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If a Top2 mutation was recovered that affected pairing, then altered wing and body pigmentation would be expected.
In December of 1982, the first such mutation was recovered from a hybrid dysgenesis screen and eventually acquired the name, Inverse regulator-a[hd1] (Rabinow et al. 1991).
The sweetbread (swd) mutation was recovered from an ethylnitrosourea-induced genome-wide mutagenesis screen because the mutants had relatively small exocrine pancreas (Yee et al., 2005).
This particular transition has been previously identified [ 16, 19, 20]; in fact in the introduction of high temperatures (45°C) in the study of Bull et al. [ 16], this particular mutation was recovered in ~85% of the isolates.
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Each mutation is recovered over a balancer chromosome.
Live heterozygous mice carrying the L100P mutation were recovered by in vitro fertilization of C57BL/6 J eggs with the cryopreserved sperm of the corresponding G1 progeny.
For example, when a hairpin structure that controls the expression levels of the MS2 coat protein was mutated, compensatory mutations were recovered that restored the hairpin [ 37].
In contrast, silent, missense, and splice junction mutations were recovered in an equivalent proportion as predicted (Table 3).
In contrast missense, stop and splice junction mutations were recovered in a slightly lower proportion than predicted (Table 2).
Only nine binding pocket mutations were recovered without other inactivating changes in fur among the 62 transformants screened; each such mutation conferred less resistance than did a Δfur allele (Fig. 4C); and two of them (furH42L and furH42V) caused slow growth.
Fub mutations were recovered by targeted mutagenesis following a hypothesis-driven experiment (see below).
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