Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 24, Issue 19, Pages 3025-3037Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E12-07-0529
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Funding
- American Cancer Society
- National Institutes of Health [R01 CA155202]
- National Science Foundation Early Faculty CAREER award
- National Science Foundation [CBET-0941143]
- Office of the Director, National Institutes of Health [DP2OD007447]
- National Institute of General Medical Sciences Center of Excellence Grant [P50 GM071508]
- Cancer Institute of New Jersey
- New Jersey Commission on Cancer Research
- National Cancer Institute [1RC1 CA147961-01]
- Johnson & Johnson Foundation
- National Institutes of Health/National Institute of General Medical Sciences [1R01 GM081686, 1R01 GM086465]
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [1262672] Funding Source: National Science Foundation
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The transition between proliferation and quiescence is frequently associated with changes in gene expression, extent of chromatin compaction, and histone modifications, but whether changes in chromatin state actually regulate cell cycle exit with quiescence is unclear. We find that primary human fibroblasts induced into quiescence exhibit tighter chromatin compaction. Mass spectrometry analysis of histone modifications reveals that H4K20me2 and H4K20me3 increase in quiescence and other histone modifications are present at similar levels in proliferating and quiescent cells. Analysis of cells in S, G(2)/M, and G(1) phases shows that H4K20me1 increases after S phase and is converted to H4K20me2 and H4K20me3 in quiescence. Knockdown of the enzyme that creates H4K20me3 results in an increased fraction of cells in S phase, a defect in exiting the cell cycle, and decreased chromatin compaction. Overexpression of Suv4-20h1, the enzyme that creates H4K20me2 from H4K20me1, results in G(2) arrest, consistent with a role for H4K20me1 in mitosis. The results suggest that the same lysine on H4K20 may, in its different methylation states, facilitate mitotic functions in M phase and promote chromatin compaction and cell cycle exit in quiescent cells.
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