
Disruption of the full-length BEND2 protein leads to reduced primordial follicle pool, impaired oocyte quality, and accelerated decline in female fertility in mice.


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Reproductive aging, characterized by a decline in female reproductive potential, is a significant biomedical challenge. A key factor in reproductive aging is the depletion of the ovarian reserve, the pool of primordial follicles in the ovary. Recent studies have implicated BEND2, a BEN domain-containing protein family member, in mammalian spermatogenesis. In the testis, Bend2 expresses two protein isoforms: full-length and truncated. Ablation of both proteins results in an arrested spermatogenesis. Because the Bend2 locus is on the X chromosome, and the Bend2-/y mutants are sterile, Bend2 ’s role in oogenesis remained elusive.

In this study, we employed a novel Bend2 mutation that completely blocks the expression of the full-length BEND2 protein but allows the expression of the truncated BEND2 isoform. However, this mutation does not confer male sterility, allowing us to investigate BEND2’s role in mice’s oocyte quality, follicular dynamics, and fertility. Our findings demonstrate that full-length BEND2 is dispensable for male fertility, and its ablation leads to impaired oocyte quality, reduced follicular formation, and an accelerated decline in fertility. These results reveal a critical role for BEND2 in oogenesis and provide insights into the mechanisms underlying reproductive aging. Furthermore, these findings hold relevance for the diagnostic landscape of human infertility.

### Competing Interest Statement

The authors have declared no competing interest.

BEND2 is a crucial player in oogenesis and reproductive aging

disruption-of-bend2-leads-to-impaired-oogenesis-and-accelerated-reproductive-aging-in-mice


Disruption of BEND2 Leads to Impaired Oogenesis and Accelerated Reproductive Aging in Mice
