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Toward a comprehensive model for induced endoreduplication.

机译:建立诱导核内复制的综合模型。

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Both the biological significance and the molecular mechanism of endoreduplication (END) have been debated for a long time by cytogeneticists and researchers into cell cycle enzymology and dynamics alike. Mainly due to the fact that a wide variety of agents have been reported as able to induce endoreduplication and the diversity of cell types where it has been described, until now no clear or unique mechanism of induction of this phenomenon, rare in animals but otherwise quite common in plants, has been proposed. DNA topoisomerase II (topo II), plays a major role in mitotic chromosome segregation after DNA replication. The classical topo II poisons act by stabilizing the enzyme in the so-called cleavable complex and result in DNA damage as well as END, while the true catalytic inhibitors, which are not cleavable-complex-stabilizers, do induce END without concomitant DNA and chromosome damage. Taking into account these observations on the induction of END by drugs that interfere with topo II, together with our recently obtained evidence that the nature of DNA plays an important role for chromosome segregation [Cortes, F., Pastor, N., Mateos, S., Dominguez, I., 2003. The nature of DNA plays a role in chromosome segregation: endoreduplication in halogen-substituted chromosomes. DNA Repair 2, 719-726.], a straightforward model is proposed in which the different mechanisms leading to induced END are considered.
机译:细胞遗传学家和研究人员对细胞内复制的生物学意义和分子机制(END)进行了很长时间的争论,研究涉及细胞周期酶学和动力学。主要是由于据报道已报道了多种试剂能够诱导核内复制和细胞类型的多样性,到目前为止,尚无明确或独特的诱导这种现象的机制,这种现象在动物中很少见,但在其他方面相当明显。已经提出在植物中常见的。 DNA拓扑异构酶II(拓扑II)在DNA复制后的有丝分裂染色体分离中起主要作用。经典的topo II毒物通过稳定所谓可裂解复合物中的酶来起作用,并导致DNA损伤和END,而真正的催化抑制剂不是可裂解复合物稳定剂,它确实会诱导END,而没有伴随的DNA和染色体损伤。考虑到这些有关干扰topo II的药物诱导END的观察结果,以及我们最近获得的证据,证明DNA的性质在染色体分离中起着重要作用[Cortes,F.,Pastor,N.,Mateos,S ,Dominguez,I.,2003。DNA的性质在染色体分离中起作用:卤素取代的染色体中的核内复制。 DNA Repair 2,719-726。],提出了一个简单的模型,其中考虑了导致END的不同机制。

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