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. 2020 Nov 20;21(22):8766. doi: 10.3390/ijms21228766

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Targeting mechanism models of tRF5-GluCTC. (A) In the normal state, RSV-induced tRF5-GluCTC binds to AGO4, leading to an increase in the gene silencing activity. Upon AGO1 depletion, AGO1-associated sncRNAs are released and compete with RSV-induced tRF5-GluCTC for the loading onto AGO4, leading to less tRF5-GluCTC in AGO4 and consequently the reduced gene trans-silencing activity of tRF5-GluCTC. (B) Upon RSV infection, AGO1 binds to mRNA targets in a tRF5-GluCTC-independent manner, subsequently helping tRF5-GluCTC to find its targets. (C) Upon RSV infection, AGO1 or other unidentified molecular partners associate with mRNA targets and deliver them to the AGO4-tRF5-GluCTC complex.