Sentence examples for mutants to show from inspiring English sources

As the increased longevity and pathogen resistance observed in glp-1 mutants has been attributed to the absence of the germline and not a specific function of the glp-1 gene [8], [20], one might expect other germline-deficient mutants to show a similar lifespan extension and pattern of broad-range resistance to pathogen infection.

Thus, we would not expect the DNA repair mutants to show resistance to oxidizing agents which is correlated with reduced ILS in C. elegans [ 8, 30].

The authors used whole seedling protein preparations for comparisons between wild type and multiple mutants to show that PP2Cs control the activity of OST1 but not of CPKs and the interdependence of the Ca2+ dependent and independent pathway.

In this article, we have used the details of the trajectories of sterile mutants to show how genetic variation plays an essential role in the evolutionary dynamics of each mutation.

In a similar fashion, FRET was performed with NBD-cholesterol and the Cy5-labeled deletion mutants to show FRET occurred between the NBD-labeled ligand and the following deletion mutants: Plin2-C1, Plin2-C2, and Plin2-I with R values ranging from 85 to 96 Å (Table 2).

Here we use this same cao-plus mutant to show that Chl b can bind to the CP43′ protein, expressed in cells exposed to low iron levels, which normally binds Chl a only.

If no other pathway was recruited downstream of Fz, we would expect the double mutant to show the same phenotype as the single bar-1 ga80) bar-1 ga80e.

Finally, o2 was the only opaque mutant to show significant alteration of starch biosynthetic gene expression.

If the increased flexibility observed upon binding drives cooperativity, we expected this mutant to show a different change in dynamics upon ligand binding.

One notable class of mutants appeared to show lethality in combination with spt10 Δ during our systematic screen.

Both the sequential deletion mutants of ADAM10 tail and the S741 to A mutant failed to show P incorporation, thus confirming that S741 is a PKC phosphorylation site.