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. 2017 Oct 27;8:1174. doi: 10.1038/s41467-017-01224-w

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© The Author(s) 2017

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. 5 — Autophagy is specifically induced by limited S-precursor supply for cysteine biosynthesis. a Autophagy induction in the shoot of serat tko and sir1-1 was determined by immunological detection of the canonical autophagy marker ATG8a and NBR1 with specific antisera. Lipidation of ATG8a (ATG8a-PE) (apparent size: 15–20 kDa) is essential for autophagosome formation and indicated by a significant shift during electrophoresis. NBR1 is a cargo receptor for selective autophagy and consequently degraded in autophagic bodies (D-NBR1) (apparent size: 50–75 kDa). b Level of ATG8a-PE and D-NBR1 shown in a were quantified (n = 3, mean ± s.e.m., one-way ANOVA, *p < 0.05). c Autophagy induction in the root of serat tko and sir1-1 was detected by MDC staining. White arrows marked the visible autophagic bodies. Scale bar, 25 µm. d Autophagy induction in the shoot of WT under sulfur deficiency was determined by ATG8a-PE level (n = 3, mean ± s.e.m., t-test, *p < 0.05)