A 'male-harming' mtDNA mutation has been identified in Drosophila and impairs male fertility without impairing other male or female functions.

Spermatozoa require GIV for specialized compartmentalized signaling to support efficient capacitation while inhibiting premature acrosome reaction.

Bi-allelic mutations in ZMYND12, encoding a novel axonemal protein interacting with TTC29 and DNAH1, cause male infertility and flagellum defects in human and Trypanosoma.

Cylicin 1 and Cylicin 2 are essential components of the sperm perinuclear theca and their loss results in impaired spermiogenesis and thus in infertility in mice and men.

ADGRG2, an orphan GPCR, when coupled to CFTR via a regional Gq signaling on the apical membrane, acts to regulate efferent duct fluid reabsorption making it essential for male fertility.

Mitochondrial genomes harbor male-fertility-reducing mutations that can be harnessed to control population viability as a novel approach to control economic and environmental pests.

Study of human, knockout mice, and in-vitro models revealed CEP78 absence is the genetical cause of cone-rod dystrophy and male infertility with multiple morphological abnormalities of sperm flagella, CEP78 interacted with IFT20 and TTC21A to modulate cilliogenesis and centriole length.

Androglobin, a newly identified mammalian globin with a unique modular structure including a protease and calmodulin binding IQ domain within a circularly permuted globin domain, is implicated in murine spermatogenesis.

Sperm production and male fertility in Drosophila melanogaster depend on transcripts generated from the AAGAG(n) repeated satellite DNA within primary spermatocytes.

In addition to its academic merits, characterizing the genetic determinants of male (in)fertility and identifying clinically actionable genetic variants can lead to improved diagnosis or even treatment of such conditions.