Female-inherited supernumerary chromosomes that lack a male-inherited homolog are transmitted to all meiotic products instead of the expected half, which indicates an additional amplification of unpaired chromosomes during meiosis.
Prdm9-generated meiotic asynapsis of homologous chromosomes in mouse subspecific hybrids causes hybrid sterility and can be reversed by introducing random stretches of consubspecific sequence (≥ 27Mb) on four chromosomes most sensitive to asynapsis.
TcMAC21 is an appropriate “next gen” mouse model for DS research, and provides a proof of concept of using artificial chromosomes to generate non-mosaic humanized animal models of chromosome disorders.
Seemingly contradictory findings of single-molecule and in vivo experiments on a major mechanism of chromosome organization are reconciled by computationally investigating mechanisms of loop extrusion that are consistent with both.
Evolutionary adaptation to a constitutive perturbation of DNA replication reveals that adaptive mutations in three conserved pathways interact to restore faithful chromosome replication and segregation.