Speakers
Takashi Akera (National Heart, Lung, and Blood Institute, USA)
The impact of genetic cheating on mammalian reproduction and speciation
Dr. Takashi Akera is a molecular biologist whose research focuses on chromosome dynamics, evolution, and non-Mendelian inheritance. He investigates how selfish genetic elements violate Mendel’s law through meiotic drive and shape mammalian reproduction and speciation. He received his PhD. in Biophysics and Biochemistry from the University of Tokyo in 2014 and completed his postdoctoral training at the University of Pennsylvania. In 2019, he joined the National Heart, Lung, and Blood Institute (NIH) as an Earl Stadtman Investigator. He has since received the NHLBI Outstanding Mentor Award (2024) and the Vilcek Prize for Creative Promise in Biomedical Sciences (2026). His laboratory combines mouse genetics, CRISPR/Cas9, high-resolution microscopy, and optogenetics to uncover the cellular and evolutionary mechanisms of meiotic drive and biased chromosome segregation.
Ahmed Balboula (University of Missouri, USA)
Spatiotemporal regulation of the oocyte spindle: New insights into aneuploidy origins
Suzanne Madgwick (Newcastle University, United Kingdom)
Studying cell cycle regulation in oocyte meiosis I by imaging mass cytometry
Marie-Emilie Terret (College de France, France)
Mechanics of oocyte divisions and impact on oocyte quality
Helena Fulkova (Institute of Experimental Medicine of the Czech Academy of Sciences, Czech Republic)
Turning back the time: Reversing DNA damage in aging oocytes
Alexander Bruce (University of South Bohemia, Czech Republic)
Beyond specification: How is the mouse blastocyst trophectoderm lineage maintained?
Kianoush Kakavand (Institute of Animal Physiology and Genetics of the Czech Academy of Sciences, Czech Republic)
Translational downregulation as a key determinant of anaphase progression in oocytes
Abstracts of the lectures, speaker profiles, and the final program, including a full list of speakers, will be updated and made available on this website.
