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. 2020 Jul 3;11:3306. doi: 10.1038/s41467-020-17163-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Membrane fractions prepared from yeast cells expressing Atg40 mutants were treated with MP in the presence or absence of Triton X-100. The samples were analyzed by immunoblotting using antibodies against HA and Kar2. Atg40-HA^MP, MP-modified Atg40-HA. The ER lumenal protein Kar2 served as a control. Kar2^MP, MP-conjugated Kar2. b ER morphology was analyzed by fluorescence microscopy. Images were focused on the center or periphery of the cells. Arrowheads indicate abnormally expanded ER sheets. c spo7-aid*-HA cells were grown on YPD agar plates in the presence or absence of IAA. The experiments were repeated independently twice (a, b) or three times (c). Scale bars: 5 μm (b), 5 mm (c).