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Wall integrity has been demonstrated to be compromised in the irx7, irx8 and irx9 mutants, causing a decrease in the breaking strength of the inflorescence stems [ 15, 35].
Plasmid pDAI- SceI-SacBN, encoding the homing endonuclease, was conjugated into single crossover mutants, causing a double-strand break resolved by either a second crossover, yielding mutant genotype, or by reversion to wild-type.
Other mutants causing a decrease in the ratio of Aβ species were mostly clustered in the lower half of TMD1 (i.e., including and right after the helix-breaking P27) but also occurred at the N-terminal region (E4R and N8A), upper TMD2 (S73andnd W74A), and C-terminal D90A.
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Second, a large number of genes are misexpressed in individual mutants causing an abundance of upregulated genes that are not miRNA targets [21], [22].
Furthermore, overexpression of CMT2B-causing Rab7a mutants caused a strong increase of soluble vimentin (Fig. 4E F).
Reintroduction of a functional RRN5 gene into Sup mutants caused a reduction in the number of rDNA repeats to close to the wild type level but did not change RNA content.
We therefore tested whether the shs1-ps mutants cause a phenotype that is similar to shs1Δ.
APC mutants cause a strong activation of canonical Wnt signaling that leads to arrest prior to gastrulation [36].
In conjunction, the data from the AJ and more basal sections suggest that the mutants cause a subcellular reshuffling of endogenous protein, possibly linked with its signalling ability.
Thus, reduced accumulation of Pio in the tracheal lumen in γCOP mutants causes a pio-like defect in dorsal branch formation.
Although most mutants caused a similar early arrest of oogenesis, these markers allowed us to discriminate several categories of phenotypes.
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