Proteostasis regulated by testis-specific ribosomal protein RPL39L maintains mouse spermatogenesis

Maintaining proteostasis is important for animal development. How proteostasis influences spermatogenesis that generates male gametes, spermatozoa, is not clear. We show that testis-specific paralog of ribosomal large subunit protein RPL39, RPL39L, is required for mouse spermatogenesis. Deletion of Rp vertical bar 39 vertical bar in mouse caused reduced proliferation of spermatogonial stem cells, malformed sperm mitochondria and flagella leading to sub-fertility in males. Biochemical analyses revealed that lack of RPL39L deteriorated protein synthesis and protein quality control in spermatogenic cells, partly due to reduced biogenesis of ribosomal subunits and ribosome homeostasis. RPL39/RPL39L is likely assembled into ribosomes via H/ACA domain containing NOP10 complex early in ribosome biogenesis pathway. Furthermore, Rp vertical bar 39 vertical bar null mice exhibited compromised regenerative spermatogenesis after chemical insult and early degenerative spermatogenesis in aging mice. These data demonstrate that maintaining proteostasis is important for spermatogenesis, of which ribosome homeostasis maintained by ribosomal proteins coordinates translation machinery to the regulation of cellular growth.

Automated summary

The study found that the ribosomal large subunit protein gene RPL39L is essential for mouse spermatogenesis, as its deletion leads to reduced fertility. Furthermore, the lack of RPL39L also affects the sperm mitochondria and flagella, which in turn affects sperm quality. These results demonstrate that maintaining proteostasis is crucial for spermatogenesis.