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. 2020 Jan 9;102(4):975–983. doi: 10.1093/biolre/ioaa002

Figure 2.

Figure 2

TESMIN deficiency leads to male infertility with spermatogenesis defects. (a) Targeting scheme of the Tesmin KO. Tesmin consists of nine exons. Exon 3, which is shared with both splicing variants, was targeted to generate the Tesmin KO mice. Sequence highlighted in gray indicates exon 3. Red characters and red box indicate the target of sgRNA and PAM sequence, respectively. Deleted region is underlined with a double line. Arrows indicate primers. (b) Genotyping by PCR. The 316-bp sequence was deleted in em1-mutant mice. (c) Tesmin-L expression in testis detected by western blotting. CALNEXIN (ubiquitously expressed marker) was used as a control. (d) Expression of Tesmin analyzed with RT-PCR using testicular cDNA obtained from Tesmin +/+, +/em1 and KO mice (top panel). Although a faint band was observed in Tesmin KO testis, the sequence of PCR products showed that Tesmin KO mouse had a 121-bp deletion that causes a frameshift (bottom panel). Red characters indicate the sequence after deletion. (e) Number of pups that were obtained by crossing Tesmin +/em1 (n = 5) and KO (n = 3) male mice with WT female partners. (f) Comparison of the testicular weight among Tesmin +/em1 and 10- and 14-day-old KO mice and adults. (g) Comparison of the gross morphology of the testis from Tesmin +/em1 and KO male adult mice (21 weeks old).