Mattei D, Scherf A
Unité de Parasitologie Expérimentale, CNRS URA 361, Institut Pasteur, Paris, France.
Mutat Res. 1994 Jul;324(3):115-20. doi: 10.1016/0165-7992(94)90055-8.
The stability of chromosome ends of the human malaria parasite P. falciparum was analysed using a polymerase chain reaction (PCR) assay that detects potential chromosome breaks that have been healed by the addition of telomere repeats. The data show that the Pf332 and Pf87 genes located in subtelomeric positions of chromosomes 3 and 11, respectively, represent fragile sites. Breakpoints were observed in different regions of these genes. In the broken genes, the DNA sequences preceding the telomere addition sites generally have complementarity to the predicted RNA template of a P. falciparum telomerase ribonucleoprotein enzyme complex. We propose a model for the creation of new telomeres in P. falciparum adjacent to broken ends containing short telomere-like sequence motifs.
利用聚合酶链反应(PCR)分析方法检测了人类疟原虫恶性疟原虫染色体末端的稳定性,该方法可检测因添加端粒重复序列而修复的潜在染色体断裂。数据表明,分别位于3号和11号染色体亚端粒位置的Pf332和Pf87基因代表了脆弱位点。在这些基因的不同区域观察到了断点。在断裂的基因中,端粒添加位点之前的DNA序列通常与恶性疟原虫端粒酶核糖核蛋白酶复合物的预测RNA模板具有互补性。我们提出了一个模型,用于在恶性疟原虫中靠近含有短端粒样序列基序的断裂末端产生新的端粒。