Sentence examples for mutants we were from inspiring English sources

Despite numerous attempts to generate Δpv1 mutants, we were unable to isolate such parasites, although control experiments were successful.

By combining gene expression analyses using 70-mer oligonucleotide 16.4 K microarrays for both wild type symbionts and nodulation defective symbiotic mutants, we were able to identify and classify more than 3,400 differentially regulated genes and associated regulators.

For example, because we were able to directly compare the native alleles to the site-directed mutants, we were able to infer that changes at other sites must be altering the functional impact and possibly the selective advantage of the Cys-to-Ser mutation.

For some mutants, we were able to identify a region in which the mutation could be localized by deficiency mapping.

With these two new mutants we were able to show a significant impact on GAG-binding affinity.

For the heterozygous and homozygous mutants, we were not able to obtain stable populations in the white state.

Using these and additional mutants, we are testing the role played by cis-elements in maintaining the chromatin and looping of Tcrb, which are essential for recombination.

From this point forward in the text, when we refer to etr1;ers1-3 mutants we are referring to both the etr1-7 ers1-3 etr1-7 ers1-3 etr1-7 ers1-3with the intent here to indicand that both etr1-9 ers1-3 etr1-9 ers1-3 etr1-9 ers1-3

Due to poor expression and stability of the Tob W93A mutant, we were unable to test the interaction of this mutant with CNOT7 in vitro, although the mutant expressed in mammalian cells for subsequent interaction assays in vivo.

By combining this strain with a previously engineered xylose reductase mutant, we were able to eliminate l-arabinitol formation and produce xylitol to near 100% purity from an equiweight mixture of d-xylose, l-arabinose, and d-glucose.

Since lysine762 localizes to the region that is deleted in the Δ716 G-CSFR mutant, we were interested in investigating whether cells expressing the K762R/G-CSFR also exhibited ligand-induced hyperproliferative responses to G-CSF.