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Production of salinomycin was fully restored in the S. albus Δ salBIII mutant when complemented in trans with the wild-type salBIII gene.
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The GLOI heterozygous mutants (+/h) clone when complemented with an episomal copy of GLOI showed an increase in the growth rate as compared to the heterozygous mutant, thereby revealing that the presence of GLOI as an episomal copy facilitates in overcoming the defect in the growth that probably has arisen because of the deletion of one of the wild type GLOI allele.
The heterozygous mutant Ld GLOI:: HYG (+/h) when complemented with an episomal copy of GLOI had a specific activity of 345±28 nmol min−1 mg−1proTable(Table 2).
The heterozygous mutant Ld GLOI :: HYG (+/h) when complemented with an episomal copy of GLOI was able to overcome the effect caused by the deletion of one of the allele of GLOI.
Complementation of the ΔhrcU mutant with HrcUAAAH produced canker lesions similar to those observed when complemented with wild-type HrcU.
At the 10 µM concentration, the ΔmgtC mutant strain grew significantly less than the wild type strain (p<0.05), reestablishing its phenotype when complemented with mgtC cloned in pBBR-5 plasmid.
Regardless, single mutant analysis has revealed that when each of these genes is knocked out, abnormalities arise in plant development and these phenotypes are corrected when complemented by the corresponding overexpression construct.
When we measured the ability of wild type PIN3 and mutant PIN3 S4A S5A to complement the pin347 mutant when expressed from a PIN3 promoter fragment, we found that the phototropism defect of the pin347 mutant was only partially complemented by the PIN3 S4A S5A transgene while it was fully complemented by wild type PIN3.
In contrast, PpHxk1 failed to complement the hxk1 hxk2 glk1 triple mutant when expressed from the same vector.
SND1, NST1, NST2, VND6 and VND7 regulate an overlapping set of targets [ 21, 25], supported by the ability of NST2, VND6 and VND7 to complement the snd1 nst1 double mutant when ectopically expressed in fibre cells [ 26, 27].
When a ΔrovA mutant strain complemented with pAraRovA was subjected to CFSE staining and flow cytometry analysis, the percentage of stained cells was restored and was even higher than that of the wild type strain.
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