Problems with the model
Genotype |
Observed Phenotype |
Simulated Phenotype |
Notes |
Viable, grows slowly with reduced size at birth and reduced size at
budding |
Viable, normal growth rate, small at birth, normal size at budding. |
Cdh1 promotes proteolysis of some activator of START. |
|
Viable, large size with an extended G2 phase |
Viable, size between WT and cdh1∆ with a slightly shorter G2. |
||
Viable |
Inviable, sister chromatid separation occurs 1.5 min after nuclear division. |
Parameter settings may be faulty or model criteria for cell viability may be too strict. |
|
Inviable in glucose, viable in galactose |
Viable in both glucose and galactose. |
Clb1 may not be a perfect backup of Clb2, which may be essential for activation of APC/Cdc20. |
|
Inviable, telophase arrest |
Inviable, division occurs in an unbudded cell. |
A delay in the onset of mitosis by the morphogenesis checkpoint may cause telophase arrest. |
|
Inviable. |
Completes 1st cycle, but no bud in the 2nd cycle. |
See discussion of the triple-antagonist strain. |
|
("triple-antagonist") |
Inviable, arrests as a "4-cell body" objects with 2 short spindles and 4C DNA content (Archambault et al., 2003). The triple-antagonist strain has additional cytokinesis defect than the double mutant sic1∆ cdh1∆. |
Inviable, telophase arrest with 2C DNA content. |
Cdc14 may trigger mitotic exit in the presence of high Clb2 kinase activity. See mutant simulation for details.
|
Inviable, similar to triple-antagonist |
Inviable, similar to triple-antagonist. |
Same as triple-antagonist. |
|
Viable |
Inviable, Esp1 active before chromosome alignment. |
The model neglects the role of Cdc5 in activating the Scc1 as the substrate for Esp1. |
|
Inviable |
Inviable for the wrong reasons. If both single mutants are viable then the double mutant would be viable as well. |
Does Clb2 have a new role in inactivating Esp1? |
|
Exits from mitosis after many hours in nocodazole |
Tightly arrests in metaphase in nocodazole. |
May be a new cross talk from the BUB2 pathway to the MAD2 pathway. |