近日,，IDIBELL研究人員確定了蛋白質(zhì)Zds1片斷在有絲分裂中發(fā)揮關(guān)鍵作用。
Bellvitge生物醫(yī)學(xué)研究所（IDIBELL）研究人員發(fā)現(xiàn)蛋白質(zhì)Zds1在有絲分裂過程中發(fā)揮關(guān)鍵性作用的機(jī)制,。相關(guān)研究論文發(fā)表在Journal of Cell Science雜志上,，這一研究取得的結(jié)果為發(fā)展靶向性癌癥療法鋪平了道路。
每一個(gè)有機(jī)體中,，細(xì)胞生長(zhǎng)和分裂成兩個(gè)子細(xì)胞的過程被稱為“細(xì)胞周期”,。細(xì)胞必須完成細(xì)胞周期過程中四個(gè)主要步驟：G1和G2期、對(duì)數(shù)生長(zhǎng)期（S期）,、染色體的分離（M期,、有絲分裂期）和分裂期（細(xì)胞分裂）。在S期或是DNA復(fù)制期,，遺傳物質(zhì)進(jìn)行復(fù)制,，在M期或有絲分裂過程中，細(xì)胞之間染色體分開復(fù)制成兩個(gè)子細(xì)胞,。
染色體的穩(wěn)定性
遺傳信息（DNA）,，從父到子（或從細(xì)胞到細(xì)胞）的傳輸是生物學(xué)上的基本問題。非整倍體,，即染色體的缺乏或過剩,，是幾乎所有人類癌癥類型中的特征,。有規(guī)律的有絲分裂對(duì)維持染色體的穩(wěn)定性尤為重要。
然而,，盡管DNA很重要性,，但很少有人知道有絲分裂產(chǎn)生的確切結(jié)果。這項(xiàng)發(fā)表在Journal of Cell Sciencs雜志的文章中,，IDIBELL研究細(xì)胞周期的小組由埃塞爾Queralt領(lǐng)導(dǎo),，研究發(fā)現(xiàn)新的有絲分裂的調(diào)控機(jī)制。
Separase蛋白是一種染色體分離和有絲分裂調(diào)控的重要組成部分,。Queralt博士首次描述了Zds1蛋白參與保持染色體完好性,，Zds1蛋白與Separase一起確保細(xì)胞到細(xì)胞之間正確的基因遺傳。
研究人員表示蛋白質(zhì)Zds1調(diào)節(jié)有絲分裂和染色體分離的分子機(jī)制需進(jìn)行深入研究,。本文采用一種模式生物酵母來開展研究,。（生物谷：Bioon.com）
doi:10.1242/jcs.097865
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Zds1 regulates PP2ACdc55 activity and Cdc14 activation during mitotic exit via its Zds_C motif
Ines Calabria, Barbara Baro, Jose-Antonio Rodriguez-Rodriguez, Nuria Russi?ol and Ethel Queralt*
At anaphase onset, highly active mitotic cyclin-dependent kinase (Cdk) is inactivated to promote exit from mitosis and completion of cytokinesis. The budding yeast Cdc14p phosphatase is a key mitotic regulator that counteracts cyclin-dependent kinase (Cdk) activity during mitotic exit. Separase, together with Zds1p, promotes the down-regulation of PP2ACdc55 in early anaphase, enabling accumulation of phosphorylated forms of Net1p and nucleolar release of Cdc14p. Here we show that the C-terminal domain of Zds1p, called the Zds_C motif, is required for Zds1-induced release of Cdc14p, while the N-terminal domain of the protein might be involved in regulating this activity. More interestingly, Zds1p physically interacts with Cdc55p, and regulates its localization via the Zds_C motif. Nevertheless, expression of the Zds_C motif at endogenous levels cannot induce timely nucleolar release of Cdc14, despite the proper (nucleolar) localization of Cdc55p. Our results suggest that the activity of PP2ACdc55 cannot be modulated solely through regulation of its localization, and that an additional regulatory step may be required. These results suggest that Zds1p recruits PP2ACdc55 to the nucleolus and induces its inactivation by an unknown mechanism.
