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A和T同聚物延伸介导恶性疟原虫中的DNA倒位，这导致基因表达丧失。

A and T homopolymeric stretches mediate a DNA inversion in Plasmodium falciparum which results in loss of gene expression.

作者信息

Pologe L G, de Bruin D, Ravetch J V

机构信息

Sloan-Kettering Institute, New York, New York 10021.

出版信息

Mol Cell Biol. 1990 Jun;10(6):3243-6. doi: 10.1128/mcb.10.6.3243-3246.1990.

DOI:10.1128/mcb.10.6.3243-3246.1990
PMID:2188111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC360690/
Abstract

Ring-infected erythrocyte surface antigen-negative isolates of Plasmodium falciparum demonstrate a complex DNA rearrangement with inversion of 5' coding sequences, deletion of upstream and flanking sequences, and healing of the truncated chromosome by telomere addition. An inversion intermediate that results in the telomeric gene structure for RESA has been identified in the pathway. This inversion creates a mitotically stable substrate for the sequence-specific addition of telomere repeats at the deletion breakpoint.

摘要

恶性疟原虫的环状感染红细胞表面抗原阴性分离株表现出复杂的DNA重排，包括5'编码序列的倒位、上游和侧翼序列的缺失，以及通过添加端粒修复截短的染色体。在该途径中已鉴定出一种导致RESA端粒基因结构的倒位中间体。这种倒位为在缺失断点处序列特异性添加端粒重复序列创造了有丝分裂稳定的底物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e37/360690/253e92e64a0c/molcellb00042-0815-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e37/360690/da7ce42096a5/molcellb00042-0813-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e37/360690/98d9a7887a40/molcellb00042-0814-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e37/360690/253e92e64a0c/molcellb00042-0815-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e37/360690/da7ce42096a5/molcellb00042-0813-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e37/360690/98d9a7887a40/molcellb00042-0814-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e37/360690/253e92e64a0c/molcellb00042-0815-a.jpg

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本文引用的文献

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