Sentence examples for mutants which show from inspiring English sources

We isolated a total of 229 mutants which show sensitivity to one or more of the DNA damaging agents used.

In the nervous system, the role of BPAG1a is also well studied because disruption of BPAG1a results in a phenotype identical to that of Dystonia musculorum (dt) mutants, which show progressive motor disorder.

Prkdc is also involved in telomere maintenance and in contrast to mice genetically engineered to lack Prkdc (i.e. null mutants), which show complete absence of DNA-PKcs activity, loss of telomere capping function and normal telomere length, cells from scid mice show not only loss of telomere capping function but also abnormally elongated telomeres.

Similarly, a deletion within Rpl24 has been identified in mouse "Belly spot and tail" (Bst) mutants, which show a kinked tail, white hind feet, and a ventral midline spot [7].

Nevertheless, as Hmg1p, which showed almost no morphologic change [8] was identified as the target candidate of lovastatin, even with very weak phenotype it may be possible to identify the candidate, suggesting that strong statistical power is needed to detect target-related mutants which show weak phenotypes (e.g., vma1, vma8 and vma11).

GFP LGG-1 accumulates in the autolysosomes in cup-5 mutants, which show impaired lysosomal function.

Additionally, for mutants, which showed significant attenuation, the complemented mutant, as far as available, was tested.

The mutants which showed lighter blue than the parental strain PAO1pClacZ were selected for further confirmation.

The exceptions were the E2/A and H4/A mutants, which showed a similar lag phase to AChE586-599, however their plateau height was affected with a drastic decrease for the E2/A mutant and an increase for the H4/A mutant.

In rt mutants, which showed specific reduction of rt transcripts (Fig. S1), the climbing abilities of flies homozygous for rt were significantly decreased compared to those of flies heterozygous for rt at all ages (Fig. 1A, Table 1).

We identified 3 groups of mutants that showed varying degrees of defects in L-form colony formation, possibly reflecting the relative importance of the genes involved in L-form formation (Fig. 3), with the majority of the mutants belonging to Group 1 mutants which showed a complete inability to form L-form colonies.