Sentence examples for most mutants that from inspiring English sources

In most mutants that showed M1 extension defects, we never observed g1P truncation, and even minor structural defects of the g1P projection (e.g., ectopic branches or minor misroutes) were much less severe than for M1.

(A ) Imaging of pachytene nuclei stained with antibodies to COH-3/4 and HTP-3 demonstrated that COH-3/4 associates with meiotic axes in most mutants that fail to establish COH-3/4-dependent SCC.

Strikingly, most mutants that displayed reduced Ser/Ser phosphorylation and binding to 14-3-3 14-3-3 14-3-3ithin cytosolic pools resembling inclusion bodies (R1441C, R1441G, R1441H, accumulated99C, L1795F and I2020T).

Although it is possible that some mutant forms might show a limited response at a lower dose and a larger response at a higher dose, our results indicate that most mutant forms that were tested at both lower and higher doses showed a "good" response at either dose.

Differences between the observed number of hits and the number expected by chance were most dramatic for mutants that dysregulated four or more IR clones (Figure 2C).

However, most of the mutants that abrogate STIL-CC/ PLK4-PB3 interaction do not promote centriole amplification when overexpressed.

A major challenge in studying achiasmate chromosome segregation mechanisms is that most of the mutants that generate natural nonexchange chromosomes have very poor spore viability.

In most cases, H3-L61X muthatshowat sensitivityivito tonene drug also show sensitivity to the other two drugs suggesting that these sensitivities share a common underlying mechanism.

The fact that most of the mutants that have evolved in these lineages were able to persist in time could be a consequence of the mutational resiliency that evolved owing to the short Hamming distance values.

The average duration of nuclear movements was 121 ± 17 min in wild-type cells and was unchanged in most of the mutants that have been examined previously, including taz1Δ, dhc1Δ, and rec12Δ mutants (Ding et al. 2004).

Thus, Kog1-body formation does not appear to play a significant role in TORC1-Sch9 signaling during acute glucose starvation since (1) Sch9 dephosphorylation occurs much faster than the accumulation of Kog1-bodies (ττ = <2.5 min versus 11 ± 3 min) and (2) most of the mutants that have a defect in Kog1-body formation behave like the wild-type strain in the Sch9 phosphorylation assay.