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. 2021 May 31;12:3263. doi: 10.1038/s41467-021-23567-1

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© The Author(s) 2021

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. 7 — Seam cell number distribution is shifted in egl-18 mutants in CB4856 (orange) compared with N2 (green) towards a higher average. Genetic variation in hsp-110 and other loci within the identified QTL regions in CB4856 may potentiate Wnt signalling and thus reinforce seam cell fate acquisition. This effect is only revealed in sensitised conditions, such as upon egl-18 loss-of-function or pop-1 RNAi.