Black carp ATG16L1 negatively regulates STING-mediated antiviral innate immune response

Copyright © 2024 Elsevier Ltd. All rights reserved..

The precise control of interferon (IFN) production is indispensable for the host to eliminate invading viruses and maintain a homeostatic state. In mammals, stimulator of interferon genes (STING) is a prominent adaptor involved in antiviral immune signaling pathways. However, the regulatory mechanism of piscine STING has not been thoroughly investigated. Here, we report that autophagy related 16 like 1 (bcATG16L1) of black carp (Mylopharyngodon piceus) is a negative regulator in black carp STING (bcSTING)-mediated signaling pathway. Initially, we substantiated that knockdown of bcATG16L1 increased the transcription of IFN and ISGs and enhanced the antiviral activity of the host cells. Subsequently, we identified that bcATG16L1 inhibited the bcSTING-mediated IFN promoter activation and proved that bcATG16L1 suppressed bcSTING-mediated antiviral ability. Furthermore, we revealed that bcATG16L1 interacted with bcSTING and the two proteins shared a similar subcellular distribution. Mechanically, we found that bcATG16L1 attenuated the oligomerization of bcSTING, which was a key step for bcSTING activation. Taken together, our results indicate that bcATG16L1 interacts with bcSTING, dampens the oligomerization of bcSTING, and negatively regulates bcSTING-mediated antiviral activity.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:148

Enthalten in:

Fish & shellfish immunology - 148(2024) vom: 10. Apr., Seite 109483

Sprache:

Englisch

Beteiligte Personen:

Peng, Yuqing [VerfasserIn]
Liu, Xiaoyu [VerfasserIn]
Tan, Shasha [VerfasserIn]
Li, Jinyi [VerfasserIn]
Tang, Le [VerfasserIn]
Liu, Youjia [VerfasserIn]
Xiao, Jun [VerfasserIn]
Wu, Hui [VerfasserIn]
Feng, Hao [VerfasserIn]

Links:

Volltext

Themen:

9008-11-1
ATG16L1
Black carp
Fish Proteins
IFN
Interferons
Journal Article
STING
SVCV

Anmerkungen:

Date Completed 09.04.2024

Date Revised 09.04.2024

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1016/j.fsi.2024.109483

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM369482352