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Hence, the muscle fiber defect in the axin1/apc1 mutants is likely also caused by late Wnt/β-catenin hyperactivation.
The biological explanation for the differences observed in the heterozygous mutants compared to homozygous mutants is likely that most of these genes are haplosufficient under the growth conditions examined.
The premature disappearance of YP170 GFP in tbc-2 mutants is likely due to premature degradation in the lysosomes as we found that YP170 GFP showed increased colocalization with Lysotracker Red, a marker for acidic compartments.
These results support the idea that gametes are unaffected by Ospie1-1 and Ospie1-2 mutandons and that the homozygous lethality of Ospie1 mutants is likely caused by a defect in embryo development.
Together, these considerations suggest that the lethality of the dRecQ4 mutants is likely a consequence of loss of both of its primary functions, namely DNA replication and DNA repair.
Thus, the microphthalmia exhibited in KTA048 mutants is likely the result of the retarded lens growth.
Similar(29)
More of these mutants were likely to make it back to the village without losing their seeds, and hence their seeds were more likely to be planted.
This higher evapo-transpiration compared to esk1 single mutants was likely due to increased opening of stomata, which are, therefore, functional in esk1.
These results indicated that the surface hydrophobicity defects of ΔpdeH and ΔpdeLΔpdeH mutants were likely due to the lowed MPG1 expression.
Further, many of these mutants are likely to provide valuable insights into the genetic regulation of color changes and light adaptation in fish and other organisms.
Therefore, the genes transcriptionally regulated by osr mutants are likely responsive to osmosensitive signaling pathways rather than secondarily responsive to tissue damage.
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