The cbbLS::kanr mutant was not expected to grow in air because this mutant, like the cbbL insertion mutant constructed by Baker et al. [10], did not produce the carboxysomal Form I RubisCO (Figure 4) and relied instead on utilization of the available intracellular inorganic carbon pool by its Form II RubisCO.
On the contrary, a pta− mutant is not expected to accumulate this intermediate (McCleary et al. 1993).
Analysis of the three-dimensional structure of PSII indicates that the mutants are not expected to cause gross structural rearrangements either.
Thus the J shaped curve expected for derived mutants is not expected and a flat distribution is predicted under neutrality, as these polymorphisms are ancient with no influx of new mutations.
However, as the polymeric starch substrates interact with at least 9 glucose moieties (Fig. 3), single mutants are not expected to change CD size specificity completely (see Table 2).
In contrast to wild-type OPA1, however, this mutant, which is not expected to bind guanine nucleotides, was unaffected by incubation with GTPγS.
The mutant was therefore not expected to show significant changes in the abundance of mRNAs or proteins involved in primary metabolism.
In the context of the whole tru pathway in E. coli, where tru precursors were present as internal controls (producing patellins), the mutant 8 was not expected to be a substrate.
As predicted by the model, no purR, purO double mutants were found, because this combination shows no increase in LacZ level over that seen for either singly mutant type and is not expected to cause any growth improvement.
The xenografts used in these studies express wild type AR, not mutant AR and are therefore not expected to bind estradiol.
