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Hence the PRC observed in our double mutants is probably caused by changes in the circadian pacemaker.

The decrease of concerted integration activity that was observed for the mutants is probably due to the defect in strand transfer activity in this assay.

Therefore, the slightly reduced level of pre-rRNA association of Noc4p variants in these mutants is probably not responsible for their failure to support growth.

All thing considered, the model that best recapitulates the phenotype of PGK Cre Dbx1DTA mutants is probably the CNCC ablation paradigm in chick [10], [12], [13].

Therefore, while RIIβ−/− mice may have enjoyed health benefits due to chronic insulin sensitivity over the course of their lifespan, insulin sensitivity in old RIIβ−/− mice did not reflect attenuation of an age-related dysfunction, and the insulin sensitivity seen in the male mutants is probably not the cause of their extended lifespan.

The meeting participants concluded that the prevalence of HBsAg mutants is probably higher than previously believed.

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The remaining 4 mutants were probably incorrectly associated with RP or have functionalities not discovered yet.

Our analysis suggests that the intermediate phenotypes of the pla/slr1 double mutants were probably due to a reduction in cell number.

Some of these mutants are probably involved in auxin-related processes, and a very few, including rh2, Lrt1, and ral1, seems to be specifically implicated in root-specific mechanisms.

The results presented above indicated that appressoria formed by ΔpdeH mutants are probably defective in penetration.

The inability to identify more conclusive evidence of linkage in ercc1 or neb mutants was probably due to the large number of changed genes: compared to SAP102, PSD-95 and Foxa3 where 21, 12 and 10 genes respectively were changed, 140 genes were changed in ercc1 mutants and 92 in neb mutants (Table 4).

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