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Background  Our interests lie in determining the genes and genetic pathways that are important for establishing and maintaining maternal-fetal interactions during pregnancy. Mutation analysis targeted to a 34 Mb domain flanked by  Trp53  and  Wnt3  demonstrates that this region of mouse chromosome 11 contains a large number of essential genes. Two mutant alleles ( l11Jus1  and  l11Jus4 ), which fall into the same complementation group, survive through implantation but fail prior to gastrulation.    Results  Through a positional cloning strategy, we discovered that these homozygous mutant alleles contain non-conservative missense mutations in the  Notchless homolog 1  ( Drosophila ) ( Nle1 ) gene. NLE1 is a member of the large WD40-repeat protein family, and is thought to signal via the canonical NOTCH pathway in vertebrates. However, the phenotype of the  Nle1  mutant mice is much more severe than single  Notch  receptor mutations or even in animals in which NOTCH signaling is blocked. To test the hypothesis that NLE1 functions in multiple signaling pathways during pre-implantation development, we examined expression of multiple  Notch  downstream target genes, as well as select members of the  Wnt  pathway in wild-type and mutant embryos. We did not detect altered expression of any primary members of the  Notch  pathway or in  Notch  downstream target genes. However, our data reveal that  Cdkn1a , a NOTCH target, was upregulated in  Nle1  mutants, while several members of the  Wnt  pathway are downregulated. In addition, we found that  Nle1  mutant embryos undergo caspase-mediated apoptosis as hatched blastocysts, but not as morulae or blastocysts.    Conclusions  Taken together, these results uncover potential novel functions for NLE1 in the WNT and CDKN1A pathways during embryonic development in mammals.

bmc genomic data

ENU mutagenesis reveals that Notchless homolog 1 (Drosophila) affects Cdkn1a and several members of the Wnt pathway during murine pre-implantation development