Sentence examples for transfer in mutant from inspiring English sources

In addition to the identical emission positions, we found that the PE fluorescence of mutant PBsome is weaker than that of WT PBsome, which probably suggests a higher efficiency of energy transfer in mutant PBsome (Figure 7C).

Soluble redox mediators only partially restored electron transfer in mutants, suggesting that soluble shuttles could not replace periplasmic protein-protein interactions.

Since growth on Fe III) citrate was not detected in the same strain in the absence of vanillate (Fig. 3A), this demonstrated the increased sensitivity of the nongrowth real-time Fe III) citrate reduction assay in detecting residual electron transfer activity in mutants.

A potential functional role of PHR1 in sulfate homeostasis was assessed by examining the root-to-shoot and shoot-to-root sulfate transfer in the phr1 mutant in comparison to the sultr1 3 and sultr2;1 single mutants and WT plants.

Moreover, according to the lower frequency of transfer in the ΔthdF mutant S. Typhimurium LT2 recipient strains, this hypothesis could be more probable than successive transfers of single SGI1 monomer into a single recipient cell.

Notably, RomR-GFP did not undergo pole-to-pole transfer in the mglA9 mutant.

PHR1 stimulated the expression of the SULTR1 3 gene under Pi deficiency, and the significance of this regulation was reflected in a decrease in the shoot-to-root sulfate transfer in the phr1 mutant relative to WT.

This nongrowth assay appears to detect residual rates of electron transfer in Δ imcH mutants that were too slow to support growth and that were not easily detectable in the traditional assay.

This indicates that in the steady-state reaction, the phosphoryl transfer step between MgATP and bicarbonate in mutant H216N has become slow enough to be rate-limiting.

In correlation with the gene transfer experiment deletion of genes BCAL1755-6 in mutant K56-2ΔL1755-6 did not result in increased susceptibility to aminoglycosides or any other antimicrobial tested (Table 4).

Our data have identified one important cellular deficit that potentially constitutes a major pathogenesis process, namely a reduction in GJ-mediated glucose transfer in the cochlea of Cx30 mutant mice.