Retroelements versus APOBEC3 family members: No great escape from the magnificent seven.
Retroelements versus APOBEC3 family members: No great escape from the magnificent seven.
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DOI：
10.3389/fmicb.2012.00275
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发表时间：
2012
影响因子：
5.2
通讯作者：
Tokunaga K
中科院分区：
文献类型：
--
作者：
Arias JF;Koyama T;Kinomoto M;Tokunaga K
逆转录因子包括一个庞大而成功的转座遗传因子家族，通过密集的渗透，数百万年来塑造了人类和其他哺乳动物的基因组。事实上，逆转录转座子现在占人类基因组的大约45%。由于它们的基因组移动性称为反转录转座，一些反转录元件可以引起遗传疾病;这种反转录转座事件不仅发生在生殖细胞中，而且发生在体细胞中，对所有细胞群体的基因组稳定性构成威胁。作为回应，哺乳动物已经发展出内在免疫机制，提供抵抗逆转录转座的有害作用。其中，胞苷脱氨酶的APOBEC 3（A3）家族的七个成员作为高活性的、内在的抗逆转录病毒宿主因子。某些A3蛋白有效地抵抗逆转录病毒如HIV-1以及其他病毒家族的感染，同时还阻断逆转录元件的转座。基于它们在生殖细胞中的优先表达，其中反转录转座子可能是活跃的，很可能A3蛋白通过哺乳动物进化获得，主要是为了抑制反转录转座，从而维持这些细胞中的基因组稳定性。本文综述了近年来在人类基因组中活跃的逆转录因子与抗逆转录因子A3蛋白之间相互作用的研究进展。
Retroelements comprise a large and successful family of transposable genetic elements that, through intensive infiltration, have shaped the genomes of humans and other mammals over millions of years. In fact, retrotransposons now account for approximately 45% of the human genome. Because of their genomic mobility called retrotransposition, some retroelements can cause genetic diseases; such retrotransposition events occur not only in germ cells but also in somatic cells, posing a threat to genomic stability throughout all cellular populations. In response, mammals have developed intrinsic immunity mechanisms that provide resistance against the deleterious effects of retrotransposition. Among these, seven members of the APOBEC3 (A3) family of cytidine deaminases serve as highly active, intrinsic, antiretroviral host factors. Certain A3 proteins effectively counteract infections of retroviruses such as HIV-1, as well as those of other virus families, while also blocking the transposition of retroelements. Based on their preferential expression in the germ cells, in which retrotransposons may be active, it is likely that A3 proteins were acquired through mammalian evolution primarily to inhibit retrotransposition and thereby maintain genomic stability in these cells. This review summarizes the recent advances in our understanding of the interplay between the retroelements currently active in the human genome and the anti-retroelement A3 proteins.
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