Moira K. O’Bryan

This study shows that Hsc70Cb is essential for spermatogenesis in Drosophila, with knockdown causing sterility and sperm defects, supporting its role in human male fertility.

This study identifies CCDC112 as essential for sperm mitochondrial sheath formation and epididymal maturation, impacting fertility and motility.

This study identifies AXDND1's role in balancing spermatogonial commitment and sperm tail formation in mice and humans, showing its necessity for fertility.

The paper investigates the role of epsilon tubulin (TUBE1) in microtubule-based structures during male germ cell development in mice, showing its essential function and link to male sterility.

The paper identifies genotype-specific meiotic impairments in infertile men with loss-of-function variants in M1AP or ZZS genes, showing different recombination failures and reproductive outcomes.

This study shows that deleting Katna1 in mouse oocytes reduces fertility, while Katnal1 deletion has no effect, with defects in MII spindle morphology and fertilization rates.

This study identifies spastin's essential role in regulating microtubule dynamics during spermatogenesis, revealing its critical impact on male gamete development and function.

This study identifies genetic subforms of non-obstructive azoospermia using exome sequencing and single-cell RNA sequencing, revealing molecular groups of genes involved in spermatogenesis.

This study shows Fancm deficiency increases crossover frequencies and disrupts gametogenesis in mice, with potential implications for human genomic instability disorders.

The paper identifies de novo mutations as a significant genetic cause of male infertility, finding several candidate genes and an enrichment of loss-of-function and missense mutations in intolerant genes.

This paper systematically reviews and validates monogenic causes of human male infertility, identifying 120 genes linked to 104 infertility phenotypes and assessing their clinical validity.

This study investigates how a mutation in mir-1 affects the motility of C. elegans by analyzing kinematic parameters and power output across age.