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We have previously shown that the K & B framework is quite restricted when it comes to explaining why recessive mutants are so common, the appearance of dominant mutations, the existence of functional recessive homozygotes, the phenomenon of overdominance, and how genetic dominance may arise from intralocus interaction [12].
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There are several possible reasons why the number of P-body-inducing mutants is so high.
The PKG I mutants were so-called SM-Iβ rescue mice [ 49].
Furthermore, the L158Q mutant was so unstable in 786-O cells that it was nearly undetectable (Fig. 1c).
Would inclusion of the Rab5Q or Rab5GTP structure be useful to show here to understand why Rab5Q mutant is so poor in intrinsic hydrolysis?
In a single large patch at the candidate ESS, the fitness of a single mutant is so that large mutations invade if and only if small mutations invade.
Would inclusion of the Rab5Q or Rab5GTP structure be useful to show here to understand why Rab5Q mutant is so poor in intrinsic hydrolysis? 6) How many cells were counted in 6c?
The poorly inducible M1 (5′-cACGTG-3′) site showed greater binding to constitutive proteins than the SARE or M3, which could explain why this mutant was so poorly inducible by hypoxia and anoxia compared to the SARE and M3.
However, since these well-organized tissue areas are rare, it could explain why the root hairs on docs1 mutant roots are so scarce.
Since the dvps4Δ7b mutant clones are so short lived and because of the possibility that the flanking genes might be affected by the deletion, we turned to RNAi-mediated knock-down [28] and a dominant negative form of dVps4, dVps4-DN as means of reducing dVps4 activity.
When the noise amplitude is smaller than the threshold, we observe that low-fitness mutants are accumulated, so that robustness to mutation is not achieved.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com