About event
Chromosome segregation in mammalian germ cells and embryos is frequently prone to errors. This leads into frequent termination of development in oviduct or in uterus. Also, the chromosome segregation errors increase risk of severe developmental or mental disorders, such as Down syndrome. It is not entirely clear why oocytes and embryos are so frequently incorrect during segregation of their chromosomes. From somatic cells it is known, that the major role in preventing these errors and aneuploidy is played by Spindle Assembly Checkpoint (SAC). This pathway prevents transition from metaphase to anaphase when spindle apparatus is not assembled properly. It does so by blocking activation of Anaphase Promoting complex (APC/C), until all chromosomes are properly arranged on the spindle. Our results show that the SAC pathway, essential in somatic cells to prevent chromosome segregation errors, is not active in mouse embryos. Instead, they activate APC/C immediately after NEBD, not leaving time for SAC activity. This might explain increased frequency of aneuploidy leading into termination of development in mammalian embryos.
More information
This event is part of the Principal Investigator Seminar Series, the schedule of seminars can be found here.
