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Note that abd-A expression expands to T3 in mutant embryos, compared to wild-type embryos.
Similarly, iridiphores are reduced in size in enz mutant embryos compared to wild-type siblings.
Subsequently, we quantified the area of punctate melanophores in enz mutant embryos compared to stellate melanophores in wild-type siblings.
Moreover, 11.7% of Mlc1v-nlacZ-24 positive cells were Ki67-negative (non-proliferating) in mutant embryos compared to 5.7% in wildtype embryos (p<0.001; data not shown).
Quantification of neural crest (AP-2α positive) and SHF (Mlc1v-nlacZ-24 β-galactosidase positive) nuclei revealed a significant decrease in neural crest cell numbers in mutant embryos compared to wildtype littermates (Fig. 8B, 8C).
The mean numbers of cells in wild-type and enz embryos were subjected to a one-tailed T-test to determine whether the decrease in cell numbers in enz mutant embryos compared to wild-type siblings was statistically significant.
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We confirmed that Gal was completely absent in Foxa2 mutant embryos (compare Figures 2B and 2E; n = 7/7).
Some ISG transcripts are highly elevated in Adar1 mutant whole embryos compared to wild-type embryos and levels return to normal in Adar1; Mavs and Adar1; Ifnar embryos, though the Adar1; Ifnar1 double-mutant embryo does not normalize ISG transcript levels as fully as Adar1; Mavs.
We measured spatial, kinematic, and dynamic antero-posterior asymmetries to biophysically characterize both resiliency to laser perturbations and failure of closure in mutant embryos and compared them to natural asymmetries in unperturbed, wild-type closure.
Littermates were used for all experiments in which normal and mutant embryos were compared.
Immunostaining (Fig. 1C D) showed that maternal Spt5 protein was significantly reduced in fogsk8 mutant embryos as compared to WT siblings.
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