Related Experiment Video
Updated: Aug 1, 2025

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
Published on: June 26, 2020
ATRX/DAXX: Guarding the Genome against the Hazards of ALT
Sarah F Clatterbuck Soper1, Paul S Meltzer1
1Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Abstract:
Proliferating cells must enact a telomere maintenance mechanism to ensure genomic stability. In a subset of tumors, telomeres are maintained not by telomerase, but through a homologous recombination-based mechanism termed Alternative Lengthening of Telomeres or ALT. The ALT process is linked to mutations in the ATRX/DAXX/H3.3 histone chaperone complex. This complex is responsible for depositing non-replicative histone variant H3.3 at pericentric and telomeric heterochromatin but has also been found to have roles in ameliorating replication in repeat sequences and in promoting DNA repair. In this review, we will discuss ways in which ATRX/DAXX helps to protect the genome, and how loss of this complex allows ALT to take hold.
Related Concept Videos
DNA Damage can Stall the Cell Cycle
Nucleotide Excision Repair
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...
Exon Recombination
Exon shuffling follows “splice frame rules.” Each exon...
DNA Damage Can Stall the Cell Cycle
Other Unique Bacteria
Inheritance of Chromatin Structures

