Human eggs are formed before birth and can remain dormant for decades before they are used. Keeping their chromosomes correctly organized during that long wait is essential for fertility – and a newly identified protein may help explain how eggs manage it.
Researchers in Japan have discovered OMC1, a protein that appears to help preserve the molecular “glue” holding chromosome copies together in immature egg cells. The study, published in Nature Aging, suggests that OMC1 helps maintain chromosome cohesion from fetal development through adulthood.
Why egg chromosomes are vulnerable
Unlike sperm, which are produced continuously after puberty, eggs are formed during the fetal stage. They then enter a dormant state called the dictyate stage, in which cell division pauses until ovulation.
During this period, a protein complex called REC8 cohesin holds together the chromosome copies created before division was paused. REC8 is not replenished during the dormant stage. As eggs age, this cohesion weakens, increasing the risk that an egg will end up with the wrong number of chromosomes—a condition known as aneuploidy. Aneuploidy is a leading cause of miscarriage, infertility and chromosomal disorders such as Down syndrome.
What OMC1 does
The research team, led by Professor Kei-ichiro Ishiguro of Chiba University, identified Omc1 by comparing gene activity in immature egg cells and male germ cells. They named the protein OMC1, short for Oocyte-specific Meiotic Chromosome protein 1.
Further experiments showed that OMC1 sits on egg chromosomes in the same locations as REC8 cohesin and remains there from the fetal stage into adulthood. When the researchers created mice lacking Omc1, REC8 began disappearing from chromosomes earlier than normal. Even young eggs from these mice showed weakened chromosome cohesion and errors in chromosome separation resembling those more often seen in older eggs.
When the researchers restored OMC1 in adult egg cells, REC8 levels on chromosomes partly recovered and chromosome errors decreased. This suggests that OMC1 actively helps keep REC8 in place rather than simply slowing the aging process itself.
A possible link to early menopause
The human counterpart of OMC1 is CCDC201. Previous genetic research has found that women homozygous for a particular stop-gain variant in CCDC201 reached menopause about nine years earlier than other women.
In the new study, the researchers tested a shortened mouse OMC1 protein corresponding to one human CCDC201 variant. The truncated protein failed to localize to egg chromosomes and could not restore chromosome cohesion. This suggests that impaired OMC1 or CCDC201 function may contribute to variation in reproductive aging, although the finding remains experimental.
What it means for fertility
The discovery does not provide a fertility treatment. It was conducted in mice and laboratory experiments, and it remains unknown whether OMC1 can be safely preserved or supplemented in human eggs.
But the work identifies a potential biological mechanism behind age-related decline in egg quality. As Professor Ishiguro noted, OMC1 should be viewed as a maintenance factor that extends the chromosomal lifespan of eggs, rather than a factor that stops aging itself.
If future research confirms similar mechanisms in humans, it could eventually inform ways to assess, protect or potentially mitigate age-related decline in egg quality. For now, the study offers an important clue to one of fertility biology’s longest-standing questions: how an egg formed before birth can keep its chromosomes intact for decades.
Source: Chiba University
