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RECQL5/Recql5 helicase regulates homologous recombination and suppresses tumor formation via disruption of Rad51 presynaptic filaments.
TLDR
This work shows that deletion of Recql5 in mice results in cancer susceptibility and identifies RECQL5 as an important tumor suppressor that may act by preventing inappropriate HR events via Rad51 presynaptic filament disruption.
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Cancer predisposition caused by elevated mitotic recombination in Bloom mice
TLDR
It is demonstrated that the increased rate of loss of heterozygosity (LOH) resulting from mitotic recombination in vivo constitutes the underlying mechanism causing tumour susceptibility in these mice.
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Transcription factors activated in mammalian cells after clinically relevant doses of ionizing radiation
TLDR
A review of the literature demonstrates that extrapolation from high doses of IR to low doses ofIR is inaccurate for most transcription factors and most IR-inducible transcripts/proteins, and that induction of transactivating proteins at low doses must be empirically derived.
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Recql5 and Blm RecQ DNA Helicases Have Nonredundant Roles in Suppressing Crossovers
TLDR
It is shown that in mouse embryonic stem (ES) cells, mutations in either the Bloom syndrome homologue (Blm) or the Recql5 genes result in a significant increase in the frequency of sister chromatid exchange (SCE), whereas deleting both Blm and RecQL5 lead to an even higher frequency of SCE.
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15-Hydroxyprostaglandin dehydrogenase, a COX-2 oncogene antagonist, is a TGF-beta-induced suppressor of human gastrointestinal cancers.
TLDR
It is determined that colonic 15-PGDH expression is directly controlled and strongly induced by activation of the TGF-beta tumor suppressor pathway, delineate an enzymatic pathway that induces colon cancer suppression.
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Regulation of alternative splicing by local histone modifications: potential roles for RNA-guided mechanisms
TLDR
Recent studies are discussed that connect two previously separate avenues of investigation, beginning with the unexpected discoveries that nucleosomes are preferentially positioned over exons and DNA methylation and certain histone modifications also show exonic enrichment, which have profound implications linking chromatin structure, histone modification and splicing regulation.
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Defective sister-chromatid cohesion, aneuploidy and cancer predisposition in a mouse model of type II Rothmund-Thomson syndrome.
TLDR
Observations provide evidence for a previously unsuspected role for Recql4 in sister-chromatid cohesion, and suggest that the chromosomal instability may be the underlying cause of cancer predisposition and birth defects in these mutant mice.
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Hu proteins regulate alternative splicing by inducing localized histone hyperacetylation in an RNA-dependent manner
TLDR
It is proposed that splicing regulators may actively modulate chromatin structure when recruited to their target RNA sequences cotranscriptionally and this “reaching back” interaction with chromatin provides a means to ensure accurate and efficient regulation of alternative splicing.
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The p97-UBXD8 complex destabilizes mRNA by promoting release of ubiquitinated HuR from mRNP.
TLDR
A previously unknown mechanism that implicates the ATPase p97, a protein-remodeling machine, in the dynamic regulation of mRNP disassembly is reported, revealing a new paradigm in RNA biology: nondegradative ubiquitin signaling-dependent disassembly ofmRNP promoted by the p97-UBXD8 complex to control mRNA stability.
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Recql5 plays an important role in DNA replication and cell survival after camptothecin treatment.
TLDR
It is reported that the deletion of RecQ helicase Recql5 in mouse ES cells and embryonic fibroblast cells resulted in a significant increase in CPT sensitivity and a profound reduction in DNA replication after the treatment with CPT, but not other DNA-damaging agents.
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