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Regular Abstract Submission

Session: Exchange Lecture 2 (SRB): Novel Methods to Assess Developmental Competency

Maternal and Paternal CENP-A Equalization is Critical for Proper Mammalian Embryo Development

Wednesday, July 30, 2025
2:15 PM - 2:30 PM EDT
Location: Chinatown Room

    Author(s)

  • Dilara N. Anbarci, PhD

    Postdoctoral Fellow
    Department of Human Genetics , University of Michigan
    Ann arbor, Michigan, United States

Abstract Authors:

Dilara N. Anbarci1, Catherine A. Tower1, Emily L. Ferrell2 , Saher S. Hammoud 1,2.3



 



1 Department of Human Genetics, University of Michigan, Ann Arbor, USA



2 Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, USA



3 Department of Urology, University of Michigan, Ann Arbor, USA


Abstract Text:

Centromeric protein A (CENP-A) maintenance has been extensively studies in the context of somatic cells, however its regulation and maintenance in germ cells and embryos is far less understood.  CENP-A has been shown to be a marker of stemness as well as being essential for faithful chromosome segregation and centromere identity, and subsequently fundamental for cell division in somatic cells. Both too little and too much CENP-A is known to cause chromosomal defects in somatic cells. In the germline, we have shown that oocyte CENP-A levels are at least 10-fold higher than in sperm. However, this inherited difference in CENP-A is quickly equalized prior to the first mitotic division by the presence of a free, cytoplasmic pool of maternal CENP-A protein. This equalization is reliant on the asymmetric recruitment of maternal CENP-C and MIS18BP1. Interestingly, reducing overall CENP-A levels does not impair equalization, but reduces total CENP-A levels in both pronuclei. However, reducing maternal CENP-C disrupts CENP-A equalization. Failure to reach optimal levels of CENP-A (either in CENP-A KD) or equalize CENP-A (as seen in CENP-C KD) leads to an increase frequency of missegregated chromosomes and micronuclei. To determine whether CENP-A equalization relies on sensing asymmetry or requires the presence of a maternal pronucleus, we generated androgenetic embryos and found that paternal CENP-A accumulation is regulated by paternal chromatin state, suggesting a paternally intrinsic mechanism for regulation of CENP-A equalization in the early embryo. Experiments are currently underway to determine whether maternal accumulation requires the presence of paternal CENP-A.