Fig. 2: Phenotypic defects produced by the Drosophila CG9222 mutation. | Communications Biology

Fig. 2: Phenotypic defects produced by the Drosophila CG9222 mutation.

From: Testis-specific serine/threonine kinase dTSSK2 regulates sperm motility and male fertility in Drosophila

Fig. 2

a CRISPR/Cas9-mediated dTSSK2 gene disruption in Drosophila. Sequencing results revealed the deletion of two bases in the coding region of the dTSSK2 gene, resulting in formation of a premature stop codon and complete removal of the S_TKc kinase catalytic domain. b The mRNA expression levels in testicular extracts from wild-type and dTSSK2−/− flies were assessed by RT-qPCR analysis. c Qualitative fertility assay of wild-type (w1118), dTSSK2−/− and P{dTSSK2}; dTSSK2−/− male flies (n = 10 per group). Data are mean ± SEM. d Live imaging of testes and seminal vesicles of the indicated genotypes. Sperm nuclei (green) are labeled with protamine GFP-Mst35Bb. Cytological examination showing defects of whole testes in dTSSK2−/− male flies. Scale bar, 100 μm. e Quantification of tail-beat frequency of sperm by wild-type (w1118) or dTSSK2 mutant males (n = 30 per group). Data are mean ± SEM.

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