- Sic1 Mutants
- sic1∆
- sic1∆ cdh1∆
- sic1∆ cdh1∆ GALL-CDC20
- sic1∆ cdc6∆2-49
- sic1∆ cdc6∆2-49 cdh1∆
- sic1∆ cdc6∆2-49 cdh1∆ GALL-CDC20
- GAL-CLB2 sic1∆
- GAL-CLB5 sic1∆
- CLB5-db∆ sic1∆
- APC-A sic1∆
- APC-A sic1∆ cdc6∆2-49
- cdc14-ts sic1∆
- cln1∆ cln2∆ sic1∆
- cln3∆ bck2∆ sic1∆
- cln1∆ cln2∆ cln3∆ sic1∆
- swi5∆
- swi5∆ GAL-CLB2
- swi5∆ cdh1∆
- swi5∆ cdh1∆ GAL-SIC1
- GAL-SIC1
- GAL-SIC1-db∆
- GAL-SIC1 cln1∆ cln2∆
- GAL-SIC1 GAL-CLN2 cln1∆ cln2∆
- GAL-SIC1 cln1∆ cln2∆ cdh1∆
- GAL-SIC1 GAL-CLN2 cln1∆ cln2∆ cdh1∆
- CLB2-db∆ multicopy SIC1
- CLB2-db∆ GAL-SIC1
- cdc14-ts GAL-SIC1
- cdc14ts then GAL-SIC1
- APC-A cdh1∆ GAL-SIC1
- APC-A cdh1∆ multi-copy SIC1
swi5∆ cdh1∆
debug: ,
test user =
test db =
Simulation:
Change of parameters: ksswi'= ksswi"=0, kscdh=0, init CDH1=CDH1T=0.
Arrest: Inviable, telophase arrest.
Experiments:
Archambault, V., Li, C.X., Tackett, A.J., Wasch, R., Chait, B.T., Rout, M.P. and Cross, F.R. (2003). Genetic and biochemical evaluation of the importance of Cdc6 in regulating mitotic exit. Mol. Biol. Cell 14:4592-4604.
[Abstract] [Article]
[Abstract] [Article]
Experimental results: Similar to the triple-antagonist. They were able to undergo DNA synthesis and nuclear division, but not cell division and arrested as binucleate cells with 4C DNA content.
Comments: Problem for the model. The double mutant swi5∆ cdh1∆ has similar phenotype to the triple-antagonist, because with Swi5 deletion, Sic1 and Cdc6 synthesis are drastically reduced. And our model is at odds with this mutant as well.
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