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增殖基因在黑腹果蝇中诱导体细胞配对缺陷并允许复制。

Proliferative genes induce somatic pairing defects in Drosophila melanogaster and allow replication.

作者信息

Riede I

机构信息

BL-Institut für Neurobiologie, Magdeburg, Germany.

出版信息

Cancer Genet Cytogenet. 1997 Sep;97(2):143-54. doi: 10.1016/s0165-4608(96)00396-2.

DOI:10.1016/s0165-4608(96)00396-2
PMID:9283598
Abstract

Drosophila tumor forming lines (malignant brain tumor, lethal giant larvae, discs large, brain tumor, and tumor suppressor gene) exhibit incomplete somatic pairing of specific regions in the salivary gland chromosomes, indicating that excessive cell proliferation correlates with somatic pairing defects in Drosophila. Alleles of malignant brain tumor enhancing the frequency of cell divisions exhibit melanizing tumors in the larvae. The giant chromosomes are defective in somatic pairing, indicating that a functional component of the chromosomes is influenced. Genes at different sites are affected, but the similarity of the phenotypes and complex complementation pattern reveals that their functions are interrelated. In the brain of malignant brain tumor recombinants and mutants in proliferative genes, polytene cells appear; wildtype does not amplify DNA in brain tissue cells. Thus, mutant proliferative genes induce the S-phase and allow replication of DNA.

摘要

果蝇肿瘤形成系(恶性脑肿瘤、致命大幼虫、盘状大、脑肿瘤和肿瘤抑制基因)在唾液腺染色体的特定区域表现出不完全的体细胞配对,这表明果蝇中过度的细胞增殖与体细胞配对缺陷相关。增强细胞分裂频率的恶性脑肿瘤等位基因在幼虫中表现出黑色素化肿瘤。巨型染色体在体细胞配对方面存在缺陷,表明染色体的一个功能成分受到影响。不同位点的基因受到影响,但表型的相似性和复杂的互补模式表明它们的功能是相互关联的。在恶性脑肿瘤重组体和增殖基因中的突变体的大脑中,出现了多线细胞;野生型在脑组织细胞中不扩增DNA。因此,突变的增殖基因诱导S期并允许DNA复制。

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