find some articles here:
The Guardian: www.theguardian.com/science/2026...
Reuters: www.reuters.com/business/hea...
The Times: www.thetimes.com/uk/science/a...
Boston Globe: www.bostonglobe.com/2026/01/09/n...

Huge thanks to @debojitsaha.bsky.social for leading this work — & to an outstanding team of co-authors: Saba Manshaei, @cavazzalab.bsky.social, Z. Holubcová, B. Maierova, A. Zielinska, L. Wartosch, M. Blaney, K. Elder & our clinical collaborators at Bourn Hall Clinic & Reprofit International (10/10)

Our findings identify centromeric cohesion protection as a modifiable determinant of egg quality.
This is, to our knowledge, the first molecular intervention shown to improve chromosome cohesion in human eggs.
(9/10)

Remarkably, SGO1 supplementation in human eggs significantly reduces premature chromatid separation and the number of single chromatids per egg.

This effect is consistent across donors. (8/10)

Human eggs show the same pattern.
Eggs from women ≥35 years have significantly reduced SGO1 and increased PSSC compared to younger donors.
Can this be rescued by supplementing SGO1? (7/10)

Crucially, restoring SGO1 levels in aged mouse eggs rescues centromeric cohesion and reduces chromosome errors to youthful levels. But what about human oocytes, do they also lose SGO1 with age? (6/10)

But how do cohesins and their protective factors change with age?
In aged mouse oocytes, we observe a decline in pericentromeric transcription, SGO1, PP2A, and centromeric cohesion.
This mirrors the dramatic rise in PSSC with age. (5/10)

We find that ongoing transcription at pericentromeres is essential to maintain SGO1 (and PP2A) on meiotic chromosomes.
Blocking transcription reduces SGO1 on chromosomes and triggers cohesion loss. (4/10)

We identify Shugoshin 1 (SGO1) as a critical protector of centromeric cohesion in mammalian eggs.
In mouse oocytes, depletion of SGO1 with siRNAs causes cohesion failure (PSSC) and alignment defects. But how is SGO1 maintained at meiotic centromeres? (3/10)

Sister chromatids must stay tightly connected until fertilization.
When cohesion fails, chromatids separate prematurely — a defect called PSSC (premature separation of sister chromatids) — leading to mis-segregation and aneuploidy. (2/10)

👉 Dive into our full review to explore these mechanisms in detail, compare strategies across species, and see how understanding protein storage in oocytes could open new paths for fertility research.
Thanks to @idajentoft.bsky.social for your great work on this review. (5/5)

But oocytes face another challenge: protein damage accumulates during the mother’s life. Proteostasis systems clear or sequester damaged proteins ensuring a rejuvenated egg. Failure here may explain age-related fertility decline, as long-lived proteins lose stability and clearance falters. (4/5)

Across species, diverse strategies have evolved to store proteins, from large filamentous assemblies to membrane bound compartments. These systems prevent premature degradation and ensure key proteins are available when needed after fertilization. (3/5)

As transcription shuts down in growing oocytes, the egg relies on maternally deposited proteins and RNAs to drive early development, until the embryo can make its own.
But how do oocytes store these proteins? (2/5)