LARGE DELETIONS RESULT FROM BREAKAGE AND HEALING OF P-FALCIPARUM CHROMOSOMES
LARGE DELETIONS RESULT FROM BREAKAGE AND HEALING OF P-FALCIPARUM CHROMOSOMES
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DOI：
10.1016/0092-8674(88)90142-0
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发表时间：
1988-12-02
期刊：
影响因子：
64.5
通讯作者：
RAVETCH, JV
中科院分区：
文献类型：
--
作者：
POLOGE, LG;RAVETCH, JV
人疟原虫恶性疟原虫表现出广泛的菌株依赖性染色体多态性，这些多态性与该生物体中抗原变异的产生有关。这些多态性可导致染色体中的大缺失，如通过脉冲场梯度凝胶电泳所确定的。我们已经调查了广泛的缺失在染色体2和8在多个地理分离的寄生虫，导致在表达的良好表征的寄生虫抗原的损失的分子基础。这些多态性染色体的结构揭示了染色体断裂和愈合的机制，通过添加端粒重复序列最合理地解释了这些核型。此外，这些基因片段在其截短的染色体上的取向揭示了最初与着丝粒元件相关的愈合的染色体在有丝分裂中是稳定和维持的。这种机制在复杂的寄生虫生命周期中可能发挥的作用的模型进行了讨论。
The human malaria parasite P. falciparum exhibits extensive strain-dependent chromosomal polymorphisms that have been implicated in the generation of antigenic variability in this organism. These polymorphisms can result in large deletions in chromosomes as determined by pulsed-field gradient gel electrophoresis. We have investigated the molecular basis for extensive deletions in chromosomes 2 and 8 in multiple geographic isolates of this parasite that result in the loss of expression of well-characterized parasite antigens. The structure of these polymorphic chromosomes reveal that a mechanism of chromosome breakage and healing by the addition of telomeric repeats most plausibly accounts for these karyotypes. Furthermore, the orientation of these gene fragments on their truncated chromosomes reveal that the healed chromosome originally associated with centromeric elements is mitotically stable and maintained. A model for the possible role of this mechanism in the complex parasite life-cycle is discussed.