bims-nocaut 2022-10-09 papers

Autophagy. 2022 Oct 05.

A Noncanonical Autophagy Function of ATG9A for Golgi Integrity and Dynamics.

Yuanyuan Meng, Qian Luo, Quan Chen, Yushan Zhu.

In mammalian cells, the Golgi apparatus serves as the central hub for membrane trafficking. Notably, the membrane trafficking and Golgi integrity are tightly regulated by reversible post-translational modifications, such as glycosylation, phosphorylation and ubiquitination. Nonetheless, how the Golgi apparatus responses to stress to ensure appropriate membrane assembly and distribution of cargo is poorly understood. The Golgi resident protein ATG9A is the only multi-spanning membrane protein in the ATG family, and has been demonstrated to traffic through the plasma membrane, endosomes, and Golgi to deliver materials for the initiation of macroautophagy/autophagy. Our recent work reveals a noncanonical function of ATG9A for Golgi dynamics and identifies a pathway for sensing Golgi stress via the MARCHF9-ATG9A axis.

Keywords: ATG9A; Golgi dynamics; Golgi stress response; MARCHF9; ubiquitination

DOI: https://doi.org/10.1080/15548627.2022.2131244

J Cell Biol. 2022 Dec 05. pii: e202206040. [Epub ahead of print]221(12):

V. cholerae MakA is a cholesterol-binding pore-forming toxin that induces non-canonical autophagy.

Xiaotong Jia, Anastasia Knyazeva, Yu Zhang, Sergio Castro-Gonzalez, Shuhei Nakamura, Lars-Anders Carlson, Tamotsu Yoshimori, Dale P Corkery, Yao-Wen Wu.

Pore-forming toxins (PFTs) are important virulence factors produced by many pathogenic bacteria. Here, we show that the Vibrio cholerae toxin MakA is a novel cholesterol-binding PFT that induces non-canonical autophagy in a pH-dependent manner. MakA specifically binds to cholesterol on the membrane at pH < 7. Cholesterol-binding leads to oligomerization of MakA on the membrane and pore formation at pH 5.5. Unlike other cholesterol-dependent cytolysins (CDCs) which bind cholesterol through a conserved cholesterol-binding motif (Thr-Leu pair), MakA contains an Ile-Ile pair that is essential for MakA-cholesterol interaction. Following internalization, endosomal acidification triggers MakA pore-assembly followed by ESCRT-mediated membrane repair and V-ATPase-dependent unconventional LC3 lipidation on the damaged endolysosomal membranes. These findings characterize a new cholesterol-binding toxin that forms pores in a pH-dependent manner and reveals the molecular mechanism of host autophagy manipulation.

DOI: https://doi.org/10.1083/jcb.202206040

J Allergy Clin Immunol. 2022 Oct;pii: S0091-6749(22)01114-9. [Epub ahead of print]150(4): 979

Retraction notice to Noncanonical autophagy in dermal dendritic cells mediates immunosuppressive effects of UV exposure J Allergy Clin Immunol Volume 145, Issue 5, May 2020, Pages 1389-1405.

Payel Sil, Jutamas Suwanpradid, Ginger Muse, Artiom Gruzdev, Liwen Liu, David L Corcoran, Cynthia J Willson, Kyathanahalli Janardhan, Sara Grimm, Page Myers, Laura Miller Degraff, Amanda S MacLeod, Jennifer Martinez.

DOI: https://doi.org/10.1016/j.jaci.2022.08.006