Journal
HEPATOLOGY
Volume 63, Issue 1, Pages 247-259Publisher
WILEY
DOI: 10.1002/hep.28281
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Funding
- National Research Foundation - Korean government [2014R1A2A1A10050775, 2011-0030043]
- National Cancer Center, Republic of Korea [NCC-1410673]
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Hepatocyte chromosome polyploidization is an important feature of liver development and seems to be required for response to liver stress and injury signals. However, the question of how polyploidization can be tightly regulated in liver growth remains to be answered. Using a conditional knockout mouse model, liver-specific depletion of Ssu72 protein phosphatase was found to result in impairment in regulation of polyploidization. Interestingly, the aberrant polyploidization in Ssu72-depleted mice was associated with impaired liver damage response and increased markers of liver injury and seemed to mimic the phenotypic features of liver diseases such as fibrosis, steatosis, and steatohepatitis. In addition, depletion of Ssu72 caused deregulation of cell cycle progression by overriding the restriction point of the cell cycle and aberrantly promoting DNA endoreplication through G(2)/M arrest. Conclusion: Ssu72 plays a substantial role in the maintenance of hepatic chromosome homeostasis and would allow monitoring of liver function. (Hepatology 2016;63:247-259)
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