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Updated: Aug 18, 2026

A High-Throughput In Situ Method for Estimation of Hepatocyte Nuclear Ploidy in Mice
Published on: April 19, 2020
c-Myc regulates cell size and ploidy but is not essential for postnatal proliferation in liver
Esther Baena1, Alberto Gandarillas, Mireia Vallespinós
1Department of Immunology and Oncology, Centro Nacional de Biotecnología/Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Cantoblanco, E-28049 Madrid, Spain.
Abstract:
The c-Myc protein is a transcription factor implicated in the regulation of multiple biological processes, including cell proliferation, cell growth, and apoptosis. In vivo overexpression of c-myc is linked to tumor development in a number of mouse models. Here, we show that perinatal inactivation of c-Myc in liver causes disorganized organ architecture, decreased hepatocyte size, and cell ploidy. Furthermore, c-Myc appears to have distinct roles in proliferation in liver. Thus, postnatal hepatocyte proliferation does not require c-Myc, whereas it is necessary for liver regeneration in adult mice. These results show novel physiological functions of c-myc in liver development and hepatocyte proliferation and growth.
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