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Plasmid insertion sites of the mutants were mapped to 169 genes by DNA sequencing (Table 1; Table S1).
The mutants were mapped using standard snip-SNP assay [32] and the three-factor mapping technique [52].
Following screening, the homozygous lethal mutants were mapped initially by crossing to the second chromosome deficiency kit, provided by the Bloomington Drosophila Stock Center.
As described in Materials and Methods, these mutants were mapped by whole-genome sequencing to a transcription unit denoted CG8316.
The mutants were mapped by meiotic recombination with visible markers, male recombination (Chen et al. 1998), and by complementation tests using the Bloomington Chromosome 2 and 3 deficiency kits.
The sites of KanR cassette insertion for the non-responsive mutants were mapped to the genome of H. influenzae by polymerase chain reaction (PCR) and sequencing of amplicons (see Materials and Methods).
Similar(52)
When the Caton et al. escape mutants are mapped onto the 1RVX structure, there are clusters of mutations that correspond to each antigenic site.
In these cases all genomic reads from the mutant were mapped back to the reference.
The sequence reads from the wild type and parR mutant were mapped to the genome sequence of the mexEF-oprN region and displayed using Artemis and Bamview.
When perturbation energies (∆∆G values) for each mutant were mapped onto the NMR structure of GxTx-1E, a well-defined surface of the toxin was identified where mutations having dramatic effects on the apparent affinity of the toxin cluster together.
This method utilizes a related genome, denoted the 'mediator', to which NGS data of both the WT and the mutant are mapped.
More suggestions(15)
transfers were mapped
transformants were mapped
changes were mapped
mutants were confirmed
mutants were recovered
mutants were obtained
mutants were discovered
mutants were set
mutants were generated
mutants were monitored
mutants were indicated
mutants were named
mutants were affected
mutants were expressed
mutants were designed
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