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Summary Binucleate cells are produced in garlic root tip cells with puromycin and with 6-dimethylaminopurine (6-DMAP), the purine component of puromycin. The possibility that the effect of puromycin on cytokinesis is due to 6-DMAP-which appears to be without short term effects on protein synthesis-is discussed.This work was supported by AI 031871 from the Centre National de la Recherche Scientifique (M-C.B.) and the University René Descartes (M-C.B. and F.L.), Paris.The authors would like to thank Miss G. Daouse and Miss M. Delage for excellent technical assistance. 相似文献
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Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions 总被引:5,自引:0,他引:5
Gorgoulis VG Vassiliou LV Karakaidos P Zacharatos P Kotsinas A Liloglou T Venere M Ditullio RA Kastrinakis NG Levy B Kletsas D Yoneta A Herlyn M Kittas C Halazonetis TD 《Nature》2005,434(7035):907-913
DNA damage checkpoint genes, such as p53, are frequently mutated in human cancer, but the selective pressure for their inactivation remains elusive. We analysed a panel of human lung hyperplasias, all of which retained wild-type p53 genes and had no signs of gross chromosomal instability, and found signs of a DNA damage response, including histone H2AX and Chk2 phosphorylation, p53 accumulation, focal staining of p53 binding protein 1 (53BP1) and apoptosis. Progression to carcinoma was associated with p53 or 53BP1 inactivation and decreased apoptosis. A DNA damage response was also observed in dysplastic nevi and in human skin xenografts, in which hyperplasia was induced by overexpression of growth factors. Both lung and experimentally-induced skin hyperplasias showed allelic imbalance at loci that are prone to DNA double-strand break formation when DNA replication is compromised (common fragile sites). We propose that, from its earliest stages, cancer development is associated with DNA replication stress, which leads to DNA double-strand breaks, genomic instability and selective pressure for p53 mutations. 相似文献
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Dopamine neurons derived from embryonic stem cells function in an animal model of Parkinson's disease 总被引:112,自引:0,他引:112
Kim JH Auerbach JM Rodríguez-Gómez JA Velasco I Gavin D Lumelsky N Lee SH Nguyen J Sánchez-Pernaute R Bankiewicz K McKay R 《Nature》2002,418(6893):50-56
Parkinson's disease is a widespread condition caused by the loss of midbrain neurons that synthesize the neurotransmitter dopamine. Cells derived from the fetal midbrain can modify the course of the disease, but they are an inadequate source of dopamine-synthesizing neurons because their ability to generate these neurons is unstable. In contrast, embryonic stem (ES) cells proliferate extensively and can generate dopamine neurons. If ES cells are to become the basis for cell therapies, we must develop methods of enriching for the cell of interest and demonstrate that these cells show functions that will assist in treating the disease. Here we show that a highly enriched population of midbrain neural stem cells can be derived from mouse ES cells. The dopamine neurons generated by these stem cells show electrophysiological and behavioural properties expected of neurons from the midbrain. Our results encourage the use of ES cells in cell-replacement therapy for Parkinson's disease. 相似文献
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Protein synthesis by amoebal ribosomes 总被引:2,自引:0,他引:2
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P Markovits S Levy D Papadopoulo S Nocentini M F Tripier P Benda 《Comptes rendus des séances de l'Académie des sciences. Série D, Sciences naturelles》1977,285(5):623-626
Using primary cultures originating from 14 day old fetal Hamster brain, we have obtained a cell line with glial morphology. These cell remain non transplantable during the first year of in vitro culture, but undergo spontaneous transformation during the second year. Following prolonged contact of the glial-like cells with 25 to 50 microgram/ml of methylnitrosourea (MNU), a malignant transformation is observed 5 months after the treatment. The lowest concentrations of (MNU) do not cause malignant transformation, but seem to inhibit (or postpone) the spontaneous transformation. After MNU treatment, cells retain their glial nature. 相似文献