Regulation of cardiomyocyte polyploidy and multinucleation

Liu et al have discovered a potent promoter of polyploidy in rat hearts. Polyploidy—multiple copies of the genome in one cell—is normal in cardiomyocytes but can also be ramped up in pathological situations, such as cardiac hypertrophy or in regenerative situations, such as after heart injury. The ability to boost or suppress polyploidy might thus have a number of heart health implications. Cardiomyocytes in the mammalian embryo divide just like regular cells, but shortly after birth, they stop dividing and continue replicating their DNA, creating cells with multiple nuclei. This multinucleation period lasts for about 3 weeks in rats and about 10 years in humans. Liu et al discovered that in the postnatal multinucleation phase in rats, levels of cyclin G1 protein shot up, whereas levels of other cell cycle regulators dropped. Cyclin G1, the team showed, boosted polyploidy in newborn rat cardiomyocytes, whereas the lack of cyclin G1 prevented polyploidy in newborn mice. Without cyclin G1, these mice were also less capable of increasing the number of their nuclei in response to cardiac overload and hypertrophy. Defective DNA Replication Impairs Mitochondrial Biogenesis In Human Failing Hearts (p 1541)