Syndecan-4 promotes cytokinesis in a phosphorylation-dependent manner
Syndecan-4 promotes cytokinesis in a phosphorylation-dependent manner
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DOI：
10.1007/s00018-010-0298-6
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发表时间：
2010-06-01
影响因子：
8
通讯作者：
Szilak, Laszlo
中科院分区：
文献类型：
--
作者：
Keller-Pinter, Aniko;Bottka, Sandor;Szilak, Laszlo
在有丝分裂期间，细胞分离，细胞-基质相互作用受到限制。胞质分裂完成后，两个子细胞仍通过细胞间桥（ICB）短暂连接，作为胞质分裂的最终步骤，细胞间桥会脱落。细胞与基质的粘附是由 syndecan-4 (SDC4) 跨膜硫酸乙酰肝素蛋白聚糖介导的。我们目前的工作表明，SDC4 在 MCF-7 乳腺癌细胞中以磷酸化依赖性方式促进胞质分裂。 SDC4的丝氨酸179磷酸化和胞外域脱落以细胞周期依赖性方式周期性变化，在G2/M期达到最大值。相反，抗磷酸化的 Ser179Ala 突变体消除了脱落。磷酸化的全长和脱落残余物沿着有丝分裂纺锤体富集，随后在 ICB 中富集，然而，适当的膜插入对于中体定位是必要的。磷酸化 Ser179Glu SDC4 的表达导致不完全脱落，而磷酸抗性 SDC4 的表达导致巨大的多核细胞。
During mitosis, cells detach, and the cell-matrix interactions become restricted. At the completion of cytokinesis, the two daughter cells are still connected transiently by an intercellular bridge (ICB), which is subjected to abscission, as the terminal step of cytokinesis. Cell adhesion to the matrix is mediated by syndecan-4 (SDC4) transmembrane heparan sulfate proteoglycan. Our present work demonstrated that SDC4 promotes cytokinesis in a phosphorylation-dependent manner in MCF-7 breast adenocarcinoma cells. The serine179-phosphorylation and the ectodomain shedding of SDC4 changed periodically in a cell cycle-dependent way reaching the maximum at G2/M phases. On the contrary, the phospho-resistant Ser179Ala mutant abrogated the shedding. The phosphorylated full-length and shed remnants enriched along the mitotic spindles, and subsequently in the ICBs, however, proper membrane insertion was necessary for midbody localization. Expression of phosphomimicking Ser179Glu SDC4 resulted in incomplete abscission, whereas expression of the phospho-resistant SDC4 led to giant, multinucleated cells.