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Loop extrusion as a mechanism for formation of DNA damage repair foci
During the repair of double-stranded DNA breaks, cohesin mediates the extrusion of loops of DNA along which phosphorylated H2AX spreads to establish a repair zone.
- Coline Arnould
- , Vincent Rocher
- & Gaëlle Legube
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Article |
Histone H3.3 phosphorylation amplifies stimulation-induced transcription
The histone variant H3.3 is phosphorylated at Ser31 in induced genes, and this selective mark stimulates the histone methyltransferase SETD2 and ejects the ZMYND11 repressor, thus revealing a role for histone phosphorylation in amplifying de novo transcription.
- Anja Armache
- , Shuang Yang
- & Steven Z. Josefowicz
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Article |
H2A.Z facilitates licensing and activation of early replication origins
DNA replication in eukaryotes requires the histone variant H2A.Z, which binds the enzyme SUV420H1 to promote the dimethylation of histone H4, in turn recruiting the origin-recognition complex to activate early replication origins.
- Haizhen Long
- , Liwei Zhang
- & Guohong Li
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Letter
| Open AccessGenome organization and DNA accessibility control antigenic variation in trypanosomes
Long-read sequencing allows the assembly of antigen-gene arrays in Trypanosoma brucei and, coupled with deletion experiments, demonstrates that histone variants act as a molecular link between genome architecture, chromatin conformation and antigen variation.
- Laura S. M. Müller
- , Raúl O. Cosentino
- & T. Nicolai Siegel
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Brief Communications Arising |
Elsässer et al. reply
- Simon J. Elsässer
- , Kyung-Min Noh
- & Laura A. Banaszynski
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Brief Communications Arising |
On the role of H3.3 in retroviral silencing
- Gernot Wolf
- , Rita Rebollo
- & Todd S. Macfarlan
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Letter |
Histone H3.3 is required for endogenous retroviral element silencing in embryonic stem cells
Transposable elements in mammalian genomes need to be silenced to avoid detrimental genome instability; here, the histone variant H3.3 is shown to have an important role in silencing endogenous retroviral elements.
- Simon J. Elsässer
- , Kyung-Min Noh
- & Laura A. Banaszynski
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Letter |
Histone H2A.Z subunit exchange controls consolidation of recent and remote memory
The authors identify a specific histone variant as a memory-suppressor that is initially reduced in expression within the hippocampus during memory formation; as a memory is consolidated to the cortex, reduced histone association with specific plasticity genes is observed, promoting stabilization of the memory.
- Iva B. Zovkic
- , Brynna S. Paulukaitis
- & J. David Sweatt
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Article |
ANP32E is a histone chaperone that removes H2A.Z from chromatin
Human protein ANP32E is a histone chaperone that promotes removal of H2A.Z from chromatin.
- Arnaud Obri
- , Khalid Ouararhni
- & Ali Hamiche
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Article |
DAXX envelops a histone H3.3–H4 dimer for H3.3-specific recognition
The crystal structures of the histone chaperone DAXX histone-binding domain bound to a histone H3.3–H4 dimer are described; DAXX wraps around the H3.3–H4 dimer and alters its conformation.
- Simon J. Elsässer
- , Hongda Huang
- & Dinshaw J. Patel
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Letter |
Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma
Recurrent histone mutations are linked to paediatric glioblastoma multiforme, an aggressive type of brain tumour.
- Jeremy Schwartzentruber
- , Andrey Korshunov
- & Nada Jabado
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Letter |
Crystal structure of the human centromeric nucleosome containing CENP-A
- Hiroaki Tachiwana
- , Wataru Kagawa
- & Hitoshi Kurumizaka
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Letter |
Structural basis for recognition of centromere histone variant CenH3 by the chaperone Scm3
- Zheng Zhou
- , Hanqiao Feng
- & Yawen Bai
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Letter |
The histone variant macroH2A suppresses melanoma progression through regulation of CDK8
The histone variant mH2A is shown to be expressed at reduced levels in many melanomas. Loss of mH2A promotes tumour growth and metastasis via transcriptional upregulation of CDK8, a known oncogene. This study therefore reveals a new tumour suppression mechanism exerted by epigenetic modifications.
- Avnish Kapoor
- , Matthew S. Goldberg
- & Emily Bernstein