Journal
JOURNAL OF CELL BIOLOGY
Volume 218, Issue 2, Pages 433-444Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201809123
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Funding
- National Institutes of Health (NIH) Transformative Research Award [R01 NS096786]
- Keck Foundation
- NOMIS Foundation
- Waitt Advanced Biophotonics Core Facility
- Razavi Newman Integrative Genomics and Bioinformatics Core Facility of the Salk Institute
- NIH National Cancer Institute Cancer Center Support Grant (NIH NCI CCSG) [P30 014195]
- National Institute of Neurological Disorders and Stroke Neuroscience Core Grant [NS072031]
- Waitt Foundation
- Chapman Foundation
- Helmsley Charitable Trust of the Razavi Newman Integrative Genomics and Bioinformatics Core Facility of the Salk Institute
- NIH NCI CCSG [P30 014195]
- Helmsley Trust
- American Diabetes Association postdoctoral fellowship [1-18-PMF-007]
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Many adult tissues contain postmitotic cells as old as the host organism. The only organelle that does not turn over in these cells is the nucleus, and its maintenance represents a formidable challenge, as it harbors regulatory proteins that persist throughout adulthood. Here we developed strategies to visualize two classes of such long-lived proteins, histones and nucleoporins, to understand the function of protein longevity in nuclear maintenance. Genome-wide mapping of histones revealed specific enrichment of long-lived variants at silent gene loci. Interestingly, nuclear pores are maintained by piecemeal replacement of subunits, resulting in mosaic complexes composed of polypeptides with vastly different ages. In contrast, nondividing quiescent cells remove old nuclear pores in an ESC RT-dependent manner. Our findings reveal distinct molecular strategies of nuclear maintenance, linking lifelong protein persistence to gene regulation and nuclear integrity.
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