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. 2018 Mar 22;9:1195. doi: 10.1038/s41467-018-03531-2

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© The Author(s) 2018

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. 8 — A proposed model of the RPL-11.2/RPL-5-PHA-4-mediated lipogenesis pathway required for nucleolar stress-induced lipid accumulation. Nucleolar stress is triggered by perturbation of pre-rRNA transcription and processing, activates PHA-4 expression, which is mediated by RPL-11.2/RPL-5 in C. elegans. Both RPL11 and RPL5 are conserved ribosomal proteins that are required for the nucleolar stress response in mammalian cells. PHA-4 subsequently binds to and transactivates the expression of the lipogenic genes pod-2 encoding acetyl-CoA carboxylase, fasn-1 encoding fatty acid synthase, and dgat-2 encoding diacylglycerol O-acyltransferase 2. Upregulated POD-2, FASN-2, and DGAT-2 expression further promotes the biosynthesis of fatty acids and triacylglycerol (TAG), leading to excessive lipid accumulation. Furthermore, the increased lipid accumulation promotes worm survival under starvation