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We also performed linkage analysis of HWC2 (Ichitani et al. 2001) and tagged this locus between the two restriction fragment length polymorphism (RFLP) markers on the long arm of chromosome 4.
Part of the observed variation in AFLP data is caused by indels (insertions or deletions) between the two restriction sites at a single locus, resulting in amplicons of different sizes.
These results suggest the GC bias between the two restriction enzymes may explain the difference in the abundance of TEs between the two BES groups.
The AFLP mutations that are primary due to point mutations within the restriction site, with a small fraction of in/dels that occurs between the two restriction enzyme sites and that should originate co-dominant AFLP loci.
Both of these values were significantly greater than the FI of the controls and remained so for the 4 days of measurement, although after the first day there was no significant difference between the two restriction groups: FI had decreased to 6.61±0.54 g/day and 7.70±0.37 g/day for low and high restriction groups, respectively (P>0.05).
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To explain this difference between the two BES groups, we examined the bias of the two restriction enzymes.
IR searched the two lines so that they met the two restrictions and so that the deviations between the observed values and the estimated values were minimal.
We can see that the two restrictions are not contradictory.
The two restrictions are pragmatic.
Differences in BM appeared between the two restricted groups after day 13 of restriction and remained for the rest of the restriction period.
The SUMO-I sequence was obtained by PCR amplification and inserted between these two restriction sites, giving vectors pET-FPSG.
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