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. 2022 Jan 3;20:5. doi: 10.1186/s12958-021-00880-4

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Effects of SLO3 deficiency on mitochondrial function. A Influence of the SLO3 mutation on mitochondrial membrane potential (MMP). Assessment of mitochondrial membrane potential by flow cytometry acquisition for JC-1-stained (a marker of MMP) cells was performed through FL1 for green and FL2 for red fluorescence. MMP is significantly reduced in mutant sperm compared with control. B Immunoblotting of sperm lysates from controls and the SLO3-mutated individual using the anti-HSP60 antibody. β-actin was used as loading control. C The expression of HSP60 is almost diminished in SLO3 mutant spermatozoa. HSP60 staining is present in the flagellar midpiece of spermatozoa from normal controls, but significantly reduced in spermatozoa from A-132. Scale bars, 20 μm