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Heterozygous mutation of Drosophila OPA1 (dOpa1) by P-element insertion results in no obvious morphological abnormalities, whereas homozygous mutation is embryonic lethal.
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).
TEAD1 null mutation is embryonic lethal and the mutant mice suffer from severe heart defects.
As has been reported for the other Brca1 mouse models, homozygosity for this mutation is embryonic lethal.
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The first attempts to study Brca2 knockout mice similarly found that the mutation was 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.
All of the mutants died during embryonic development, indicating that the conditional mutation is embryonically lethal.
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.
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