The ploidy conveyor of mature hepatocytes as a source of genetic variation
Andrew W. Duncan,
Matthew H. Taylor,
Raymond D. Hickey,
Amy E. Hanlon Newell,
Michelle L. Lenzi,
Susan B. Olson,
Milton J. Finegold and
Markus Grompe
Additional contact information
Andrew W. Duncan: Oregon Stem Cell Center, Papé Family Pediatric Research Institute, Oregon Health & Science University
Matthew H. Taylor: Oregon Health & Science University
Raymond D. Hickey: Oregon Stem Cell Center, Papé Family Pediatric Research Institute, Oregon Health & Science University
Amy E. Hanlon Newell: Oregon Health & Science University
Michelle L. Lenzi: Oregon Health & Science University
Susan B. Olson: Oregon Health & Science University
Milton J. Finegold: Texas Children’s Hospital, Houston, Texas 77030, USA
Markus Grompe: Oregon Stem Cell Center, Papé Family Pediatric Research Institute, Oregon Health & Science University
Nature, 2010, vol. 467, issue 7316, 707-710
Abstract:
Polyploidy in liver cells Many liver cells are polyploid, containing 4, 8, 16 or more times the haploid chromosome complement, although the significance of the phenomenon is not known. A study in mice now shows that hepatocytes can both increase and decrease their ploidy in vivo. Ploidy reversal was previously thought to be exclusive to meiosis, but this work shows that it can also occur in normal somatic cells. Increases in ploidy occur through failed cytokinesis, and decreases as a result of multipolar mitosis. The resulting genetic heterogeneity might be advantageous following hepatic injury when 'genetically robust' cells could be selected from a pre-existing pool of diverse genotypes.
Date: 2010
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:467:y:2010:i:7316:d:10.1038_nature09414
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DOI: 10.1038/nature09414
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