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mutation rate by exposure to antibiotic (10^{-6}~mbox{mut} times mbox{gen}) σ Conjugation rate of bacteria (10^{-5}~mbox{day}^{-1}) (E_{max}) Maximum killing rate of antibiotic (26.4~mbox{day}^{-1}) (E_{50}) Antibiotic concentration for half max.
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Conjugation rates of 25 haploid isolates of F1-hybrid gametes between Microbotryum lychnidis-dioicae and M. silenes-dioicae backcrossed to parental, non-hybrids isolates provided evidence of assortative mating depending on the species' specific MAT region.
Hence the ratio of conjugation rate to phage infection rate is ∼5, meaning a F+ cell has a higher probability of encountering a F− and conjugating than being infected by a M13 phage within the regime defined by our inoculation conditions.
To understand the relative encounter frequencies, we can compare the conjugation rate to phage infection rate at the beginning of mixing.
As previously reported (Wan et al. 2011), the maximum conjugation rate is of the same order of magnitude as the estimated encounter rate.
The only unknown parameter is the penalty factor of conjugation rate due to infection (P λ).
As shown in Fig. 5b, as the amount of IgG was increased, the conjugation rate gradually increased, and when IgG reached 122.178 μg, the conjugation rate reached the highest level which can be determined as the optimal amount of IgG.
The conjugation rate then should be limited by physical factors and the probability of finding recipient cells.
By using meiotic products from F1-hybrids to backcross with parental (non-hybrid) gametes, the paired alleles at the mating type locus in particular were manipulated to be from the same species (homospecific backcross) or the alternate species (heterospecific backcross) for the comparison of conjugation rates.
Horizontal gene transfer (primarily conjugation) could explain this persistence, but it has been suggested that very high conjugation rates would be required.
These results are promising; however, based on low cisplatin-glutathione conjugation rates, a recent study by Peklak-Scott et al. concluded that cisplatin resistance attributed to GSTP1 is not caused by cisplatin conjugation, but rather modulation of other signaling pathways [92].
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