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

HIV-1 Rev蛋白诱导通常保留在细胞核中的单剪接HIV-1转录物（4kb-RNA）的输出。然而，4kb-RNA是如何输出的还没有很好的理解，因为这样的转录本应该有可能利用CRM 1依赖性或TAP依赖性输出，或两者兼而有之。为了了解输出机制，我们产生了模型RNA底物，再现了4kb-RNA在非洲爪蟾卵母细胞中的输出情况，并详细研究了Rev的作用。我们发现，这样的模型RNA基板利用专门的CRM 1依赖的出口途径中存在的Rev。最重要的是，这一承诺的一个单一的RNA出口途径是通过Rev的能力，不仅诱导CRM 1依赖的出口，但也抑制TAP依赖的出口。

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.