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Lee, Changwook
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Human atlastins are sufficient to drive the fusion of liposomes with a physiological lipid composition

Author(s)
Jang, EunhongMoon, YeojinYoon, So YoungDiaz, Joyce Anne R.Lee, MiriamKo, NahoPark, JongseoEom, Soo HyunLee, ChangwookJun, Youngsoo
Issued Date
2023-02
DOI
10.1083/jcb.202109090
URI
https://scholarworks.unist.ac.kr/handle/201301/64337
Fulltext
http://dx.doi.org/10.1083/jcb.202109090
Citation
JOURNAL OF CELL BIOLOGY, v.222, no.4, pp.e202109090
Abstract
The dynamin-like GTPase atlastin is believed to be the minimal machinery required for homotypic endoplasmic reticulum (ER) membrane fusion, mainly because Drosophila atlastin is sufficient to drive liposome fusion. However, it remains unclear whether mammalian atlastins, including the three human atlastins, are sufficient to induce liposome fusion, raising doubts about their major roles in mammalian cells. Here, we show that all human atlastins are sufficient to induce fusion when reconstituted into liposomes with a lipid composition mimicking that of the ER. Although the fusogenic activity of ATL1, which is predominantly expressed in neuronal cells, was weaker than that of ATL2 or ATL3, the addition of M1-spastin, a neuron-specific factor, markedly increased ATL1-mediated liposome fusion. Although we observed efficient fusion between ER microsomes isolated from cultured, non-neuronal cells that predominantly express ATL2-1, an autoinhibited isoform of ATL2, ATL2-1 failed to support liposome fusion by itself as reported previously, indicating that cellular factors enable ATL2-1 to mediate ER fusion in vivo. Atlastins regulate the structure and function of the endoplasmic reticulum (ER). In this study, using reconstituted proteoliposomes with a lipid composition mimicking that of the ER, Jang et al. show that all human atlastins are sufficient to drive membrane fusion.
Publisher
ROCKEFELLER UNIV PRESS
ISSN
0021-9525
Keyword
HEREDITARY SPASTIC PARAPLEGIAHOMOTYPIC ER FUSIONVERTEX RING DOMAINGOLGI-APPARATUSMEMBRANEPROTEINSGTPASESSNARESASSOCIATIONPATHWAY

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