2. Academic Validation
  3. lncRNA Sensing of a Viral Suppressor of RNAi Activates Non-canonical Innate Immune Signaling in Drosophila

lncRNA Sensing of a Viral Suppressor of RNAi Activates Non-canonical Innate Immune Signaling in Drosophila

  • Cell Host Microbe. 2020 Jan 8;27(1):115-128.e8. doi: 10.1016/j.chom.2019.12.006.
Liqin Zhang 1,  Wen Xu 1,  Xinlei Gao 1,  Wenjie Li 1,  Shuishui Qi 1,  Dongyang Guo 1,  Olugbenga Emmanuel Ajayi 1,  Shou-Wei Ding 2,  Qingfa Wu 3
Affiliations

Affiliations

  • 1 Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
  • 2 Department of Microbiology and Plant Pathology, Institute for Integrative Genome Biology, University of California, Riverside CA, USA.
  • 3 Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: wuqf@ustc.edu.cn.
PMID: 31917956 DOI: 10.1016/j.chom.2019.12.006
Abstract

Antiviral immunity in insects is mediated by the RNA interference (RNAi) pathway. Viruses evade Antiviral RNAi by expressing virulence factors known as viral suppressors of RNAi (VSR). Here, we report the identification of VINR, a Drosophila VSR-interacting long non-coding (lnc) RNA that activates non-canonical innate immune signaling upon detection of the dsRNA-binding VSR of Drosophila C virus (DCV). VINR is required for the induction of antimicrobial peptide (AMP) genes but dispensable for Antiviral RNAi. VINR functions by preventing the ubiquitin proteasome-dependent degradation of Cactin, a coiled-coil and arginine-serine-rich domain-containing protein that regulates a non-cannonical antimicrobial pathway for AMP induction. CRISPR-Cas9 knockout of VINR in Drosophila cells enhances DCV replication independently of Antiviral RNAi, and VINR-knockout adult flies exhibit enhanced disease susceptibility to DCV and bacteria. Our findings reveal a counter counter-defense strategy activated by a lncRNA in response to the viral suppression of the primary Antiviral RNAi immunity.

Keywords

Cactin; Deaf1; Drosophila; IMD pathway; RNAi immunity; Toll pathway; counter counter-defense; lncRNA; viral suppressors of RNAi; virus.

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