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Previously described caps mutations are embryonic lethal [7] and, as expected, capspB1 was also lethal.
According to the literature reviewed, mice homozygous for targeted null Evi1 mutations are embryonic lethal and are characterized by widespread hypocellularity and poor/disrupted development of the cardiovascular and neural crest-derived cells[20].
Homozygous En-1 mutations are embryonic lethal.
Because homozygous Msx-1 and Msx-2 mutations are embryonic lethal, analyses of Msx gene function in the adult mammary gland are largely absent.
Although traditional homozygosity mapping or exome sequencing has uncovered many genes for these conditions, these approaches may fall short for genes under strong selective pressure or for genes in which homozygous loss-of-function mutations are embryonic lethal.
In contrast, few diseases have been identified so far that are caused by mutations in type B-lamins, though this could simply reflect that such mutations are embryonic lethal [ 6].
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The first attempts to study Brca2 knockout mice similarly found that the mutation was embryonic lethal.
Heterozygous mutation of Drosophila OPA1 (dOpa1) by P-element insertion results in no obvious morphological abnormalities, whereas homozygous mutation is embryonic lethal.
While most heterozygous BHD+/−/CMV-Cre mice showed no obvious abnormalities at age of 18 months, the homozygous mutation was embryonic lethal and BHD−/− mutants died between 3.5 dpc and 8.5 dpc, underscoring the importance of BHD in development.
The mutation is embryonic lethal with abnormal vasculogenesis [ 87, 112].
At the restrictive temperature, the dyn-1 mutation is embryonic lethal (Harris et al., 2001).
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