Table 2.
Summary of phenotypic disturbances observed in Smad2hSmad3ki intercross progeny
| Age | +/+ | Smad2hSmad3ki/+ | Smad2hSmad3ki/Smad2hSmad3ki | RS/EDa | AADb |
|---|---|---|---|---|---|
| E9.5 | 15 | 16 | 6 | 4 | 0 |
| E15.5 | 4 | 11 | 4 | 0 | 2 |
| E16.5 | 15 | 28 | 8 | 6 | 4 |
| Total (%)c | 34 (32%) | 55 (51%) | 18 (17%) | ||
| Weanlings (%)c | 33 (32%) | 60 (58%) | 10 (10%) |
The presence of resportion sites (RS) or empty decidua (ED) at the time of dissection suggests that some mutants die with more severe developmental abnormalities. Insufficient material for genotype determination.
Number of Smad2hSmad3ki/hSmad3ki embryos with abnormal anterior development (AAD).
Percentage of total embryos or weanlings genotyped. A loss of more than half of Smad2hSmad3ki homozygotes was observed across more than three generations of breeding. The surviving homozygotes show normal fertility, and in homozygous crosses, ∼50% of the embryos develop normally, whereas the others die in utero or at birth due to anterior patterning defects. Since the Smad2hSmad3ki mice were maintained on a mixed (C57BL/6J × 129Sv//Ev)F1 background, these distinct phenotypes may be due to genetic background differences.