Adele Marston

Chromosome segregation in mitosis and meiosis.

Adele Marston is Professor in Cell Biology at the University of Edinburgh. Her group aims to discover fundamental molecular mechanisms that direct chromosome structure and segregation during mitosis and meiosis. The goal is to understand how errors in human oocyte meiosis and the first mitotic divisions of the human embryo arise and contribute to infertility. 

Adele obtained her PhD from the University of Oxford, in the lab of Jeff Errington, and carried out postdoctoral work with John Chant at Harvard University and Angelika Amon at MIT. In 2005, she moved to the Wellcome Centre for Cell Biology in Edinburgh to establish her independent research group as a Wellcome Research Career Development Fellow and has been successively funded by Wellcome Senior Fellowships, Wellcome Investigator awards and a Wellcome Discovery award (2026). 

portrait photo of Adele Marston
Adele Marston

In 2021, she became Director of the (formerly Wellcome) Centre for Cell Biology. She is also Director of the Wellcome Discovery Research Platform for Hidden Cell Biology, established in 2023 and Co-Director of the Wellcome Integrated Cellular Mechanisms PhD programme since 2019. She is an EMBO member (2019), Fellow of the Royal Society of Edinburgh (2022) and recipient of the Genetics Society Mary Lyon Medal (2024).

Mansour Aboelenain, Eleanor Casey, Alexander Julner Dunn, Tiasha Ghosh, Marina Hamaia, Dilara Kocakaplan, Lori Koch, Matheus Leitão, Lucia Massari, Lucy Munro, Gerardus Pieper, Hollie Rowlands, Maya Rowley and Matthew Turner.


Chromosome Segregation in Mitosis and Meiosis

Specialization of chromosome segregation mechanisms in meiosis

Meiosis generates gametes with half the parental genome through two consecutive chromosome segregation events, meiosis I and meiosis II. Meiotic errors are prevalent in humans, accounting for frequent miscarriages, birth defects and infertility. Our vision is to elucidate the molecular basis of the adaptations that sort chromosomes into gametes during meiosis. We use budding and fission yeast as general discovery tools, and Xenopus and mouse oocytes to uncover meiotic mechanisms in vertebrates. Using patient-donated oocytes and ovarian tissue, we address the relevance of our findings for human fertility.

Structural and functional organisation of meiotic chromosomes

During meiosis, chromosomes undergo extensive remodelling for transmission into gametes. Chromosomes are broken and reciprocally exchanged in prophase, specifically cohered at centromeres during meiosis I and permanently separated at meiosis II. The cohesin complex is a major definer of chromosome structure, establishing intra and inter-sister chromatid linkages and providing the context for spatial control of homolog interactions. Cohesin defines a specialized chromosomal domain, called the pericentromere, surrounding each budding yeast centromere. We discovered that cohesin extrudes a chromatin loop on either side of the centromere until halted by convergent genes at pericentromere borders. We revealed that cohesin acetylation prevents extrusion through pericentromere borders and demonstrated that this boundary formation is critical for meiotic chromosome segregation. Therefore, we determined how chromosome loops are positioned to functionally structure the genome. A key ongoing focus is to understand how pericentromere structure influences its role as a signalling platform that safeguards chromosome segregation, both in the model yeast system and in human oocytes. 

Specialization of meiotic kinetochores

Kinetochores link centromeric nucleosomes to microtubules for chromosome segregation. Our goal is to understand how the kinetochore is adapted to perform its meiosis-specific functions in suppression of meiotic recombination, directing the co-segregation of sister chromatids during meiosis I, and maintaining linkages between sister chromatids until meiosis II. We defined the proteomic landscape of yeast kinetochores and centromeric chromatin during meiosis, revealing extensive remodelling during prophase and meiosis I. We are now addressing the mechanism of kinetochore remodelling, as well as its functional importance. In many organisms, sister kinetochores are fused in meiosis I, while a lack of fusion in human oocytes may account for susceptibility to segregation errors and fertility problems. Ongoing work in Xenopus, mouse and human oocytes aims to test this hypothesis.


Figure showing chromosome segregation in oocytes

Figure legend.

A. Molecular mechanism for condensin recruitment to pericentromeres. Interface between budding yeast condensin and shugoshin was identified through biochemistry, alphafold and functional analyses in vivo. 

B. Conformation of budding yeast pericentromeres in the presence or absence of microtubule-based tension. Hi-C maps of a 50kb region surrounding centromere 10.

C. Human oocytes lose centromeric cohesion protection with age. Shugoshin 2 (SGO2) forms a bridge between sister kinetochores in young oocytes, but the bridge structure tends to be lost from older oocytes.

Wang M, Robertson D, Zou J, Spanos C, Rappsilber J and Marston AL (2025) Molecular mechanism targeting condensin for chromosome condensation. EMBO J. 44, 705-735. 

Mukherjee A, Spanos C and Marston AL † (2024) Distinct roles of spindle checkpoint proteins in meiosis. Current Biology. 34, 3820-3829

Koch LB, Spanos C, Kelly V, Ly T, Marston AL (2024) Rewiring of the phosphoproteome executes two meiotic divisions in budding yeast. EMBO J. 43, 1352-1383.

Mihalas BP, Pieper GH, Aboelenain M, Munro L, Srsen V, Currie CE, Kelly DA, Hartshorne GM, Telfer EE, McAinsh AD, Anderson RA, Marston AL (2024) Age-dependent loss of cohesion protection in human oocytes. Current Biology 34, 117-131.

Paldi F, Alver B, Robertson D, Schalbetter SA, Kerr A, Kelly D, Baxter J, Neale MJ and Marston AL† (2020). Convergent genes shape budding yeast pericentromeres. Nature, 582, 119-123.


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