Loss of BECN1 does not compromise autophagosome formation but alters cargo selection and HLA-restricted antigen presentation of B cells.

Authors

Svenja L Walter, Felix Baur Lermer, Sophie Buchser, Sibilla Sander, Kennith Brian Castelino, Marcel Wacker, Eanna Fennell, Lisa Rieble, Saskia von Boxberg, Sandra Schmid, Christopher A Hess, Laure-Anne Ligeon, Juliane Walz, Muriel Mari, Fulvio Reggiori, Jörn Dengjel, Christian Münz

Published in

Autophagy. Aug 21, 2026. Epub Aug 21, 2026.

Abstract

BECN1 (beclin 1) is a member of the nucleation complex and considered crucial for induction of macroautophagy/autophagy, leading to the formation and ultimate degradation of autophagosomes. We found that in human B lymphoblastoid cell lines (LCLs) deficient of BECN1 (BECN1-KO), autophagosome formation was intact and autophagic flux could be induced upon nutrient starvation or MTOR inhibition. Remarkably, autophagosomal cargo differed significantly between BECN1-KO and control (CTRL) LCLs, revealing a preferred formation of autophagosomes at the endoplasmic reticulum (ER) and not at endosomes/lysosomes in BECN1-KO LCLs. Endosomal TLR3 (toll like receptor 3) was less frequently incorporated within autophagosomes in BECN1-KO LCLs. Additionally, several proteins of the ER-resident peptide loading complex for MHC class I antigen presentation were found enriched in autophagosomes from BECN1-KO LCLs, resulting in a diminished detection of BECN1-KO LCLs by T cells. Hence, BECN1 seems to be dispensable for autophagosome formation but rather contributes to cargo selection of phagophores and immunosurveillance.

PMID:
42625472
Bibliographic data and abstract were imported from PubMed on 21 Aug 2026.

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