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Related Concept Videos

Other Unique Bacteria01:18

Other Unique Bacteria

Magnetic bacteria exhibit a directed movement called magnetotaxis, driven by structures called magnetosomes. These magnetosomes consist of chains of magnetic particles made of either magnetite (Fe₃O₄) or greigite (Fe₃S₄) and are organized in a linear conformation by a protein scaffold within invaginations of the cell membrane. The bacteria align along the north–south magnetic field lines, much like a compass needle. They are typically microaerophilic or anaerobic and are commonly found near the...
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Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
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Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
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...
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Nucleotide Excision Repair

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DNA Damage Can Stall the Cell Cycle

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Related Experiment Video

Updated: May 29, 2026

Immunofluorescence Microscopy of γH2AX and 53BP1 for Analyzing the Formation and Repair of DNA Double-strand Breaks
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AT cells are not radiosensitive for simple chromosomal exchanges at low dose.

Megumi Hada1, Janice L Huff, Zarana S Patel

  • 1USRA Division of Life Sciences, Houston, TX 77058, USA.

Mutation Research
|September 6, 2011
PubMed
Summary

Cells with ATM or NBS mutations show increased chromosomal aberrations after high radiation doses. However, this study reveals that ataxia telangiectasia cells do not exhibit heightened sensitivity to low-dose radiation.

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Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH
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Immunofluorescence Microscopy of γH2AX and 53BP1 for Analyzing the Formation and Repair of DNA Double-strand Breaks
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Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation
11:24

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Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH
07:54

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

Published on: August 19, 2014

Area of Science:

  • Radiobiology
  • Cell Biology
  • Genetics

Background:

  • Cells deficient in ATM (ataxia-telangiectasia) or NBS (Nijmegen breakage syndrome) exhibit elevated chromosomal aberrations post high-dose ionizing radiation.
  • Previous research indicated a larger quadratic dose-response for aberrations in ATM/NBS-deficient cells compared to normal fibroblasts.

Purpose of the Study:

  • To investigate the response of ATM-deficient cells to low-dose ionizing radiation.
  • To determine if the increased chromosomal aberration sensitivity observed at high doses persists at low doses in ATM-deficient cells.

Main Methods:

  • Chromosomal aberration analysis was conducted on cells at low dose-rates (0.5Gy/d).
  • ATM kinase inhibitor (KU-55933) and siRNA knockdown were used to assess ATM's role in normal cells.
  • Comparison of aberration yields between wild-type, ATM-deficient, and NBS-deficient cells.

Main Results:

  • ATM-deficient cells showed no increased sensitivity to chromosomal exchanges at radiation doses below 1Gy.
  • Normal lung fibroblasts treated with an ATM inhibitor or ATM siRNA did not show increased exchanges at doses ≤0.5Gy.
  • The high background level of exchanges in AT cells complicated low-dose response analysis.

Conclusions:

  • The heightened sensitivity of ataxia-telangiectasia cells for chromosomal exchanges observed at high radiation doses is not present at low doses.
  • ATM kinase activity is crucial for the response to higher radiation doses but less so at very low doses.