- Clb1 Clb2 Mutants
- clb1∆ clb2∆
- CLB1 clb2∆
- CLB1 clb2∆ cdh1∆
- CLB1 clb2∆ pds1∆
- TAB6-1 CLB1 clb2∆
- CLB2-db∆
- CLB2-db∆ in galactose
- CLB2-db∆ multicopy SIC1
- CLB2-db∆ GAL-SIC1
- CLB2-db∆ multicopy CDC6
- CLB2-db∆ GAL-CDC6
- CLB2-db∆ clb5∆
- CLB2-db∆ clb5∆ in galactose
- GAL-CLB2
- Multicopy GAL-CLB2
- GAL-CLB2 sic1∆
- GAL-CLB2 cdh1∆
- APC-A GAL-CLB2
- swi5∆ GAL-CLB2
- cln1∆ cln2∆ cln3∆ GAL-CLB2
- GAL-CLB2-db∆
CLB1 clb2∆ cdh1∆
debug: ,
test user =
test db =
Simulation:
Change of parameters: ksb2'=0.0003, ksb2"=0.013 (=33% of WT), kscdh=0, init CDH1=CDH1T=0.
Experiments:
Cross, F.R. (2003). Two redundant oscillatory mechanisms in the yeast cell cycle. Dev. Cell 4:741-752.
[Abstract] [Article]
[Abstract] [Article]
Experimental results: Supplementary Fig. 1 & Table 6. Double mutant clb2∆ cdh1∆ (CLB1 gene intact) grows well in galactose medium, but exhibited poor viability when transferred to glucose medium.
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Deletion of CDH1 gene should help clb2∆ to make Esp1 higher at mitosis, and better to satisfy that viability criterion. Conversely, deletion of the CLB2 gene should help the viability of cdh1∆ also.
Perhaps Clb2 has some additional role(s) at mitotic exit, not included in our wiring diagram and not carried out by Clb1. For instance, Clb2-kinase is most likely needed to phosphorylate and activate Cdc5 (Cheng et al., 1998; Kotani et al., 1998), which in turn is needed for Cdc14 release. Hence, for cdh1∆ cells which depend on Cdc14 and CKIs for survival, further deletion of CLB2 will lower Cdc5 activity, causing reduction in Cdc14 release and CKI production, thereby preventing mitotic exit.
In galactose, mutant simulation is viable as observed.:
