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We sequenced six mutant clones derived from the E. coli KLY strain and systematically searched for inversions.
To summarize, this study uses 21 population samples of Ara- cells taken at 0, 1,000, 2,000,..., 20,000 generations from the evolving Ara-1 population, and 5 neutrally marked Ara+ mutant clones derived from generations 0, 5,000, 10,000, 15,000 and 20,000 of the same population.
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We assessed the identities of cells in the clones derived from single btd mutant type II neuroblasts by examining cell fate marker expression.
Positive clones were detected by fluorescence, and inducible expression of the EGFP-bound GTPase mutant proteins, and of HA-Dock10.1 in clones derived from C33, was confirmed by western blot analysis (Fig. 4).
Clones derived from single wild-type or bantam mutant neuroblasts were compared for neuroblast growth and for the number of progeny produced.
We induced GFP-marked mosaic clones derived from single wild-type or trx mutant type I or II neuroblasts and assessed the identities of cells in the clones by examining the expression of cell fate markers in a time-course study.
We prepared two independent clones (derived from different plaques after initial virion rescue) for each WT and mutant viruses.
Pregnancy outcomes for some of the clones derived from primary fetal fibroblasts were reported previously30,31.
Five positive cell clones derived from different single cells were screened from 56 clones.
All clones derived from the B. anthracis/B.
Compared with the controls, 3243A>G MitoTALENs significantly reduced the percentage of mutant mtDNA in all of the sub-clones derived from the MELAS-iPSCs (Figs. 3A, 3B, and S3A).
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