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In humans, there are two A-type cyclins - an embryonic-specific cyclin A1 and a somatic cyclin A2. Cyclin A1 is only expressed in meiosis and very early embryos, whereas cyclin A2 is present in proliferating somatic cells

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Genome doubling is an underlying cause of cancer cell aneuploidy and genomic instability, but few drivers have been identified for this process. Due to their physiological roles in the genome reduplication of normal cells, we hypothesised that the oncogenes cyclins E1 and E2 may be drivers of genome doubling in cancer. We show that both cyclin E1 (CCNE1) and cyclin E2 (CCNE2) mRNA are significantly associated with high genome ploidy in breast cancers. By live cell imaging and flow cytometry, we show that cyclin E2 overexpression promotes aberrant mitosis without causing mitotic slippage, and it increases ploidy with negative feedback on the replication licensing protein, Cdt1. We demonstrate that cyclin E2 localises with core preRC (pre-replication complex) proteins (MCM2, MCM7) on the chromatin of cancer cells. Low CCNE2 is associated with improved overall survival in breast cancers, and we demonstrate that low cyclin E2 protects from excess genome rereplication. This occurs regardless of p53 status,

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Duplicating chromosomes once each cell cycle produces sister chromatid pairs which separate accurately at anaphase. polytene chromosomes can also separate prior to metaphase through a spindle-independent mechanism termed Separation-Into-Recent-Sisters (SIRS). Both reduplication responses require the spindle assembly checkpoint protein Mad2. While Mad2 delays anaphase separation of metaphase polytene chromosomes Mad2s control of overall mitotic timing ensures efficient SIRS. Our results pinpoint mechanisms enabling continued proliferation after genome reduplication a finding with implications for cancer progression and prevention. DOI: http://dx.doi.org/10.7554/eLife.15204.001 species of fruit fly Stormo and Fox discovered two distinct ways in AR-231453 which cells respond to extra chromosome duplications. One response occurs in cells that were experimentally engineered to undergo an extra chromosome duplication. These cells delay division so that the chromosome separation machinery can somehow ...

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Cyclin A2 (encoded by CCNA2) is responsible for activating the cyclin-dependent kinases CDK1 and CDK2 to induce S-phase chromosome duplication and initiate mitosis. As both underexpression and overexpression of cyclin A2 have been linked to poor outcome in tumors, the role of cyclin A2 in tumor progression is unclear. Because complete loss of cyclin A2 is embryonically lethal, Kanakkanthara and colleagues developed a hypomorphic Ccna2 allele (Ccna2H) with reduced expression of cyclin A2 to better understand its role in tumorigenesis. Ccna2−/H mice had a marked reduction in cyclin A2 protein in tissues with a high mitotic index but relatively normal levels in tissues with less actively dividing cells. Ccna2−/H mice were more susceptible to spontaneous and carcinogen-induced tumors than Ccna2+/+ mice, indicating that cyclin A2 insufficiency promotes malignant transformation. Mouse embryonic fibroblasts (MEF) from Ccna2−/H mice exhibited increased aneuploidy due to chromosome segregation ...

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The mammalian A-type cyclin family consists of two members, cyclin A1 (encoded by Ccna1) and cyclin A2 (encoded by Ccna2). Cyclin A2 promotes both G1/S and G2/M transitions, and targeted deletion of Ccna2 in mouse is embryonic lethal. Cyclin A1 is expressed in mice exclusively in the germ cell lineage and is expressed in humans at highest levels in the testis and certain myeloid leukemia cells. To investigate the role of cyclin A1 and possible redundancy among the cyclins in vivo, mice bearing a null mutation of Ccna1 were generated. Ccna1-/- males are sterile due to a block of spermatogenesis before the first meiotic division, whereas females are normal. Meiosis arrest in Ccna1-/- males is associated with increased germ cell apoptosis, desynapsis abnormalities and reduction of Cdc2 kinase activation at the end of meiotic prophase. Cyclin A1 is therefore essential for spermatocyte passage into the first meiotic division in male mice, a function that cannot be complemented by the concurrently ...

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CCNA1 (cyclin A1), Authors: Immacolata Vocca, Gianmarco Muzi, Francesca Pentimalli, Antonio Giordano. Published in: Atlas Genet Cytogenet Oncol Haematol.

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Cdk1 (historically known as cdc2) is a member of the cyclin-dependent Ser/Thr kinase family. Cdk1 was originally identified as a catalytic subunit of the highly conserved protein kinase complex known as the M-phase promoting factor (17, 18). The kinase activity of Cdk1 is controlled at several levels, namely (a) at the level of regulatory Cdk1 phosphorylations; (b) at the level of activation through binding to cyclins such as B1; and (c) at the level of inactivation by inhibitors such as p21cip1 and p27Kip1.. The cell division cycle is a fundamental and highly complex process that is conserved in all eukaryotic cells. The conventional view is that in mammalian cells, progression through G1 phase is driven by the activities of Cdk4 and Cdk6, which associate with D-type cyclins. Entry into the S phase and initiation of DNA replication requires the activity of Cdk2, which is activated by E-type cyclins in the late G1 and S phases and by A-type cyclins in the S and G2 phases. Finally, entry into M ...

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