Sentence examples for resistant genome from inspiring English sources
Replication of the DEB025res genome proved, unlike replication of the WT genome, to be efficient in CypA KD cells, indicating that the drug resistant genome is less dependent on CypA (and thus likely on the cis-trans isomerase activity) for efficient replication.
Furthermore, preliminary data suggests that rescue of fertility by having ∼2.5% of resistant genome upon cutting, is inefficient, meaning that many recombinant genomes are required for in each stem cell to produce progeny.
Indeed, it is likely that the recombinants observed represent a small fraction of amount of homologous repair, since the sibling genomes will presumably be the more available partners for repair but will not contribute restriction resistant genomes.
The survivors of restriction enzyme selection are homoplasmic reflecting a strong selection against the starting genomes that acts to completion in a single generation with little opportunity for a slow amplification of the resistant genomes.
When the two lysates were pooled, only FLAG-tagged, V-073-resistant virus was recovered, demonstrating that the immunoprecipitation was specific for capsids harboring proteins from the V-073-resistant genome.
Whereas 87% of (CBA/H × SJL) F1 rAMLs (i.e. 2 rAML-susceptible genomes) harbour Sfpi1 point mutations (16), only 67% of (CBA/H × C57BL) F1 rAMLs [i.e. one rAML-susceptible genome (CBA/H) and one rAML-resistant genome (C57BL)] harbour this point mutation (18).
There was no RNase-resistant genome left in the NP-40-treated supernatant of full-genome replicons, although density gradient analysis of the NP-40-treated supernatant of dORF replicon cells clearly showed the coexistence of the HCV genome and core proteins at a peak of 1.18 g/mL.
Introgressing LEW Crgn1 and Crgn2 loci into the WKY (CRGN-susceptible) genome has been shown to reduce the incidence of disease, but the effects exerted by both WKY Crgn1 and Crgn2 in a LEW (CRGN-resistant) genome have not been previously investigated.
1) The drug-bound product must interact with proteins made by the drug-resistant genome; 2) the interaction between drug-bound products and resistant proteins must inhibit an essential step in the infectious cycle of the virus; and 3) the ratio of drug-susceptible to drug-resistant products synthesized in the cell must be high enough to poison the function of the resistant variant.
To detect endonuclease-resistant genomes in crude viral preps (CVPs) or Optiprep fractions, only benzonase-treated CVPs were utilized so that all non-encapsidated genomes were degraded.
Thus, for a capsid inhibitor, trans-encapsidation of newly arising drug-resistant genomes by the intracellular excess of drug-susceptible capsids should provide an additional mechanism to reduce the reservoir of drug-resistant genomes packaged in drug-resistant capsids.
