Sentence examples for mutants to a from inspiring English sources

Moreover, restoring InsP3R function in insulin producing cells (IPCs) in the larval brain rescues the feeding deficit, growth and lethality in the itpr mutants to a significant extent.

For testing embryonic lethality in heterozygous mothers, we crossed the mutants to a him-5 strain and tested the F1 progeny as described above.

We show that a set of 9 SNPs allows the linkage of C. elegans mutants to a 5 8 megabase sub-chromosomal region.

We then crossed double mutants to a stock with a green compound balancer CyO-TM3-GFP, which constitutively expresses GFP from the Hsp70 promoter during all developmental stages, and selected Fak56CG1, Dcas1/CyO-TM3-GFP embryos, to separate double homo- and heterozygotes for analysis of the cuticles of double homozygotes (Figs 2A).

Our observation that short ssDNA primers interact with the full length Q169 mutants to a greater extent than wild type hTERT implies that in the context of full length hTERT, Q169 negatively regulates the overall strength of the interaction with short telomeric primers.

In this study, we found that Mg2+ supplementation can also partially suppress the gonadogenesis defect of gon-2 mutants to a degree that approaches that observed for the gtl-2 mutations; supplementation of the medium with 50 mM Mg2+ increased the frequency of non-vulvaless gon-2 q388 gon-2 q388animalst 23.5° fraised% (n = 763) to 64% (n = 968).

Here, we examined the sensitivity of exon 20 insertion mutants to an Hsp90 inhibitor currently in the clinic.

Similarly to budding yeast, fission yeast rif1-PP1 also restored growth to hsk1-89 mutonts, to an extent comparable to that conferred by rif1-Δ.

To further compare the Al resistance phenotype of ral1 mutant with WT, we exposed roots of WT and the mutant to a series of Al concentrations.

Results from relative water loss tests clearly showed that overexpression of OsNCED4 in the 129B08/nced3 mutant background successfully complements the severe water loss phenotype of the mutant to a level similar to that of Col-0 (Fig. 6).

Vice versa, activation of Akt by insulin reversed the phenotype of the ORF4 mutant to a significant extent.