Ghosh S, Paweletz N
Chromosoma. 1987;95(2):136-43. doi: 10.1007/BF00332186.
The interaction between centrosomes and kinetochores was studied in multinucleate cells induced by Colcemid treatment or by random cell fusion. Except for prematurely condensed chromosomes (PCC) of the G2-phase, PCCs do not develop their own spindle area. Perhaps the maturation promoting factor (MPF) fails to activate these centrosomes. In such PCCs, the kinetochore-centrosome interaction was found to be non-specific: sometimes only a few chromosomes of a group could establish connections with centrosomes, sometimes chromosomes from the same PCC group developed microtubule (MT) attachment with different centrosomes (not the pair), and sometimes kinetochores of PCC groups failed to interact with MTs. These findings explain the abnormal mitotic behaviour of PCCs as seen in the light microscope. These PCCs develop micronuclei or normal nuclei by nuclear re-formation in telophase. All the different PCC groups revealed kinetochores with kinetochore plates. It was shown that transformation of presumptive kinetochores to a trilaminar kinetochore does not depend on nuclear envelope breakdown or on the degree of chromosome condensation. This may be induced by the MPF which may initiate different events like chromosome condensation, nuclear envelope breakdown and kinetochore transformation by secondary factors. Other observations like establishment of connections by different chromosome groups to a common centrosome, kinetochore attachment of PCCs to different centrosomes, interaction of one kinetochore with two centrosomes, kinetochores being stretched and bent to receive microtubules and finally the failure of some kinetochores to develop MT attachment, all strongly suggest that the kinetochores serve as the point of termination rather than the nucleation sites of kinetochore MTs.
在秋水仙酰胺处理诱导或随机细胞融合产生的多核细胞中,研究了中心体与动粒之间的相互作用。除了G2期的早熟凝集染色体(PCC)外,PCC不会形成自身的纺锤体区域。也许成熟促进因子(MPF)未能激活这些中心体。在这类PCC中,发现动粒与中心体的相互作用是非特异性的:有时一组中只有少数几条染色体能与中心体建立连接,有时来自同一PCC组的染色体与不同的中心体(而非一对中心体)形成微管(MT)附着,有时PCC组的动粒未能与MT相互作用。这些发现解释了在光学显微镜下所见PCC异常的有丝分裂行为。这些PCC在末期通过核重新形成形成微核或正常核。所有不同的PCC组都显示有带动粒板的动粒。结果表明,推定动粒向三层动粒的转变不依赖于核膜破裂或染色体凝集程度。这可能是由MPF诱导的,MPF可能通过次要因素引发不同事件,如染色体凝集、核膜破裂和动粒转变。其他观察结果,如不同染色体组与一个共同中心体建立连接、PCC的动粒与不同中心体附着、一个动粒与两个中心体相互作用、动粒被拉伸和弯曲以接收微管,以及最后一些动粒未能形成MT附着,都强烈表明动粒作为动粒微管的终止点而非成核位点。