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. 2020 Apr 8;11:1741. doi: 10.1038/s41467-020-15555-8

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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. 6 — C. elegans heritably adapts to P. vranovensis exposure via a mechanism that requires CYSL-1, CYSL-2, and RHY-1. Briefly, our data indicates that parental exposure of C. elegans to P. vranovensis results in the activation of the SKN-1 transcription factor and increased expression of the cysteine synthases cysl-1 and cysl-2 and the predicted O-acyltransferase rhy-1 in offspring. These three genes are required for the observed increase in offspring survival in response to P. vranovensis infection.