ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
BLOC1S1 Attenuates B. Melitensis 16M LPS-Triggered Autophagy by Spatial Confinement of TDP-43.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- BLOC1S1 Attenuates B. Melitensis 16M LPS-Triggered Autophagy by Spatial Confinement of TDP-43.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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14 authors.
Funding
Abstract
Biogenesis of lysosome-related organelles complex 1 subunit 1 (BLOC1S1) is considered to have anti-Brucella potential. However, the effect of BLOC1S1 on Brucella autophagy has not yet been studied. This study investigates the interplay between Brucella lipopolysaccharide (LPS) and BLOC1S1 in modulating autophagy within goat spermatogonial stem cells (mGSCs-I-SB). Using LPS from B. melitensis 16M, its capacity is demonstrated to induce AMPK-dependent autophagy, contrasting with Escherichia coli LPS, which shows no significant effect. Mechanistically, B. melitensis 16M LPS activates AMPK signaling, elevates LC3B-II/LC3B-I ratios, and upregulates lysosomal and pro-inflammatory genes. BLOC1S1 overexpression attenuates autophagy, reducing autolysosome formation (TEM) and LC3B-II/I ratio. RNA sequencing and proteomic analyses reveal BLOC1S1-mediated transcriptional reprogramming of lysosomal pathways and mitochondrial metabolism. Co-immunoprecipitation and subcellular localization studies reveal that TDP-43 is a key interacting partner and that BLOC1S1 sequesters TDP-43 in the cytoplasm, inhibiting its nuclear translocation-dependent ATG7 mRNA stability and enhancing autophagy. These findings delineate a dual regulatory mechanism: B. melitensis 16M LPS-driven, AMPK-dependent autophagy induction, and BLOC1S1-mediated autophagic suppression through spatial control of TDP-43. These results advance understanding of host-pathogen interactions in brucellosis and identify BLOC1S1 as a potential therapeutic target for bacterial persistence and TDP-43-related pathologies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.