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We have demonstrated that OsSND2 can regulate MYBs and SCWs CESA genes expression (Figs. 5f, 6d and 7a), and that snd2 mutants have lower cellulose contents (Fig. 5e) and exhibit no change in morphology (Fig. 5d).
We confirmed our previous findings that fat-6;fat-7 double mutants have lower fat stores than wild type [23].
Stearoyl-CoA desaturase deficient worms (fat-6;fat-7 double mutants), as well as SREBP deficient worms (sbp-1 mutants) have lower fat stores, slower growth, and reduced fertility compared to wild type.
Until recently, it has been assumed that drug-resistant mutants have lower fitness and tend not to spread because they will be out-competed by wild-type strains [11].
On the other hand, if most but not all of N mutants have lower fitness than the parent clone, one of these mutants can be selected by chance as only a limited number of cells are chosen at random after fitness-dependent growth.
Surprisingly, only one of these four mutants, Δ yphA, exhibited higher intracellular FC production than the wild-type, whereas the three other mutants have lower FC production than the wild-type.
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Furthermore, female mutants had lower body weight, were leaner, had reduced glycogen levels, and were less fecund than controls.
Compared to control flies, dSdc mutants had lower expression of brain insulin-like peptides, were less fecund, more sensitive to starvation, and had reduced life span.
These mutants had lower affinities to HSPA5 in vitro, and SIL1-HSPA5 interastion as well as HSPA5 function was found to be crucial for neuronal migration ex vivo.
In S. sonnei, all of the mutants had lower fitness (p < 0.0001); in E. coli, the mutants had the same or lower fitness than the ancestor at 37°C (Table 3).
Flow-cytometry revealed that the mutant had lower auto-fluorescence levels and a higher fluorescein isothiocynate staining efficiency.
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