However, quantitative evaluation of these mutants was not well established.
These results suggest that hypersensitivity to glucose in the sfar4 knockout mutants was not caused by osmotic response (Fig. 3; Additional file 8: Fig. S6).
The vestibular phenotype of the mutants was not different from wild-types as determined by time on the rotarod, head stability tests and physiological responses to vestibular stimulation.
The value of ΔCp for unfolding of these mutants was not greatly affected relative to wild-type, indicating that the change in solvent accessibility for unfolding was similar.
Meanwhile, the onset of progeny production in c30f12.4 mutants was not delayed and progeny was steadily produced at the age when reproduction ceased in the wild type (Fig. 2D and 2E).
In vitro replication of the HA-expressing ILTV mutants was not affected, and infection of chickens revealed a reduced but still considerable virulence, similar to that of a UL50 gene deletion mutant without foreign gene insertion.
The expression yield of the deglycosylated mutants was not significantly affected, indicating that glycosylation at Asn-201 was not required for a proper processing and secretion of this protein by P. pastoris.
However, the larger average mEPSC amplitude in GluR1-S831A mutants was not multiplicative (Fig. 4C).
Since the progenitor chromosome for these mutants was not known, DNA from homozygous individuals was extracted.
First, we observed that the survival of Toll-9−/− mutants was not affected by Ecc15 oral infection (Figure S1).
This is probably due to the fact that the loss of spectrin immunoreactivity in these mutants was not complete.
