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Exact(19)
We confirmed that the crt-1 bz29) crt-1 bz29 defective in axon regeneration of D-type mutantneurons followasg axotomy (Fig. 6b andefectiveentary Table 1).
The isiA- mutant was defective in state transition.
The isiA- mutant was defective in state transition and sensitive to high light.
Further, differential expression of purine and pyrimidine biosynthesis genes purL, cdd and carB is likely required for bacteria-nematode interaction as P. temperata purL mutant was defective in supporting H. bacteriophora growth and completely inhibited infective juvenile formation.
As ileS mutant was defective in supporting nematode growth and infective juvenile formation, induction of this gene in P. temperata suggests potential importance of amino acid Ile in nematode development.
Another hint may come from the distinct phenotypes of P.a.-kerV mutant in an acute mouse pulmonary infection model and a burn-mouse model, where the mutant was defective in the former model while as fit as the wild-type in the latter.
Similar(41)
Thus, the FUS-521H mutant is defective in recruitment to damage sites and repair complex formation despite being present in the nucleus.
The ral1 mutant is defective in vascular pattern development both during embryogenesis and postembryonically.
The mutant is defective in root elongation in all root types during the first 2 weeks after germination.
Our observations with H486R mutant show that this mutant is defective in its interaction with CYLD.
Then, why the ts mis17-362 mutant is defective in CenH3 recruitment?
More suggestions(15)
mutant was low
mutant was rtM204I
mutant was non-motile
mutant was unable
mutant showed defective
mutant was active
mutant was hypersensitive
mutant was indistinguishable
mutant was susceptible
mutant was available
mutant was dependent
mutant was stable
mutant was resistant
mutant was identical
mutant was unaffected
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