Predictions (i):
We assume that Cdc6 is a weaker inhibitor to Clb5 kinase than is Sic1, hence, whenever the activity of Clb5 kinase is important, sic1∆ will have very different effects than cdc6∆2-49.
| Genotype | Phenotype |
triple-cln triple-cln sic1∆ triple-cln cdc6∆2-49 |
Inviable, G1 arrest ( Wittenberg et al., 1990 ). Viable, large ( Tyers, 1996 ). Inviable, G1 arrest (prediction). |
cln1∆ cln2∆ cln3∆ is rescued by sic1∆ but not by cdc6∆2-49.
Note: In the triple-cln and the triple-cln cdc6∆2-49 mutants, although START ransition is delayed for many hours, but eventually the cell grows large enough (in the model) for Clb5-dependent kinase activity to drive [ORI] to 1. This is a serious problem for the model. To account for the inviability of the triple-cln mutant, in this model, we set the following rule for G1 arrest:
Our rule for G1 arrest is that a cell must reach [ORI]=1 before the time it takes for a wild type cell in the same medium to divide twice (202.4 min in glucose and 293.4 min in galactose), otherwise it is considered G1-arrested.
For the quadruple mutant triple-cln cdc6∆2-49, [ORI] =1, at t=225 min, greater than two wt cycle times = 202.4 min.
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