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Journal Article

RECQL5 controls transcript elongation and suppresses genome instability associated with transcription stress.

MPS-Authors
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Söding,  J.
Research Group of Computational Biology, MPI for Biophysical Chemistry, Max Planck Society;

Fulltext (public)

2086652.pdf
(Publisher version), 3MB

Supplementary Material (public)

2086652_Suppl_1.xlsx
(Supplementary material), 567KB

2086652_Suppl_2.xlsx
(Supplementary material), 81KB

2086652_Suppl_3.xlsx
(Supplementary material), 54KB

2086652_Suppl_4.xlsx
(Supplementary material), 67KB

2086652_Suppl_5.pdf
(Supplementary material), 5MB

Citation

Saponaro, M., Mitter, R., Kantidakis, T., Kelly, G. P., Heron, M., Williams, H., et al. (2014). RECQL5 controls transcript elongation and suppresses genome instability associated with transcription stress. Cell, 157(5), 1037-1049. doi:10.1016/j.cell.2014.03.048.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0024-AF4E-9
Abstract
RECQL5 is the sole member of the RECQ family of helicases associated with RNA polymerase II (RNAPII). We now show that RECQL5 is a general elongation factor that is important for preserving genome stability during transcription. Depletion or overexpression of RECQL5 results in corresponding shifts in the genome-wide RNAPII density profile. Elongation is particularly affected, with RECQL5 depletion causing a striking increase in the average rate, concurrent with increased stalling, pausing, arrest, and/or backtracking (transcription stress). RECQL5 therefore controls the movement of RNAPII across genes. Loss of RECQL5 also results in the loss or gain of genomic regions, with the breakpoints of lost regions located in genes and common fragile sites. The chromosomal breakpoints overlap with areas of elevated transcription stress, suggesting that RECQL5 suppresses such stress and its detrimental effects, and thereby prevents genome instability in the transcribed region of genes.