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DNA double-stranded breaks

DNA double-stranded breaks

To flag neurons that have experienced genotoxic stress, researchers developed an in vivo sensor using an adeno-associated viral vector, called PRISM. Because a cell’s DNA damage response (DDR)—which activates in response to stressors such as environmental toxins or the buildup of misfolded proteins—also responds to invading pathogens, PRISM has an easier time transfecting cells whose damage response mechanisms are preoccupied with existing DNA damage. Once inside, the virus hijacks the neuron’s DNA replication machinery, which reverts an engineered frameshift mutation in the virus and thereby prompts the production of a fluorescent protein that can be observed via microscopy.

Infographic: DNA Damage Viewed with Unprecedented Clarity

Amanda Heidt | Aug 15, 2022 | 2 min read

A new genetic sensor called PRISM makes use of a host cell’s DNA replication machinery to trigger fluorescence in neurons with damaged DNA.

DNA Damage Viewed with Unprecedented Clarity

Amanda Heidt | Aug 15, 2022 | 3 min read

A new tool called PRISM draws on virus-host interactions and a DNA repair pathway to help researchers visualize how cellular stress may contribute to neurodegenerative disease.

Without This Enzyme, Insertions Thrive in the Yeast Genome

Katarina Zimmer | Mar 1, 2019 | 3 min read

A study underscores the importance of Dna2 in maintaining the integrity of the genetic code.

the literature infographic dna repairing

Infographic: How Stray DNA Can Land in Double-Strand Breaks

Katarina Zimmer | Mar 1, 2019 | 1 min read

A study on yeast illuminates how insertions may occur.

Base Editing Now Able to Convert Adenine-Thymine to Guanine-Cytosine

Catherine Offord | Oct 25, 2017 | 8 min read

With the arrival of a new class of single-nucleotide editors, researchers can target the most common type of pathogenic SNP in humans.

Brain Activity Breaks DNA

Sabrina Richards | Mar 24, 2013 | 3 min read

Researchers find that temporary double-stranded DNA breaks commonly result from normal neuron activation—but expression of an Alzheimer’s-linked protein increases the damage.