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. 2020 Nov 3;11:5387. doi: 10.1038/s41467-020-19170-5

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Inactivation of the HUSH component MPP8 leads to increased expression of bidirectionally-transcribed full-length young LINE-1s (L1PA1 and L1PA2), as well as primate-conserved LINE-1s with potential co-opted roles in gene regulation, (some enriched in long non-coding RNAs). Nucleic acid sensing ensues through dsRNA sensors MDA5 and RIG-I, leading to MAVS signaling and activation and secretion of type I IFNs. IFN-α/β then act on the same cells or bystander cells to mediate induction of IFN-stimulated genes through JAK-STAT signaling. MPP8-depletion is also accompanied by DNA damage and is a factor commonly downregulated in cancers, where its decreased mRNA expression is associated with a dominant IFN immune subtype signature.