Abstract
Inositol hexakisphosphate kinase-1 (IP6K1) is required for male fertility, but the underlying mechanisms have been elusive. Here, we report that IP6K1 is required for multiple aspects of male germ cell development. This development requires selective interactions between germ cells and Sertoli cells, namely apical ectoplasmic specialization. Spermiation (sperm release) requires tubulobulbar complexes. We found that the apical ectoplasmic specialization and tubulobulbar complexes were poorly formed or disrupted in IP6K1 KOs. Deletion of IP6K1 elicited several aberrations, including: 1, sloughing off of round germ cells; 2, disorientation and malformation of elongating/elongated spermatids; 3, degeneration of acrosomes; 4, defects in germ-Sertoli cell interactions and 5, failure of spermiation. Eventually the sperm cells were not released but phagocytosed by Sertoli cells leading to an absence of sperm in the epididymis.
Highlights
Inositol hexakisphosphate kinase (IP6K) comprises a family of three kinases, namely IP6K1, IP6K2 and IP6K31–3
Deletion of IP6K1 in mice was shown to elicit male infertility[1,11]. In agreement with this finding, we observed a complete absence of offspring from IP6K1 deleted males, whereas fertility appeared normal in IP6K1 KO females (Fig. S1a)
We examined the sexual behavior and ability of mice to mate, which appeared to be normal in the IP6K1 KO males (Fig. 1b)
Summary
Inositol hexakisphosphate kinase (IP6K) comprises a family of three kinases, namely IP6K1, IP6K2 and IP6K31–3. They found that the chromatoid body is absent in IP6K1 KO round spermatids, and the mutant spermatids failed to complete differentiation[11] Despite these advances, the influence of IP6K1 upon male germ cell development has not been fully delineated. Developing round and elongating/elongated spermatids must maintain stable attachments with Sertoli cells to prevent sloughing of immature germ cells from the seminiferous epithelium, which may result in infertility[21]. In mice apical TBCs are transiently formed at spermatogenic stage VII prior to sperm release and function to remove excess cytoplasm from spermatids[27] and to remove adhesion junctions between spermatids and Sertoli cells[26,28]. Defects of apical TBCs caused by chemical treatment or genetic mutation result in spermiation failure[30,31,32]
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