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The cell cycle is a series of discrete events in eukaryotic cells.The most important events of the cell cycle are faithful replication of the genome and precise segregation of the daughter genomes into the daughter cells formed at division.The cell-cycle control system triggers the major processes of the cell cycle to ensure: 1) all cell cycle events occur in the correct ordered and sequential progression from G 1 to M phase, 2) each event is triggered only once per cycle and in a complete, irreversible fashion, and 3) the cell cycle works properly even if parts of the system malfunction.B cyclin / cyclin dependent kinase 1 (Cdk1) complexes are essential for mitotic entry and progression.Cyclin B1 and B2 are the mitotic B cyclins in mammalian somatic cells.Cyclin B1 is an essential gene for mouse embryogeneisis, but cyclin B2 is dispensable.However, RNA interference (RNAi) studies in human somatic cells show that either cyclin B 1 or B2 can promote mitosis when 95-99% of cyclin B1 or B2 are depleted.Mammalian cyclin B1 and B2 are co-expressed.They are detectable beginning in G1, rise slowly through S phase then rapidly in G2, peaking in late G2 or early M, and degraded approximately after metaphase.To explore the differential effects of these B cyclins on mitosis entry and progression, we examined quantitatively the effect of cyclin B1 or cyclin B2 expression on mitotic time and the ability of either cyclin to overcome the G2 arrest imposed by depletion of both B cyclins.To do this, we generated stable cell lines inHela cell and MG63 osteoblast with inducible expression of cyclin B1-EGFP or cyclin B2-EGFP recombinant genes that are not recognized by cyclin B1 and B2 siRNAs.We conclude that cycB1 and cycB2 are interchangeable for gross ability to promote G2 and M transition.