This was true when Tbx1 was restored to both the mesoderm and endoderm of tbx1 mutants, or when combined Wnt11r and Fgf8a were restored to the mesoderm.
However, we have observed that the rfa2 -D x mutant promotes adaptation when combined with yku70 Δ, similar to that observed for rfa1 -t11.
Similarly, it has been shown that the hyper-lengthening of telomeres in rif2Δ as well as rif1Δ rif2Δ mutants is greatly reduced when combined with a yku70Δ mutation (Mishra and Shore, 1999).
Perhaps as expected, ctf4 Δ mutants also were unfit when combined with the other polymerase mutations and very unfit when combined with the telomere-defective cdc13 -1 allele.
Hypervesiculating mutants show reduced fitness when combined with mutations that limit OMV production, indicating OMV production is required for maintaining envelope integrity (Schwechheimer and Kuehn 2013).
In such cases, single mutants would show a lack of independence when combined, with double mutants exhibiting phenotypes of one or the other single mutant, or a phenotype worse than either single mutant but to a lesser degree than would be expected from independently acting mutations.
We wished to determine if opposite shifting Pol II and GTF TSS mutants were suppressive or additive when combined, for example, similarly to the combination of TFIIB and TFIIF alleles or combination of Pol II GOF and LOF mutants exhibiting suppression of TSS defects and growth phenotypes.
Neither tfg2 upstream shifting allele could rescue lethal LOF Pol II mutants, in contrast to rescue of lethal Pol II LOFs when combined with GOF mutants (Kaplan et al. 2012).
Genetic screens in yeast have shown that elg1 mutants have synthetic growth defects when combined with genes that are involved in homologous recombination, DNA repair, replication fork restart, checkpoint response and sister chromatid cohesion [2], [3], [12].
