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原生动物和真菌细胞表面变异性的遗传和表观遗传机制。

Genetic and epigenetic mechanisms underlying cell-surface variability in protozoa and fungi.

作者信息

Verstrepen Kevin J, Fink Gerald R

机构信息

Laboratory for Systems Biology, VIB, B-3001 Leuven, Belgium.

出版信息

Annu Rev Genet. 2009;43:1-24. doi: 10.1146/annurev-genet-102108-134156.

Abstract

Eukaryotic microorganisms have evolved ingenious mechanisms to generate variability at their cell surface, permitting differential adherence, rapid adaptation to changing environments, and evasion of immune surveillance. Fungi such as Saccharomyces cerevisiae and the pathogen Candida albicans carry a family of mucin and adhesin genes that allow adhesion to various surfaces and tissues. Trypanosoma cruzi, T. brucei, and Plasmodium falciparum likewise contain large arsenals of different cell surface adhesion genes. In both yeasts and protozoa, silencing and differential expression of the gene family results in surface variability. Here, we discuss unexpected similarities in the structure and genomic location of the cell surface genes, the role of repeated DNA sequences, and the genetic and epigenetic mechanisms-all of which contribute to the remarkable cell surface variability in these highly divergent microbes.

摘要

真核微生物已经进化出巧妙的机制来在其细胞表面产生变异性,从而实现差异性黏附、快速适应不断变化的环境以及逃避免疫监视。酿酒酵母和病原体白色念珠菌等真菌携带一组黏蛋白和黏附素基因家族,这些基因允许它们黏附于各种表面和组织。克氏锥虫、布氏锥虫和恶性疟原虫同样含有大量不同的细胞表面黏附基因库。在酵母和原生动物中,该基因家族的沉默和差异表达都会导致表面变异性。在这里,我们讨论了细胞表面基因在结构和基因组位置上意想不到的相似性、重复DNA序列的作用以及遗传和表观遗传机制——所有这些都促成了这些高度不同的微生物中显著的细胞表面变异性。

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