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. 2018 Sep 4;27(24):4218–4230. doi: 10.1093/hmg/ddy313

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© The Author(s) 2018. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Genetic interaction between Grhl2 and Grhl3 overexpressing alleles results in severe SB. (A–C) Among experimental litters generated by intercross of Grhl2^Axd/+ and Grhl3^{+/+:TgGrhl3/0} mice, all compound heterozygous fetuses exhibited severe SB. Note the very large size of the SB lesion that extends as far rostrally as the forelimb bud at E13.5 (C) (^*P < 0.001; significant difference among genotypes, Chi-square). (D) Analysis of PNP length among embryos at E9–10.5 shows that compound heterozygous, Grhl2^Axd/+;Grhl3^{+/+:TgGrhl3/0} embryos have significantly enlarged PNPs from E9.5 (15–19 somite stage) onwards (^*, significant difference from all other genotypes, P < 0.001). At E10.5 (28–31 somites) the PNP length of Grhl2^Axd/+;Grhl3^{+/+;TgGrhl3/0} embryos is also greater than in wild type (^#, P < 0.01). (E) In the caudal region of E9.5 embryos, mRNA abundance of Grhl2 and Grhl3 corresponds with the presence of the Grhl2^Axd and Grhl3^TgGrhl3 alleles, with no indication of reciprocal regulation (^*, differences from wild-type expression level, P < 0.01).