Barrier-to-autointegration factor: a first responder for repair of nuclear ruptures
| Autor: | Charles T Halfmann, Kyle J. Roux |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Genome instability DNA damage Nuclear Envelope Cell Barrier-to-autointegration factor Mutation Missense Review Biology 03 medical and health sciences 0302 clinical medicine medicine Animals Humans Molecular Biology Cell Nucleus Genetic Diseases Inborn Intracellular Signaling Peptides and Proteins Nuclear Proteins Cell Biology Compartmentalization (psychology) Nuclear DNA Cell biology DNA-Binding Proteins Cytosol 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Nucleus Developmental Biology |
| Zdroj: | Cell Cycle |
| Popis: | The nuclear envelope (NE) is a critical barrier between the cytosol and nucleus that is key for compartmentalization within the cell and serves an essential role in organizing and protecting genomic DNA. Rupturing of the NE through loss of constitutive NE proteins and/or mechanical force applied to the nucleus results in the unregulated mixing of cytosolic and nuclear compartments, leading to DNA damage and genomic instability. Nuclear rupture has recently gained interest as a mechanism that may participate in various NE-associated diseases as well as cancer. Remarkably, these rupturing events are often transient, with cells being capable of rapidly repairing nuclear ruptures. Recently, we identified Barrier-to-Autointegration Factor (BAF), a DNA-binding protein involved in post-mitotic NE reformation and cytosolic viral regulation, as an essential protein for nuclear rupture repair. During interphase, the highly mobile cytosolic BAF is primed to monitor for a compromised NE by rapidly binding to newly exposed nuclear DNA and subsequently recruiting the factors necessary for NE repair. This review highlights the recent findings of BAF's roles in rupture repair, and offers perspectives on how regulatory factors that control BAF activity may potentially alter the cellular response to nuclear ruptures and how BAF may participate in human disease. |
| Databáze: | OpenAIRE |
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