R-loops and genomic instability in Bre1 (RNF20/40)-deficient cells

We have proposed that maintenance of genomic stability may constitute the basis for the tumor-suppressing activity of the Bre1 (RNF20/RNF40) complex. Revisiting the evidence we presented in our recent publication, we discuss the mechanism by which maintenance of genomic stability by the Bre1 complex...

Full description

Saved in:
Bibliographic Details
Published inCell cycle (Georgetown, Tex.) Vol. 11; no. 16; pp. 2980 - 2984
Main Authors Chernikova, Sophia B., Brown, J. Martin
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 15.08.2012
Landes Bioscience
Subjects
Animals
Binding
Biology
Bioscience
Calcium
Cancer
Cell
Cell Death
Chromosomal Instability
Chromosomes, Mammalian - genetics
Chromosomes, Mammalian - metabolism
CIN
Cycle
DNA - metabolism
DNA Breaks, Double-Stranded
Extra Views
Gene Silencing
Genomic Instability
H2B monoubiquitination
H3K79
Heterochromatin - genetics
Heterochromatin - metabolism
Histones - genetics
Histones - metabolism
homologous recombination
Landes
Mice
Neoplasms - genetics
Neoplasms - metabolism
Nucleic Acid Conformation
Organogenesis
Proteins
R-loop
RNA Processing, Post-Transcriptional
RNA, Messenger - genetics
RNA, Messenger - metabolism
RNA:DNA hybrids
Transcription, Genetic
Ubiquitin-Protein Ligases - genetics
Ubiquitin-Protein Ligases - metabolism
Ubiquitination
Online AccessGet full text

Cover

More Information
Summary:We have proposed that maintenance of genomic stability may constitute the basis for the tumor-suppressing activity of the Bre1 (RNF20/RNF40) complex. Revisiting the evidence we presented in our recent publication, we discuss the mechanism by which maintenance of genomic stability by the Bre1 complex is achieved through coordination of events during transcription. Among many functions of Bre1, we focus on the two that, when defective, could lead to the formation of R-loops, the RNA:DNA hybrid structures regarded as a major source of genomic instability. Specifically, we discuss the role of Bre1-mediated H2B ubiquitination in the 3′-end processing of replication-associated histone mRNA and in heterochromatic gene silencing and show how disturbance of these two functions may result in the specific pattern of chromosomal abnormalities we observe in the Bre1-depleted cells.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1538-4101
1551-4005
DOI:10.4161/cc.21090