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The occurrence of HIV-1 recombination in vivo can be explained by the ability of the nascent viral strand to switch RNA templates during reverse transcription [44], and it necessitates super-infection of the target cell with two or more viruses, each carrying a different HIV-1 genome.
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When an incorrect dNTP is incorporated onto the 3′ terminus of the primer strand, the pol helps to switch the primer terminus from the pol to the exo subdomain, facilitating cleavage of the 3′-terminal nucleotide residue.
There may be alternative explanations but the important point is that the result was to switch strands at the AGCA/GGTT breakpoint as shown by the pattern of divergent sites we described above.
Similarly, the first 84 nucleotides of AF124829 and AF124832 match to Mal d 1.02 (typical SNPs are shown at the bottom of Table 5), while the remaining sequence matches to Mal d 1.01 making these accessions also putative erroneous sequences due to strand switching.
Beginning with the inner strands (right strand of left hand, left strand of right hand) cross the left strand above the right, switching each strand to the opposite hand.
This mechanism posits that breaks induce invasion of homologous duplex, followed by replicative extension of the invading strand, that is strand switching (see Arand et al., 2013).
Now the right and center strand will switch places.
However, the frequency by which either base pair appears on CCC DNA also depends on the mechanism for plus strand DNA synthesis, which requires that nascent plus strands switch templates from r5 to r3 (Figure 1A).
The error-free branch of PRR, still largely uncharacterized, competes with Rad52-mediated homologous recombination for substrates, and likely repairs these substrates by recombination between sister-strands, through either template strand switching or copy choice mechanisms [20].
Therefore, genes whose strand switched due to relocation of the origin likely experienced strong shifts in mutational pressure.
The twisted strands should switch hands.
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