Quantitative Insights into Age-Associated DNA-Repair Inefficiency in Single Cells.

08:00 EDT 20th August 2019 | BioPortfolio

Summary of "Quantitative Insights into Age-Associated DNA-Repair Inefficiency in Single Cells."

Although double-strand break (DSB) repair is essential for a cell's survival, little is known about how DSB repair mechanisms are affected by age. Here we characterize the impact of cellular aging on the efficiency of single-strand annealing (SSA), a DSB repair mechanism. We measure SSA repair efficiency in young and old yeast cells and report a 23.4% decline in repair efficiency. This decline is not due to increased use of non-homologous end joining. Instead, we identify increased G1 phase duration in old cells as a factor responsible for the decreased SSA repair efficiency. Expression of 3xCLN2 leads to higher SSA repair efficiency in old cells compared with expression of 1xCLN2, confirming the involvement of cell-cycle regulation in age-associated repair inefficiency. Examining how SSA repair efficiency is affected by sequence heterology, we find that heteroduplex rejection remains high in old cells. Our work provides insights into the links between single-cell aging and DSB repair efficiency.


Journal Details

This article was published in the following journal.

Name: Cell reports
ISSN: 2211-1247
Pages: 2220-2230.e7


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Medical and Biotech [MESH] Definitions

A poly(ADP)-ribose-binding protein that functions in the rejoining of DNA single-strand breaks that arise following treatment with alkylating agents or ionizing radiation. It interacts with DNA LIGASE III and POLY ADP RIBOSE POLYMERASE in BASE EXCISION REPAIR, and may also function in DNA processing and chromosome recombination in GERM CELLS.

Locations, on the GENOME, of GENES or other genetic elements that encode or control the expression of a quantitative trait (QUANTITATIVE TRAIT, HERITABLE).

A single-stranded DNA-binding protein that is found in EUKARYOTIC CELLS. It is required for DNA REPLICATION; DNA REPAIR; and GENETIC RECOMBINATION.

A MutL protein and component of the DNA MISMATCH REPAIR system. Its ENDONUCLEASE activity introduces SINGLE-STRAND DNA BREAKS which create entry points for EXO1 exonuclease to remove the strand containing the mismatch. It may also function in DNA DAMAGE signaling.

The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.

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