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. 2021 Apr 28;19:86. doi: 10.1186/s12915-021-01017-0

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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. 4 — Prdm9-deficiency causes spermatogenic arrests in tubular stages IV and XIV of SHR rat. a Testicular histology using PAS-H staining. Illustrative examples of all 14 rat tubule stages. Degenerated cells in seminiferous tubules from adult (71 dpp) mutants stain intensively with PAS-H (blue-purple) at stages IV and XIV (red arrows). P, pachytene spermatocytes; RSP, round spermatids; ESP, elongated spermatids; S, Sertoli cells; Pl, preleptotene; L, leptotene; D, diplotene; Z-P, zygotene-pachytene spermatocytes; MI, metaphase I spermatocytes. Quantification of cells in all stages is presented in Fig. 5. b Increased apoptosis in mutant rat stage IV and XIV tubules confirmed by labeling apoptosis (TUNEL), acrosome (PNA), and DNA (Hoechst 33342)