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Exact(27)
In summary, as shown in Figure 2 and Table S3, the vast majority of the hygromycin B-sensitive membrane traffic mutants were defective for uptake of Rb+, a more specific test of K+ defects than hygromycin B sensitivity.
In addition, these mutants were defective in replication fork regeneration and sister chromatid cohesion.
As shown in Figure 3B, these mutants were defective in silencing at the kinetochore domain.
These HIV-1 mutants were defective for reverse transcription in cells but not in a standard ERT assay [29].
All these mutants were defective in Swi1-Swi3 complex formation, suggesting the importance of the Swi1 Swi3 complex in suppression of spontaneous DNA damage during unperturbed DNA replication.
Similar to the SH1000 genetic background, the LAC* graS and imp mutants were defective in biofilm maturation, and again the biofilm phenotype could be complemented through plasmid expression.
Similar(32)
In addition to the secretion defect, ecs mutants are defective in transformation competence [7] and biofilm formation [10].
Homozygous adult male mutants are defective in testosterone synthesis, and administration of testosterone could largely rescue the mutant defects.
(D) The Pri2 cysteine mutants are defective in iron incorporation into newly translated Pri2 polypeptide.
Furthermore, Pri2 cysteine mutants are defective in loading of the entire DNA pol α-primase complex onto early replication origins resulting in defective initiation.
At the permissive temperature, the mutants are defective in 55Fe incorporation into nascent Pri2 polypeptide and exhibit reduced loading of multiple pol-prim subunits onto early replication origins.
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