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Understanding the constellation of changes unique to H3.3 mutants should allow identification of additional subtypes and driver genes.
Further characterization of these mutants should allow the identification of molecular determinants of starch-dependent hydrogen production and supply targets for future biotechnological improvements.
In future studies homologous expression in Staphylococcus mutants should allow for the isolation of T7SS protein complexes to shed light on the architecture of the entire secretion system.
The implementation of genetic strategies to bypass embryonic lethality in Sucla2 mutants should allow the recovery and study of adult animals with global or tissue-specific Sucla2 deficiency to provide additional insights into disease pathogenesis and mtDNA biology.
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The small number of genomic loci tagged by insertion of gene-disruption library constructs in plants from our mutant collection should allow the recovery of insertion sites and the analysis of moss genes affected in transformants with altered phenotypes.
Again, as the mutant must arise at the front, this means that the probability of surfing should increase with λ (as for fixed m and K, a higher value of λ should allow more mutants to be born before wild types 'catch up' to the mutant population at the leading edge).
Recent advances in the area of F. tularensis genetics should allow for mutants to be readily made in this genetic background.
Interestingly, we found distinct modalities between apical and basal expulsion of ph mutant cells and further studies of this phenomenon should allow parallels to be made with the modified adhesive and polarity properties of different types of epithelial tumors.
The comparison of global gene expression patterns in the rel-proficient and the rel-deficient mutant strain at inducing and non-inducing conditions should allow to define the regulatory networks involved in the stringent response.
If it is possible to screen or select for cellular phenotypes, for example using FACS or drug resistance gene expression, this should allow genome-wide screening of genetic mutants in S2 cells.
Co-CRISPR selects for mutation in the unc-22 gene, with mutant homozygotes identified in the F2 progeny of co-injection marker positive animals, or less frequently in the F1 progeny (Kim et al. 2014), though haploinsufficiency of the unc-22 locus in 1% nicotine should allow for identification of unc-22 mutant heterozygotes in F1 animals (Moerman and Baillie 1979).
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