Hoxd1 is not expressed in hindbrain of embryos. Expression of Hoxd1 begins at E8.5 in caudal lateral mesoderm (Pitera et al. 2001). At E9.5 to E11.5 Hoxd1 expression is observed in prosomeres p2 and p3 of the diencephalon, dermatomes, urogenital tubercle, gut endoderm, and tail bud (Wolf et al. 2001, Pitera et al. 2001). Expression is inducible by retinoic acid in embryos (Pitera et al. 2001) and embryonic stem cells (Mazzoni et al. 2013), however it is unknown if the induction is direct or indirect. NGF induces Hoxd1 in nociceptors (Guo et al. 2011).
In embryonic stem cells treated with retinoic acid the activation of Hoxd1 chromatin is accompanied by loss of methylation at lysine-27 of histone H3 (H3K27me3) and loss of polycomb repressive complex 2 (PRC2) (Mazzoni et al. 2013). As observed at other Hox genes, gain of histone acetylation and gain of methylation at histone H3K4 may also occur. The Mll2 complex methylates H3K4 in fibroblasts (Wang et al. 2009). Like other Hox gene clusters, the Hoxd cluster changes position relative to other loci in the nucleus during activtion (Williamson et al. 2014, Lonfat and Duboule 2015).