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Progeny of the 3'Δ3 mutant were repaired to wild type (wt) while those from the remaining four mutants were heterogeneous, exhibiting a wt secondary structure.
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These results suggest that most of the DSBs that cannot be repaired as crossovers in msh4 mutants are repaired using inter-sister recombination.
Still, many of the extra DSBs observed in dpy-28 single mutants are repaired via a CO intermediate (despite the presence of RTEL-1), which suggests the existence of a counteracting mechanism that promotes CO formation.
Following transfection of the ribozyme construct in AsPC-1 cells, mutant p16 mRNA molecules were repaired and p16 protein synthesis restored.
The kinetics of γ-H2AX foci disappearance (Fig 2B) confirmed that in XRCC4-mutant cells, the DNA lesions were repaired, although with lower efficiency than in wt cells, as the percentage of foci remaining at 24 h was 5 ± 8% in XRCC4 wt cells and 19 ± 7% in XRCC4 m/m.
In one blastomere, only one mutant allele was repaired * Some blastomeres failed to be amplified by PCR.
This suggested that DSBs induced in the osrecql4-2 mutant could be repaired by DNA repair systems, including HR, under normal growth conditions, since HR can proceed slowly without RecQ helicase [ 48].
Evidence that CFTR processing mutants could be repaired by a direct rescue approach is the observation that many second-site suppressors can rescue ΔF508 CFTR and other CFTR processing mutants.
Additionally, only one mutant allele (A−28G−25/G−28G−25) was repaired in 3/28 (10.7%) cells, resulting in heterozygosity (Fig. 2E).
However, homozygous mutant embryos could not be repaired in way because of the lack of WT alleles.
Mismatch repair mutants mlh1 displayed 14.5% survival, suggesting that Mn2+ induces an increased load of mismatches that cannot be repaired.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com