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Based upon the in vitro data, this level of drug exposure would be expected to result in clinical activity against most of the mutants characterised in Table 1, with the exception of T315I, and is therefore consistent with the responses observed in patients harbouring imatinib-resistant point mutations.
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The msl1 mutants characterised here block local spreading in a dominant fashion even when wild-type subunits are available.
Mutant plants characterised in certain depression resulted in reduction of sizes of vegetative and generative organs, and of plant bodies on the whole.
Mutants were initially characterised in batch culture using glucose as carbon substrate and strains with all three modifications shown to form ethanol efficiently and rapidly at temperatures in excess of 60 °C in yields in excess of 90% of theoretical.
The mutant used and characterised in those studies was as described here (David Owen, personal communication).
Similarly, reformatting the mutant scFv 4.9M characterised in this study into a bivalent diabody resulted in a molecule with tight antigen binding (Kd 8 n M; J Krauss, unpublished results).
Crucially, however, the design of the created pyrE mutant strain is such that its pyrE allele can be rapidly (2 days) restored to wild-type using an appropriate ACE correction vector allowing the specific in-frame deletion mutant to be characterised in a clean, wild-type background.
Crucially, the mutants made are always characterised in an otherwise wild-type background as the pyrE mutant is always converted back to prototrophy, using ACE, prior to phenotypic characterisation.
From our present analysis of previously uncharacterised ALK mutants, and in light of other reports concerning ALK mutant variants, the accumulated data suggests that the ALK mutations observed and characterised in neuroblastoma to date fall into three classes.
Another gene involved in folate metabolism was characterised in the brown midrib 2 (bm 2) mutant, in which a functional MTHFR gene showed reduced transcript levels.
While the phenotype of GBB loss of function has been characterised in detail, to our knowledge over expression of GBB has only been used to rescue mutant phenotypes (McCabe et al., 2003; McCabe et al., 2004; Goold and Davis, 2007).
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