Open Access Research article

A quantitative model of the initiation of DNA replication in Saccharomyces cerevisiae predicts the effects of system perturbations

Rohan D Gidvani1, Peter Sudmant2, Grace Li2, Lance F DaSilva1, Brendan J McConkey1, Bernard P Duncker1* and Brian P Ingalls12*

Author Affiliations

1 Department of Biology, University of Waterloo, Waterloo, ON, Canada

2 Department of Applied Mathematics, University of Waterloo, Waterloo, ON, Canada

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BMC Systems Biology 2012, 6:78  doi:10.1186/1752-0509-6-78

Published: 27 June 2012

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Additional file 1:

Figure S1.In vivochromatin fractionation results for Cdc6 as assayed via Western blotting.

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Additional file 2:

Figure S2.In vivochromatin fractionation results for Cdc45 as assayed via Western blotting.

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Additional file 3:

Figure S3.In vivochromatin fractionation results for Mcm2 as assayed via Western blotting.

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Additional file 4:

Table S1.Sample conversion of densitometry values to molecules per cell values for a Cdc45-myc timecourse experiment[66].

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Additional file 5:

Figure S4. Levels of model components when Cdc6, Cdt1 or Dbf4 have been reduced to 10% of their wild-type levels.

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Additional file 6:

Figure S5. The combination of DNA replication and whole cell cycle models does not alter either’s behaviour in isolation[45].

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Additional file 7:

Figure S6.Mutant phenotypes reported in whole cell cycle model are unaltered in the combined model[45].

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Additional file 8:

Figure S7. Comparison of Cdc20 time-varying profiles as originally modeled by Chen [24] versus our modified version [45].

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Additional file 9:

Table S2. Summary of simulated cell cycle mutants in the internal DNA replication initiation model. Table S3. Comparison of cell cycle mutants simulated by Chen et al. [45] and by the combined model [7,45,55,60,73,74,94-97].

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