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However the full extent of genome-associated resistance was not restored by the single mutation D320E.
This protein was apparently transformed into a phosphodiesterase by the single mutation of the bridging glutamate residue of this enzyme to a lysine (E183K).
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The identification of emb-29 (g52ts ) as an allele of cdc-25.2 was further confirmed by CRISPR/Cas9 gene editing where we rescued the mutation and recreated the temperature-sensitive phenotype by editing the single mutation in a wild-type background.
The remaining complexes were obtained from the previously built LSTc SC18 complex by applying the single mutation Asp225 → Gly in silico to generate the LSTc NY18 complex and the double mutation Asp225 → Gly/Asp190 → Glu to generate the LSTc AV18 complex.
Recombinant viruses encoding various combinations of these Vero cell adaptation mutations did not demonstrate enhanced replication in Vero cells over that exhibited by the single mutations.
In this part of the Amazon basin, it may be possible to predict treatment failure with sulfadoxine-pyrimethamine equally well by determination of either of the single mutations dihydrofolate reductase 164L or dihydropteroate synthase 540E.
Genetic interactions are thus defined for those cases in which the growth of the double mutant is different to its (expected) growth in the absence of any relationship (expected growth is usually quantified by the multiplicative effect of the single mutations (see [18], [19] and Materials and Methods).
Under this approximation, the distribution of net ΔΔ G values for multiple mutations can be computed from the distribution of ΔΔ G values for single mutations by performing convolutions of the single-mutation ΔΔ G distribution [ 3], meaning that W m for arbitrary m can be computed solely from the distribution of ΔΔ G values for single mutations.
Defects conferred by the single dinG mutation in cells that carry an oppositely oriented rrn are suppressed by RNase H over-expression and by the rpoC* mutation.
Expression of glucosinolate biosynthetic genes was slightly but significantly reduced by the single myb mutations, while the double mutation resulted in a drastic decrease in expression of these genes.
Specific interactions between the receptor and ligand are crucial for the function and activation of this receptor, as implied by the single point mutation, H305Q, causing symptoms of Type II Rickets.
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