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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...

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Studies of Chaperone-Cochaperone Interactions using Homogenous Bead-Based Assay
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Published on: July 21, 2021

Hsp90 modulates CAG repeat instability in human cells.

David Mittelman1, Kristen Sykoudis, Megan Hersh

  • 1Human Genome Sequencing Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Cell Stress & Chaperones
|April 8, 2010
PubMed
Summary

Heat shock protein 90 (Hsp90) stabilizes CAG repeat lengths in human cells. Impairing Hsp90 causes repeat contractions, suggesting a role in generating genetic variation.

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Area of Science:

  • Molecular biology
  • Genetics
  • Evolutionary biology

Background:

  • Heat shock protein 90 (Hsp90) is a molecular chaperone involved in evolution by revealing cryptic variation.
  • Hsp90 inhibition sensitizes cancer cells to DNA-damaging agents, suggesting a role in DNA repair.

Purpose of the Study:

  • To investigate the role of Hsp90 in modulating the stability of nucleotide repeats.
  • To explore how Hsp90 influences genetic variation and phenotypic expression.

Main Methods:

  • Impairment of Hsp90 in human cells.
  • Inhibition of the recombinase Rad51.
  • Analysis of CAG repeat track stability and gene-inactivating point mutations.

Main Results:

  • Hsp90 impairment induced tenfold contractions of CAG repeat tracks in human cells.
  • Inhibition of Rad51 caused similar increases in repeat instability.
  • Hsp90 inhibition did not affect the rate of gene-inactivating point mutations.

Conclusions:

  • Hsp90, through homologous recombination via Rad51, stabilizes CAG repeat tracts.
  • Hsp90 may facilitate the expression of new phenotypes by inducing genetic variation through modulation of repeat lengths.