heterozygote controls are phenotypically normal and have been previously shown to have minimal changes in global gene expression [26]. (A-F) Expression of TrkC, Runx3, and Etv1. TrkC and Runx3 immunoreactive neurons are reduced to less than 10% of controls. Small Etv1 immunoreactive neurons, most of which co-express Islet2, are unaffected. (G, H) Neurons expressing TrkB persist in Brn3a-/- mice at P0, but the distribution of the protein is markedly altered, with increased expression in axons and less expression in discrete cell bodies. (I-R) Expression of nociceptor markers Runx1, TrkA and Ret. The absolute number of Runx1 positive neurons is significantly decreased across the rostrocaudal extent of the ganglion (K, paired t-test, P = 0.001), and this loss is in excess of the overall decrease in cell number as assayed by Islet1 expression (L, paired t-test, P = 0.0004). TrkA expression is markedly diminished in the knockout (M, N). Small diameter neurons co-expressing Runx1 and Ret (O, arrows) are absent from the knockout, but a population of large diameter Ret+ neurons that are negative for Runx1 and TrkA, and may represent a class of mechanoreceptors, persist (O, P, arrowheads). HT, heterozygote control; KO, knockout.

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