Sentence examples for mutants by expressing from inspiring English sources

Attempts to rescue the efflux defects of the UTI89 mutants by expressing the deleted secretin in trans from expression plasmids were not successful, and thus we cannot rule out that the observed defects were caused by secondary effects of the deletion mutations.

We also analyzed whether the Baz variants could rescue the phenotype of baz zygotic mutants by expressing them zygotically from paternally derived transgenes (zygotic expression of BazS980A GFP does not cause a dominant phenotype because it is expressed later and at lower levels than when contributed maternally).

To determine which of these 910 differentially expressed genes were affected due to the loss of TBPH expression, we replaced TBPH in the G2 mutants by expressing TBPH under the control of its endogenous proximal promoter region.

Both ICP2-sensitivity and OmpU expression were restored to the clinical toxR mutants by expressing ompU in trans or by reverting the toxR allele to wild-type (data not shown), indicating that these mutant toxR alleles are necessary and sufficient for ICP2 resistance and that this resistance is mediated through loss of OmpU expression.

However, since we were unable to rescue the aldicarb hypersensitivity of the eat-6 mutants by expressing EAT-6 in the ACh neurons, other experiments are necessary to determine the mechanisms by which EAT-6 regulates presynaptic neurotransmission.

This result was unexpected, as Doi and Iwasaki reported successful rescue of the levamisole hypersensitivity of the eat-6 ad467 eat-6 ad467and01) eat-6 ad601 eat-6 ad601at-6 in the mutants [8].

This trans-inhibitory activity of E3 opened the possibility to rescue translation of SINV ΔDLP mutant by expressing VV E3L gene in MEF cells.

Further, the production of 1 can be restored in the Δ ltmK mutant by expressing ltmK in trans.

We studied the physiological effects of the Q555X hSynI mutant by expressing it in primary hippocampal neurons from SynI KO mice.

We were also able to induce the mutant defects by expressing mutant TBA-1 protein in wild-type animals.

To be able to assess the flower primordium initiation in plants that have lost most SYD and BRM activity, we employed the syd-5 null mutant and a conditional BRM mutant, generated by expressing an artificial micro RNA (aMIR) against BRM in adult plants (Wu et al., 2012).