Antisense inhibition of CAS, the human homologue of the yeast chromosome segregation gene CSE1, interferes with mitosis in HeLa cells.
We have analyzed the effects on HeLa cells of reduction of the CAS protein, the human homologue to yeast chromosome segregation protein CSE1. Expression of CAS antisense cDNA decreases the amount of CAS protein in HeLa cells and perturbs progression from G2 (retards transition from G2) to G1 in the cell cycle. Increased levels of cyclin B in CAS antisense transfected cells correlated with an arrest in G2 phase or mitosis. This arrest upon CAS attenuation is consistent with observations that yeast with CSE1 mutations are defective in mitosis and cyclin B degradation.
Ogryzko
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Laboratory of Molecular Growth Regulation, National Institute of Child Health and Development, and Laboratory of Molecular Biology, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
Brinkmann
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Howard
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BH
Pastan
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I
Brinkmann
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U
D029563:Cellular Apoptosis Susceptibility Protein; D016213:Cyclins / Q000378:metabolism; D016373:DNA, Antisense / Q000494:pharmacology*; D018076:DNA, Complementary; D018274:Electroporation; D005434:Flow Cytometry; D016193:G1 Phase / Q000235:genetics*; D016195:G2 Phase / Q000235:genetics*; D006367:HeLa Cells; D006801:Humans; D011506:Proteins / Q000037:antagonists & inhibitors*; D014162:Transfection
D029563:Cellular Apoptosis Susceptibility Protein; D016213:Cyclins; D016373:DNA, Antisense; D018076:DNA, Complementary; D011506:Proteins