We wished to determine whether the lethality caused by A-Myb, c-Myb, and v-Myb was due to a lethal effect in all cells, or whether these neomorphic proteins might cause specific defects in cell viability, proliferation, and differentiation.
To confirm that the lethality of spg is due to the spg locus, we were able to rescue this lethality by driving a UAS-spg cDNA with the early nanos-GAL4 driver (n = 208).
However, double knockout mice exhibit lethality by E9.5 with a complete absence of the OFT and right ventricle, indicating that Foxc1 and Foxc2 are partially functionally redundant (Seo and Kume, 2006).
Next, we tested whether it could rescue the lethality caused by a null mutation in the alpha subunit [9].
Thus, employing these ubiquitous drivers to express elements aimed at reducing AMPK expression or function results in a complete phenocopy of the lethality caused by a null mutant.
Despite Smt3, Aos1, Uba2 and Ubc9 being essential genes [11], [12], a siz1Δsiz2Δ strain is viable [13], albeit with a clonal lethality, manifested by a nibbled phenotype which is caused by the 2µ plasmid [16].
To determine if the lethality caused by a reduced maternal supply of SUMO is due to cycling defects, 0- to 3-hour wild-type and sumo04493 GLC embryos were stained with DAPI to visualize DNA.
Knockout of CBFb in mouse leads to embryonic lethality caused by a failure of hematopoiesis [ 12, 13], a phenotype very similar to that caused by knockout of Runx1.
