and reconstitution systems reveal the membrane remodeling ability of LC3B and ATG16L1 to form phagophore-like membrane cups.

Autophagy

Department of Molecular, Cellular and Developmental Biology and Life Sciences Institute, University of Michigan, Ann Arbor, MI, USA.

Published: November 2024

AI Article Synopsis

  • Macroautophagy is a crucial cellular process that helps clear and recycle unwanted materials, but its detailed mechanisms are still not fully understood.
  • A recent study by Jagan et al. identified the roles of two proteins, LC3B and ATG16L1, in creating membrane structures needed for autophagy.
  • Their research highlights that the C-terminal membrane-binding domain of ATG16L1 is essential for forming these membrane cups and converting them into autophagic vesicles, providing new insights into how autophagy works.

Article Abstract

Macroautophagy/autophagy is a conserved pathway allowing the cell to clear and recycle unwanted materials. While decades of research have revealed molecular players and their hierarchical relationships in autophagy, the detailed mechanism by which these molecules function remains largely unknown. In a recent study, Jagan et al. revealed the membrane remodeling ability of two important proteins, MAP1LC3B/LC3B and ATG16L1, in autophagy. LC3B and the ATG12-ATG5-ATG16L1 complex function synergically to induce the formation of phagophore-like membrane cups on membranes both and . In addition, the authors showed that the recently characterized C-terminal membrane-binding domain of ATG16L1 is required for the cup formation and the subsequent transition to autophagic vesicles. Together this research provides more insight into the molecular function of LC3B and ATG16L1, as well as a possible mechanism for phagophore biogenesis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11572233PMC
http://dx.doi.org/10.1080/15548627.2024.2406127DOI Listing

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