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In hmx4 morphants, r6 and r7 expression of cyp26b1 is strongly reduced, while cyp26c1 in r3 and r4 is unaffected ( Fig.?4F�CG), suggesting that caudal rhombomeres, which require the highest RA levels for patterning, are most disrupted in the hmx4 morphant hindbrain. As we observe near-normal or reduced cyp26 levels in hmx4 morphants, changes in RA degradation do not explain a reduction in signaling activity. In contrast, the strong reduction in aldh1a2 expression suggests that reduced RA synthesis is responsible for the signaling deficiency. We therefore hypothesized that the phenotypes we observe in hmx4 morphants are caused by an early loss of RA synthesis. To test this idea, we treated morphants with a low dose of exogenous RA. A 1?nM dose causes no detectable morphological phenotypes, MK-4827 cell line and does not induce hmx4 expression (Fig. S2). hmx4 morphants treated with 1?nM RA show a rescue of eye field narrowing, neural tube closure and vagal motor neuron specification ( Fig.?5). To quantify Selleckchem CPI-1205 these rescues, we scored phenotypic frequencies ( Fig.?5E, J, O). While no control embryos (n?=?83) nor embryos treated with 1?nM RA (n?=?82) show eye field narrowing at 48?hpf, 41% (��?17%, n?=?97) of hmx4 morphants display this phenotype. When hmx4 morphants are treated with 1?nM RA, this frequency decreases to 24% (��?11%, n?=?83), a statistically significant rescue (��2?=?6.95, p?DEF6 a strong reduction in this class of neurons. When hmx4 morphants are treated with 1?nM RA, the frequency of this phenotype decreases by more than half to 35% (��?10%, n?=?71), a statistically significant rescue (��2?=?23.7, p?