Special Issue "Chromatin Assembly"

Guest Editor
Prof. Dr. Alexandra Lusser
Division of Molecular Biology, Biocenter, Innsbruck Medical University, Innsbruck, Austria
Website: http://mol-biol.i-med.ac.at/staff/a_lusser.html
E-Mail: alexandra.lusser@i-med.ac.at
Phone: +43 512 9003 70210
Fax: +43 512 9003 73100

Dear Colleagues,

In eukaryotic cells genomic DNA and the highly conserved histone proteins form a nucleoprotein complex that is termed chromatin. Chromatin is a dynamic entity that varies in structure throughout the cell cycle. The basic repeating unit of the chromatin, the nucleosome, consists of 147 bp of DNA wrapped around an octamer of the histones H2A, H2B, H3 and H4.  Chromatin assembly is a tightly regulated process that occurs during DNA replication, when parental and de novo synthesized histones are distributed among newly replicated DNA strands. Moreover, nucleosome assembly is required during transcription and in DNA repair and recombination. Thus, chromatin assembly is an integral part of many important DNA-utilizing processes.

In recent years it has become apparent that different mechanisms are used to assemble chromatin in a highly specific way involving a multitude of factors. The major components of chromatin assembly pathways are histone chaperones and ATP-dependent factors belonging to the SNF2 family of proteins. Several factors, such as the histone chaperones CAF1 or ASF1 or the ATPase ISWI, have been found to play important roles in replication-dependent assembly. In contrast, the chaperones Hira, Daxx and Dek and the ATPases CHD1, SWR1 and ATRX have been linked to replication-independent incorporation of histone variants. This Special Issue on Chromatin Assembly is dedicated to the review of recent developments in the field as well as to the featuring of research contributions that will further our understanding of the mechanisms that govern establishment and maintenance of the chromatin structure in the cell.

Alexandra Lusser
Guest Editor

Submission

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• histone chaperone
• chromatin remodelling factor
• histone variant exchange
• replication-dependent chromatin assembly
• de novo chromatin assembly
• chromatin disassembly
• heterochromatin assembly
• histone H1 incorporation

Type of Paper: Article
Title: A TMA-Based Evaluation of Tumor Prognosis by Immunohistochemistry for Chromatin Assembly Factor-1 (CAF-1)p60
Author: Stefania Staibano
Affiliation: Department of Biomorphological and Functional Sciences, Pathology Section, Chief of Head and Neck Morphofunctional Pathology Unit, University Federico II of Naples, School of Medicine, via Pansini 5, 80131 Naples, Italy; E-Mail: staibano@unina.it
Abstract: The traditional clinical and morphological parameters does not allow a reliable characterization of the biological behaviour of malignant tumors. There is the urgent need for the identification of new molecular alterations predictive of tumor prognosis. The epigenetic, post-synthetic modification of chromatin proteins regulating the access to DNA information is involved in the pathogenesis and evolution of most malignancies. The Chromatin Assembly Factor-1 (CAF-1), istone chaperone, with a highly specialized role in DNA replication and in DNA-repair process, has been shown to be a new, sensible marker of cell proliferation with a prognostic role in many human tumors. We will describe the role of CAF-1/p60 protein as a new prognostic marker for a series of malignant human tumors with different histogenesis, evaluated by immunohistochemistry on tissue microarrays sections.

Type of Paper: Review
Title: FACT as a Regulator of Free Histones Levels
Authors: Douglas Maya, Macarena Morillo-Huesca, Sebastián Chávez and Mari-Cruz Muñoz-Centeno
Affiliation: Departamento de Genética, Avda. Reina Mercedes nº6, 41012 Sevilla, Spain; E-Mail: mcmunoz@us.es (M.-C.M.-C.)
Abstract: FACT is an essential chromatin assembly factor which mediates chromatin transactions during the progression of different essential DNA-related events, such as transcription, replication and repair. To avoid deleteriuous effects of free histones accumulation, cells keep a delicate balance between histones levels and chromatin assembly. Accordingly, histones levels are regulated transcriptionally, posttranscriptionally, translationally and posttranslationally. Recently, our group has demonstrated a novel source of free histones in yeast cells, as excess histones can be originated by eviction from chromatin due to a dysfunction in chromatin reassembly during transcription. The general similarities between histone trafficking during all the chromatin transactions suggest that DNA repair or DNA replication might also result in the excess of free histones when chromatin assembly is dysfunctional. Our results also point out a so-far unknown connection between chromatin dynamics and the regulation of the cell cycle, as the free histones accumulation induces a G1(START) arrest which is mediated by CLN3. This G1 delay allows cells to reduce free histone levels before DNA replication, through the Rad53-mediated histone degradation pathway. This model involve that chromatin reassembly factors, as FACT, are essential players in regulating the free histones released from dynamic chromatin and couples chromatin transaction to cell cycle progression. A review of the field will help to understand this new protective function of chromatin assembly factors.

Type of Paper: Review
Title: Epigenetics: New Questions in The Response to Hypoxia
Authors: Joel I. Perez-Perri and Pablo Wappner
Affiliation: Instituto Leloir and FBMC, FCEyN, Universidad de Buenos Aires; CONICET, Patricias Argentinas 435, C1405BWE Buenos Aires, Argentina;
E-Mail: PWappner@leloir.org.ar (P.W.)
Abstract: Reduction in oxygen levels below normal concentrations, plays important roles in different normal and pathological conditions, such as development, tumorigenesis and stroke. Organisms exposed to hypoxia trigger changes at both cellular and systemic levels to recover oxygen homeostasis. Most of these processes are mediated by Hypoxic Inducible Factors, HIFs, a family of transcription factors that directly induce the expression of several hundred genes in mammalian cells. Although different aspects of HIFs regulation are well known, it is still unclear by which precise mechanism HIFs activate transcription of their target genes. At the same time, hypoxia provokes a dramatic shut down of general transcription that seems lay in part on epigenetic changes, but the process is poorly understood. In this review we discuss the current knowledge on chromatin changes involved in HIF dependent gene activation, as well as other epigenetic changes, not necessarily linked to HIF, that take place under hypoxic conditions.