Sentence examples for mutants were due from inspiring English sources

Previous studies suggested that PLA1 and PLA2 genes regulate the rate of leaf maturation (Kawakatsu et al.[2006]) and that the small leaves in pla mutants were due to precocious leaf maturation.

To unequivocally show that the observed phenotypes of the mutants were due to the lack of Pngl, we investigated the effect of Pngl transgene expression in these mutants.

These data further suggested that the NMJ defects observed in TBPH mutants were due to a lack of new synaptic bouton formation rather than to increased presynaptic retraction.

To confirm that the defects observed in lin-23 mutants were due to a lack of BAR-1/β-catenin regulation, we constructed double bar-1; lin-23 mutants.

These data together suggests that increased O-GlcNAc modification of some proteins in cells transfected with PHB mutants were due to increased activity of OGT, most probably as a result of increased tyrosine phosphorylation of OGT.

To verify that the NMJ defects observed in the Ago2 null mutants were due to loss of Ago2 activity and not genetic background, we also analyzed larvae carrying a genomic Ago2 transgene in an Ago2 null background, P{Ago2}; Ago2414 larvae [35].

These results suggest that most collateral responses observed in the ciprofloxacin-resistant mutants are due to the observed efflux mutations.

Polydactyly in Dkk1 mutants is due to an interaction with Wnt7a, which regulates digit number (Adamska et al., 2004).

While previous reports suggest that these two molecules act cell-autonomously in the PVD, our results show that the disorganized PVD dendritic arbors in these mutants are due to the abnormal SAX-7 localization patterns in epidermal cells.

Researchers have therefore hypothesised that the presence of these mutants is due to cheating in vivo, and that siderophore mutants could be used as 'Trojan horses' to ferry antibiotic-susceptibility alleles into infections and render them more sensitive to treatment (Harrison et al., 2006; Brown et al., 2009; Jiricny et al., 2014; Andersen et al., 2015).

Unexpectedly, however, we have discovered that this prostate defect could be rescued by three different methods: renal grafting, explant culture in the presence of androgens, and administration of dihydrotestosterone (DHT) to pregnant mice, indicating that the prostate defect in Shh mutants is due to insufficient levels of androgens.