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. 2018 Apr 17;26(1):162–178. doi: 10.1038/s41418-018-0108-5

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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 — Model of CISD function. We propose that the CISD protein family and CED-13 compete to regulate CED-9 function in the process of physiological germline apoptosis. a In the absence of a cellular signal that initiates physiological germline apoptosis, CISD functions in an anti-apoptotic/pro-survival manner. However, it is not known if this is by CISD protein(s) interacting with CED-9 and/or CED-13. b The dysregulation of any member of the cisd gene family results in increased germline apoptosis. This could be through increased CED-13 inhibition of pro-survival CED-9, given that ced-13(RNAi) suppress the increased germline apoptosis observed in animals with disrupted cisd function.