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. 2023 Oct 27;150(21):dev201593. doi: 10.1242/dev.201593

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© 2023. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 1. — Establishment of Actl7b-deficient mice. (A) Graphical representation of CRISPR-Cas9-mediated gene editing of the Actl7b locus using two guide RNAs (black arrowheads) targeting the intron-less Actl7b-coding sequence. 473 bp were deleted, causing a frameshift leading to a premature stop. (B) Agarose gel of genotyping polymerase chain reaction of Actl7b^+/+, Actl7b^+/− and Actl7b^−/− mice (wild-type band, 607 bp; KO band, 134 bp). (C) Actl7b expression and ACTL7B immunolocalization during spermiogenesis based on literature (Hisano et al., 2003; Tanaka et al., 2003; Guo et al., 2018). ES, elongating spermatids; P, pachytene spermatocytes; RS, round spermatids; S, spermoatogonia; SP, spermatozoa. (D) Immunohistochemical staining against ACTL7B on Bouin-fixed, paraffin wax-embedded Actl7b^+/+, Actl7b^+/− and Actl7b^−/− testis sections counterstained with Hematoxylin. Scale bars: 20 μm.