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Reduced CHMP7 Expression Compromises Telomere Integrity in Mammalian Cells
Romina Burla1,2, Mattia La Torre1, Klizia Maccaroni1
1Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome, 00185 Rome, Italy.
Cells
|February 12, 2026
Summary
The ESCRT machinery, crucial for nuclear envelope reassembly, also maintains telomere integrity. Disrupting key factors like CHMP7 leads to DNA damage and telomere defects, highlighting new therapeutic targets.
Area of Science:
- Cell Biology
- Genetics
- Molecular Biology
Background:
- Nuclear envelope reassembly during mitosis requires the ESCRT machinery, initiated by BAF1 and LEM2.
- Telomeres are enriched at the reforming nuclear envelope, suggesting a potential role for ESCRT factors in telomere maintenance.
Purpose of the Study:
- To investigate the contribution of ESCRT factors to telomere integrity during nuclear envelope reassembly.
- To explore the functional relationships between ESCRT components and known telomere regulatory pathways.
Main Methods:
- Investigated the effects of reducing ESCRT factor CHMP7 on DNA damage, heterochromatin, and telomere structure.
- Analyzed the contribution of other ESCRT components (TSG101, VPS28, CHMP4B, AKTIP/Ft1) to telomere integrity.
- Performed genetic interaction analyses to map pathways involving CHMP7, CHMP4B, AKTIP/Ft1, TNKS1, BAF1, and LEM2.
Main Results:
- Reduction of CHMP7 caused DNA damage, heterochromatin disorganization, and telomere defects (sister telomere associations, telomere free ends).
- TSG101, VPS28, CHMP4B, and AKTIP/Ft1 also contribute to telomere integrity, with varying strengths.
- CHMP7 functions in a common pathway with CHMP4B and AKTIP/Ft1, and in parallel to TNKS1.
- BAF1 and LEM2 are involved in safeguarding telomeres during nuclear envelope reassembly.
Conclusions:
- ESCRT factors play a significant role in maintaining telomere integrity during nuclear envelope reformation.
- Findings provide new insights into nuclear deformation disorders like aging and cancer.
- Identified potential targets for modulating telomere maintenance pathways.
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