Egg protein helps keep chromosomes paired as eggs age, mouse study finds

Researchers in Japan have found a protein that egg cells appear to use to protect their chromosomes during the years they wait to be released. The protein, named OMC1, helps keep a molecular “glue” in place that holds each chromosome’s two copies together. In mice that could not make it, young eggs showed the kind of chromosome errors usually seen in old eggs, and the females had fewer and fewer pups as they aged.¹² The study was published in the journal Nature Aging on October 29, 2026.²

What the researchers found

Every egg a woman will ever release is formed before she is born. Each one then pauses partway through meiosis, the special kind of cell division that makes eggs and sperm, and stays paused until ovulation. In humans that can be thirty, forty or even fifty years later.²

During that long pause, a ring-shaped protein structure called REC8 cohesin holds the paired copies of each chromosome together. The egg does not make new REC8 once it enters this resting stage, so the supply it starts with has to last its whole reproductive life.² As females age, this cohesion slowly wears down, making it more likely that an egg ends up with the wrong number of chromosomes. That condition, called aneuploidy, is a major cause of infertility, miscarriage and conditions such as Down syndrome.¹

The new protein, OMC1 (short for “oocyte-specific meiotic chromosome protein 1”; oocyte is the scientific word for an immature egg), sits on the egg’s chromosomes in the same places as REC8 cohesin. It stays there from the fetal stage into adulthood.² Before this study, it was unclear whether eggs had any active way to protect their cohesin, or whether the glue simply decayed while the egg waited.²

How they found it

The team compared gene activity in fetal egg cells with that in young male germ cells, which go through a similar stage of division but do not pause for years. Of roughly 12,000 genes active in fetal eggs, only about 1,800 were specific to females.¹ They narrowed the list further using a mouse strain whose eggs fail to reach the long resting stage.¹

That search pointed to a gene listed in databases as Ccdc201, which had been described as not making a protein at all. The researchers found that it does make a protein, one shared across animals with backbones, and renamed it Omc1.¹ In mice, the protein appeared in the nuclei of egg cells from around day 17.5 of embryonic development and was not found in developing sperm cells.¹ Detailed imaging placed OMC1 within nanometers of REC8 on the chromosomes.¹

What happened in mice without it

To see what the protein does, the team used the gene-editing tool CRISPR to make mice without a working Omc1 gene.¹ At first glance the females looked normal. Their ovaries held a comparable reserve of eggs, and their eggs could start and resume division in the lab without obvious problems.¹

Closer looks told a different story:

• The glue went on normally, then faded early. In fetal eggs without OMC1, REC8 attached to the chromosomes as usual. But during the long resting stage, it began to disappear from the chromosomes.¹ This suggests OMC1 is not needed to set up the glue, only to keep it.¹
• Young eggs acted old. Even eggs from young mice showed weakened chromosome cohesion and errors in chromosome separation that resemble those often seen in aged eggs.²
• Fertility dropped early. The females had progressively smaller litters than normal mice of the same age and produced almost no pups after 30 weeks.¹ Embryos made from their eggs in the lab developed less well and more slowly, starting when the mice were as young as 8 weeks old.¹

The team also put OMC1 back into adult mouse eggs. REC8 levels on the chromosomes partly recovered and chromosome errors went down.² Unlike REC8 itself, newly made OMC1 could still attach to chromosomes in fully grown eggs.¹

According to coverage of the study, Professor Kei-ichiro Ishiguro said OMC1 should be seen not as something that stops aging itself, but as a maintenance factor that extends the chromosomal lifespan of eggs.²

What it does not show yet

This is mainly a mouse study.² The available reports describe the gene as shared across animals with backbones, but they do not describe tests in human eggs.¹ Whether OMC1 plays the same role in women, and whether differences in it help explain why some women’s eggs age faster than others’, is not addressed in these reports.

Restoring OMC1 in adult mouse eggs was a lab experiment. It partly brought back the glue and reduced errors, but the reports do not say it was tested as a treatment or that it changed how many healthy pups were born.² Mouse aging also differs from human aging: in mice, more than 95% of chromosome-bound cohesin is gone by 17 months of age, a far steeper drop than measured in women’s eggs.³

Finally, OMC1 slows the loss of one structure. It does not address the other side of egg aging, the shrinking number of eggs. A review of the field describes female fertility decline as driven by both falling egg quality and falling egg quantity.³

Who is behind it

The two reports available to Biohack describe the team’s affiliations slightly differently. One lists Sakie Iisaka, Shuhei Yoshida, Tomoya S. Kitajima and Kei-ichiro Ishiguro as being from Kumamoto University, working with colleagues at Chiba University and RIKEN.¹ The other says the work was led by Ishiguro of the Graduate School of Medicine at Chiba University, with Iisaka and Ryuki Shimada of Chiba University and Kitajima and Yoshida of the RIKEN Center for Biosystems Dynamics Research.² The reports do not describe the study’s funding or any company ties.

How it fits the field

Loss of chromosome glue is widely seen as a leading reason eggs decline with age. A review from Jilin University in China, published in Mechanisms of Ageing and Development, called weakened chromosome cohesion “a leading cause of oocyte competence decrease.”³ In women aged 20 to 32, roughly 20% of eggs have chromosome errors; by the mid-thirties, more than half do.³ Eggs from women over 40 show roughly a one-quarter to one-third drop in key cohesin proteins compared with eggs from women in their twenties.³

Other groups are trying to act on this problem. In January 2026, scientists linked to Ovo Labs, a company that wants to sell the approach, reported injecting a different chromosome-protecting protein, Shugoshin 1, into donated human eggs.⁴ They said the share of eggs with defects fell from 53% to 29%, and from 65% to 44% in women over 35.⁴ Those results were presented at the British Fertility Conference in Edinburgh, and the team said it was in talks with regulators about a clinical trial.⁴ Experts noted that a key open question is whether better eggs lead to embryos with fewer genetic errors.⁴

The OMC1 work is different in kind. It does not test a fix. It points to a natural maintenance system inside the egg that seems to slow the glue’s decline from before birth onward.²

What to watch next

• Whether other labs confirm OMC1’s role in mice and look for it in human eggs.
• Whether OMC1 levels fall in older eggs, which the current reports do not describe.
• Whether restoring OMC1 changes not just chromosome errors but the health of embryos and offspring.
• How this fits with protein-based approaches such as the Shugoshin 1 work now heading toward trials.⁴

For now, the finding is a piece of basic biology from mice: a protein that helps eggs hold on to their chromosome glue longer, and whose loss makes young eggs look older.²