本期封面所示為具有額外中心體的一個人細(xì)胞中的一個過渡性多極紡錘體中間形態(tài)。圖上所示微管為紅色,，中心體為綠色,，染色體為白色,。
很多腫瘤細(xì)胞的一個顯著特征是染色體不穩(wěn)定（CIN）,，即全部染色體數(shù)量的增加或減少速度加快,。CIN的機(jī)制一直是一個有很多爭論的話題,。人們長期所持的一個觀點(diǎn)是，額外的中心體（它們與CIN有關(guān)聯(lián)性）通過誘導(dǎo)混亂的多極紡錘體組裝和非對稱的細(xì)胞分裂來促使染色體錯誤分離,。但是現(xiàn)在,，長期活細(xì)胞成像顯示，CIN癌細(xì)胞很少經(jīng)歷多極分裂,，而且甚至當(dāng)它們經(jīng)歷這種分裂的時候,，所產(chǎn)生的也主要是無法生存的后代。相反,，額外中心體癌細(xì)胞僅僅是經(jīng)過一個過渡性的多極紡錘體階段,，在這個階段，“異常動粒微管附著體”會積累,。很多附著錯誤即使在額外中心體聚集形成正確雙極紡錘體之后仍存在,，從而增加染色體錯誤分離的可能性。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 460, 278-282 (9 July 2009) | doi:10.1038/nature08136
A mechanism linking extra centrosomes to chromosomal instability
Neil J. Ganem1, Susana A. Godinho1 & David Pellman1
1 Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Children's Hospital, Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
Chromosomal instability (CIN) is a hallmark of many tumours and correlates with the presence of extra centrosomes1, 2, 3, 4. However, a direct mechanistic link between extra centrosomes and CIN has not been established. It has been proposed that extra centrosomes generate CIN by promoting multipolar anaphase, a highly abnormal division that produces three or more aneuploid daughter cells. Here we use long-term live-cell imaging to demonstrate that cells with multiple centrosomes rarely undergo multipolar cell divisions, and the progeny of these divisions are typically inviable. Thus, multipolar divisions cannot explain observed rates of CIN. In contrast, we observe that CIN cells with extra centrosomes routinely undergo bipolar cell divisions, but display a significantly increased frequency of lagging chromosomes during anaphase. To define the mechanism underlying this mitotic defect, we generated cells that differ only in their centrosome number. We demonstrate that extra centrosomes alone are sufficient to promote chromosome missegregation during bipolar cell division. These segregation errors are a consequence of cells passing through a transient 'multipolar spindle intermediate' in which merotelic kinetochore–microtubule attachment errors accumulate before centrosome clustering and anaphase. These findings provide a direct mechanistic link between extra centrosomes and CIN, two common characteristics of solid tumours. We propose that this mechanism may be a common underlying cause of CIN in human cancer.
