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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
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Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Laminins are the Adhesive Proteins of Basal Lamina00:55

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Laminins are heterotrimeric proteins with high molecular mass found in the extracellular matrix. Each laminin molecule is composed of three chains, viz. alpha, beta, and gamma, coded by five, four, and three paralogous genes, respectively. Laminins are categories based on the compositions of the three chains.
In humans, the five forms of alpha chains are LAMA 1, LAMA 2, LAMA 3, LAMA 4, and LAMA 5. The four forms of beta chains are LAMB 1, LAMB 2, LAMB 3, and LAMB 4. The three forms of gamma...
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Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model
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Genomic instability in laminopathy-based premature aging.

Baohua Liu1, Jianming Wang, Kui Ming Chan

  • 1Department of Biochemistry, University of Hong Kong, 21 Sassoon Road, Hong Kong.

Nature Medicine
|June 28, 2005
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Mutations in lamin A cause premature aging by disrupting DNA repair mechanisms. Unprocessed prelamin A and truncated lamin A lead to genomic instability and cellular defects, contributing to progeroid syndromes.

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Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Premature aging syndromes are linked to mutations in nuclear proteins maintaining genomic integrity.
  • Lamin A is crucial for nuclear lamina structure; its truncation causes Hutchinson-Gilford progerial syndrome (HGPS).
  • Defects in Zmpste24, a prelamin A maturating enzyme, also lead to progeroid phenotypes.

Purpose of the Study:

  • To investigate the role of Zmpste24 deficiency and unprocessed prelamin A in DNA damage response and repair.
  • To understand the molecular mechanisms linking lamin A processing defects to genomic instability and premature aging.

Main Methods:

  • Analysis of DNA damage, chromosome aberrations, and aneuploidy in Zmpste24-deficient mouse embryonic fibroblasts (MEFs) and bone marrow cells.
  • Assessment of DNA repair protein recruitment (53BP1, Rad51) to DNA lesions.
  • Functional studies in wild-type MEFs expressing unprocessible prelamin A.

Main Results:

  • Zmpste24-deficient cells exhibit increased DNA damage, chromosome aberrations, and sensitivity to DNA-damaging agents.
  • Impaired recruitment of 53BP1 and Rad51 to DNA lesions was observed in Zmpste24-/- MEFs and HGPS fibroblasts.
  • Delayed checkpoint response and defective DNA repair were evident in Zmpste24-deficient cells and cells expressing unprocessible prelamin A.

Conclusions:

  • Unprocessed prelamin A and truncated lamin A negatively impact DNA damage response and repair pathways.
  • This perturbation leads to genomic instability, a potential contributor to laminopathy-based premature aging syndromes.
  • Defective DNA repair in laminopathies highlights a critical link between nuclear lamina integrity and genome stability.