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To explain the presence of accessions that were aromatic even though they did not have any of the known mutations, we sequenced the BADH2 gene.
To test for possible PAX2 mutations we sequenced RT-PCR products of the experimentally derived d30 sheep fetuses.
For the determination of germline mutations we sequenced in addition to the tumor tissues from each patient adjacent not affected normal colonic tissue.
To search for more cancer-associated TRKB point mutations, we sequenced the exons comprising the TRKB kinase domain from genomic DNA of 28 human tumor cell lines, from several tissue origins (data not shown).
To identify somatic mutations we sequenced the first 33 of the 35 STAG2 exons in 50 flow sorted clinical samples.
We were also surprised not to find products that correspond to a simple 4-base fill-in and blunt join among any of the TALEN mutations we sequenced.
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To understand the molecular nature of the su(wsp 1 mutation, we sequenced the coding region of the genomic DNA of the east locus.
Based on the bulldog phenotypic data and the sec24d position, at a zero recombination distance from the mutation, we sequenced sec24d as a suitable candidate gene.
In order to identify this suppressor mutation, we sequenced BicD and its four proximal neighboring genes Sgt, Aac11, fws and CG5110 from homozygous BicDPA66 Su(66) flies.
To verify that our Rut-C30 strain did contain the mutation we sequenced the gene and the reported mutation was detected.
To confirm that sec8Δ1 only disrupts the sec8 gene and provide an accurate molecular description of this mutation, we sequenced the sec8 genomic region in sec8Δ1 mutants.
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mutations we estimated
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