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By using this additional virus, we wanted to distinguish whether the phosphosites and the PRR mutants were responsible for either the totality or just a subset of the functions previously ascribed to M2 during B-cell infection [17], [30] [32].
These results implied that the abnormally short cilia in pc mutants were responsible for the relatively decreased rates of urine flow compared to wild-type kidneys, and that this led to the accumulation of urine and distension of the tubules and ducts in the pronephros.
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Importantly, this result suggests that Pio protein is the critical target whose reduced secretion in γCOP mutants is responsible for the specific DB defects observed in γCOP mutants.
Our results suggest that the observed premature Wnt signaling in oto mutants is responsible for repressing hesx1 in the anterior neural plate.
We therefore do not favor the hypothesis than the high hemocytes figures in Toll-9−/− mutants are responsible for embryonic lethality.
These results indicate that the compound heterozygote pattern of these two functional-inactive mutants is responsible for complete lactose intolerance in the infant.
Accumulation of secondary, accessory mutants is responsible for the further increase in the level of the resistance and often restored replication capacity [ 20- 22].
Most probably, selection of resistant mutants is responsible for this phenomenon [ 30]; degradation of the drug in the growth medium is not assumed, as regrowth was not observed for any other tested strain.
3) The set of experiments that would convincingly show that the reduction in secreted LPS in the flrA and motB mutants is responsible for their failure to induce apoptosis would be to 1) show that secreted fractions from the wild type but not the mutant cells can induce apopotosis, and 2) show that depletion of LPS from the wild type cells (for example with the antibody used in Koropatnick et al).
This mutant is responsible for familial amyotrophic lateral sclerosis, a chronic, progressive neuromuscular disorder [ 72].
Single α-Spec lm88 mutants did not, suggesting that the dlt mutation in the double mutant was responsible for the suppression (Table 1, Rows 17−22).
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