A novel activity of HIV-1 Rev protein to remodel export RNPs in directing virus-specific RNA export

HIV-1 Rev蛋白诱导输出通常保留在细胞核中的单剪接HIV-1转录本(4kb-RNA)。然而，4kb-RNA是如何输出的还不清楚，因为这样的转录本应该有可能利用CRM1依赖或TAP依赖的输出，或两者兼而有之。为了了解输出机制，我们构建了模拟非洲爪哇卵母细胞输出4kb-RNA情况的模型RNA底物，并详细研究了REV的作用。我们发现，在REV存在的情况下，这种模型RNA底物仅利用CRM1依赖的输出途径。最重要的是，这种对单一RNA输出途径的承诺是通过REV不仅诱导CRM1依赖的输出而且抑制TAP依赖的输出的能力实现的。

HIV-1 Rev protein induces export of singly spliced HIV-1 transcript (4kb-RNA) that is normally retained in the nucleus. However, how 4kb-RNA is exported is not well understood, since such a transcript should have possibility of utilizing CRM1-dependent or TAP-dependent export, or both. To understand the export mechanism, we generated model RNA substrates that recapitulated the situation of export of 4kb-RNA in Xenopus oocytes, and investigated the action of Rev in detail. We found that such model RNA substrates utilized exclusively CRM1-dependent export pathway in the presence of Rev. Most importantly, this commitment to a single RNA export pathway is achieved by Rev's ability not only to induce CRM1-dependent export but also to suppress TAP-dependent export.