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3C), giving values inversely proportional to density. The proportion of ENCC-free areas was similar for controls, DH, and beta1-null mutants (34.72��1.52, 36.32��2.22 and 35.54��2.00, respectively), but significantly increased within the proximal small intestine of DM (47.04��2.52, P[https://en.wikipedia.org/wiki/Tuclazepam tuclazepam] the interplay between ��1-integrins and SOX10. The behavior of vagal NCC at the time of foregut invasion was compared among genotypes. X-Gal staining of E10.5 whole-mount embryos showed stained cells in the stomach region and, irrespective of the genotype of the embryos, cells moving in lines to colonize the midgut (see black arrows, Fig. 4A), suggesting an absence of additional defects in DM compared to single mutants at this stage. One day later (E11.5), the results were different (Fig. 4B). X-Gal and TUJ1 stainings on whole-mount gut preparations revealed a slight delay in [http://www.selleckchem.com/products/XAV-939.html XAV-939 research buy] Sox10lacZ/+, beta1-null, and DH embryos compared to controls, with the front of migrating ENCC in the mutants stopping in the final quarter of the midgut, or just before the caecum ( Fig. 4B first column). This delay was clearly exacerbated in DM embryos (cells never [http://www.selleckchem.com/products/Tenofovir.html selleck compound] reached the second half of the midgut, n=5; Fig. 4B). Network disorganization was also visible in colonized regions of the DM gut, suggesting that DM defects are detected by E11.5. The observation of other NCC derivatives such as cranial ganglia, dorsal root ganglia and peripheral nerves by X-Gal staining or neurofilament (NF) whole-mount immunohistochemistry revealed no obvious differences between DM and single mutants at this stage ( Fig. 4B) or earlier (data not shown), suggesting that a cooperative requirement of Sox10 and Itgb1 is required for ENCC migration along the gut only. To determine whether ENS defects in DM were overcome after E14.5, guts from newborn mice were photographed and stained for TUJ1 and X-Gal. As shown in Fig. 5, the aganglionic gut segment in DM often extended above the caecum and affected the last third of the small intestine (Fig. 5A, compare position of black arrows). The ENS network was also more disorganized in colonized regions of DM compared to other genotypes (Fig. 5A and B). The postnatal survival of these animals was monitored up to 5 weeks of age (Table 1). Almost all Sox10lacZ/+ and DH survived, but 43% of beta1-null and 100% of the DM died before weaning.