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Engineered SAC has identified a putative rate-limiting step for the GTPase reaction and shown that GTPase-deficient oncogenic Ras mutants are not irreversibly impaired.
Notably, the DDT defects of Polα/Primase/Ctf4 mutants are not the consequence of increased sister chromatid distance, but are instead caused by altered single-stranded DNA metabolism and abnormal replication fork topology.
Equivalent mutants are not counted to calculate the score.
(3) The fitness differences between the wild type and the RT mutants are not constant.
Also, osm-9 mutants are not defective in chemotaxis to acetic acid (data not shown).
In our fly pricking model, the cepR and cepI mutants are not attenuated (Figure 5E).
Thus, the two mutants are not impaired for DNA repair after exposure to CPT or gamma rays.
In addition, these proteasome mutants are not sensitive to chemicals that perturb the cell wall (data not shown).
Tah18-5H8 and tah18-5I5 mutants are not sensitive to CPT at the permissive temperature (this work Fig. 1-B).
This indicates that the signal pathways defined by these mutants are not required for wound-induced growth inhibition.
A limiting case of negative interaction where double mutants are not viable is termed synthetic interaction; the first systematic studies characterized this class [8].
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