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In a forward genetic screen for zebrafish craniofacial mutants, we isolated the b1075 mutant allele.
Through a forward genetic screen for craniofacial mutants, we isolated a zebrafish mutant in which the first cysteine of the second zinc finger of Gata3 is mutated.
Among the 19 mutants, we isolated nine complementation groups, of which four correspond to mei-217, mei-218, mei-9, and nod.
Of the mutants we isolated, unc-18 sy671), unc-18 sy671 thes work, has defocus in twofdisthist sub-steps of sperm transfer: initiation and continued transfer.
To isolate only those with non-developmental mating defects, we screened through the mutants we isolated for defects in morphology, focusing on those with wild-type anatomy.
In a screen for sperm-transfer-defective mutants, we isolated two mutants, sy671, defective in sperm-transfer initiation, and sy672, defective in the continued transfer of sperm.
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For each suppressor mutant, we isolated DNA from root cultures of approximately five pooled M3 plants.
We also tested whether the spt16 mutants that we isolated are dominant for repression of the SER3 pr - HIS3 reporter.
Moreover, none of the mutants that we isolated from our screen for M1 defects exhibited abnormalities during the proximal phase of axon extension.
Surprisingly, we found that not one of the spt16 mutants that we isolated confers a growth defect at elevated temperatures (39°) or in the presence of HU, phenotypes that have been previously described for other spt16 alleles, including spt16 -G132D and spt16 -T828I/P859S (Formosa et al. 2001).
To test whether this effect can be reproduced in our apoc2 mutant zebrafish, we isolated plasma from adult WT and mutant zebrafish and transfused them into WT and apoc2 mutant larva recipients through cardinal vein injection.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com