Sigrist S J, Lehner C F
Department of Genetics, University of Bayreuth, Federal Republic of Germany.
Cell. 1997 Aug 22;90(4):671-81. doi: 10.1016/s0092-8674(00)80528-0.
We demonstrate that fizzy-related (fzr), a conserved eukaryotic gene, negatively regulates the levels of cyclins A, B, and B3. These mitotic cyclins that bind and activate cdk1(cdc2) are rapidly degraded during exit from M and during G1. While Drosophila fizzy has previously been shown to be required for cyclin destruction during M phase, fzr is required for cyclin removal during G1 when the embryonic epidermal cell proliferation stops and during G2 preceding salivary gland endoreduplication. Loss of fzr causes progression through an extra division cycle in the epidermis and inhibition of endoreduplication in the salivary gland, in addition to failure of cyclin removal. Conversely, premature fzr overexpression down-regulates mitotic cyclins, inhibits mitosis, and transforms mitotic cycles into endoreduplication cycles.
我们证明，与fizzy相关的（fzr）基因是一种保守的真核基因，它对细胞周期蛋白A、B和B3的水平起负调控作用。这些与细胞周期蛋白依赖性激酶1（cdk1，即cdc2）结合并激活它的有丝分裂细胞周期蛋白，在退出M期和G1期时会迅速降解。虽然之前已表明果蝇的fizzy是M期细胞周期蛋白降解所必需的，但当胚胎表皮细胞增殖停止时，G1期以及唾液腺内复制前的G2期细胞周期蛋白的清除则需要fzr。fzr缺失除了导致细胞周期蛋白清除失败外，还会使表皮细胞通过一个额外的分裂周期，并抑制唾液腺内复制。相反，过早的fzr过表达会下调有丝分裂细胞周期蛋白，抑制有丝分裂，并将有丝分裂周期转变为内复制周期。
