Tuesday, November 24, 2009

Polyphenols and Polyunsaturated Fatty Acids Boost the Birth of New Neurons, Study Finds

ScienceDaily (Nov. 24, 2009) — Universitat Autònoma de Barcelona (UAB) researchers have confirmed that a diet rich in polyphenols and polyunsaturated fatty acids, patented as an LMN diet, helps boost the production of the brain's stem cells -neurogenesis- and strengthens their differentiation in different types of neuron cells. read more....

Histone modifications are specifically relocated during gene activation and nuclear differentiation

OPEN ACCESS

Katharina S Heyse , Susanne E Weber and Hans Joachim Lipps

BMC Genomics 2009, 10:554doi:10.1186/1471-2164-10-554
Published: 24 November 2009

Abstract (provisional)

Background
Post-translational histone modifications (PTMs) and their specific distribution on genes play a crucial role in the control of gene expression, but the regulation of their dynamics upon gene activation and differentiation is still poorly understood. Here, we exploit the unique genome organization of ciliates to analyse PTM dynamics during gene activation in the differentiated cell and during nuclear differentiation. In the macronucleus of these cells the DNA is organized into nanochromosomes which represent independent functional units. Therefore ciliated protozoa represent a simplistic model system to analyse the relevance of histone modifications and their localization for gene expression and differentiation.

Results
We analysed the distribution of three PTMs on six individual nanochromosomes, two of which are silenced in the vegetative cell and only activated during sexual reproduction. We show that a specific relocation of these PTMs correlates with gene activation. Moreover, macronuclear-destined sequences in the differentiating macronucleus display a distribution of PTMs which differs significantly from the PTM patterns of actively transcribed genes.

Conclusions
We show for the first time that a relocation of specific histone modifications takes place during activation of genes. In addition, we demonstrate that genes in a differentiating nucleus are characterised by a specific distribution and composition of PTMs. This allows us to propose a mechanistic model about the relevance of PTMs for gene activation, gene silencing and nuclear differentiation. Results described here will be relevant for eukaryotic cells in general.

The complete article is available as a provisional PDF

Monday, November 23, 2009

Complement-Derived Anaphylatoxin C3a Regulates In Vitro Differentiation and Migration of Neural Progenitor Cells

STEM CELLS
Volume 27 Issue 11;Pages 2824-2832
Published Online: 25;Sep;2009
Noriko Shinjyo 1, Anders Ståhlberg 2, Mike Dragunow 3, Milos Pekny 2, Marcela Pekna 1 *1Department of Medical Chemistry and Cell Biology, Institute of Biomedicine, Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
2Center for Brain Repair and Rehabilitation, Department of Clinical Neuroscience and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
3Department of Pharmacology and The National Research Centre for Growth and Development, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand

Keywords: C3a, ERK1/2 phosphorylation, Neural progenitor cells, Neuronal differentiation, Migration, neuroprotection, neurogenesis.

New Discovery About Formation of New Brain Cells

ScienceDaily (Nov. 23, 2009) — The generation of new nerve cells in the brain is regulated by a peptide known as C3a, which directly affects the stem cells' maturation into nerve cells and is also important for the migration of new nerve cells through the brain tissue, reveals new research from the Sahlgrenska Academy published in the journal Stem Cells. (read more)

A Periplasmic Reducing System Protects Single Cysteine Residues from Oxidation

(Related to the previous post, the source paper of the previus news)

Science 20 November 2009, Vol. 326. no. 5956, pp. 1109 - 1111, DOI: 10.1126/science.1179557
Matthieu Depuydt,1 Stephen E. Leonard,2 Didier Vertommen,1 Katleen Denoncin,1 Pierre Morsomme,3 Khadija Wahni,4,5 Joris Messens,4,5 Kate S. Carroll,2 Jean-François Collet1,*

de Duve Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
2 Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109–1048, USA.
3 Institut des Sciences de la Vie, Université catholique de Louvain, B-1348 Louvain-la-Neuve, Belgium.
4 Department of Molecular and Cellular Interactions, Vlaams Instituut voor Biotechnologie (VIB), Vrije Universiteit Brussel, B-1050 Brussels, Belgium.
5 Structural Biology Brussels, Vrije Universiteit Brussel, B-1050 Brussels, Belgium.

Keywords:  thiol group, cysteine,  disulfide bonds, oxidation,  sulfenic acids, sulfonic acids,  DsbG, DsbC,  thioredoxin-related proteins.

Saving The Single Cysteine: New Antioxidant System Found

Medical News Today, Article Date: 23 Nov 2009 - 1:00 PST
We've all read studies about the health benefits of having a life partner. The same thing is true at the molecular level, where amino acids known as cysteines are much more vulnerable to damage when single than when paired up with other cysteines.  read more....

Keywords: cysteines, new antioxidant system, DsbG, hyperoxidation, antioxidant therapies,

GUÍA PRÁCTICA DE NECESIDADES EDUCATIVAS ESPECIALES

Original book : At a glance: a practical guide to children's special needs

Autor: Viv EAST y Linda EVANS
Traductor: Pablo Manzano
ISBN: 978-84-7112-609-2
Fecha de la edición: 25/11/2009

Keywors: Necesidades Educativas Especiales, Ataxia de Friedreich, Plan Educativo Individualizado (PEI)

Búsqueda y análisis de fármacos en modelos de ataxia de Friedreich

Ros Cantera, Sheila,
Tesis doctoral del Departamento de Genética de la UV.
Editorial: Instituto de Biomedicina de Valencia, CSIC; Universitat de València, Fecha de publicación: 17-Sep-2009

Keywords: Ataxia de Friedreich, Frataxina, Riboflavina, deferiprona, deferoxamina, amrinona, crisina,


Trabajo completo / full text : http://digital.csic.es/bitstream/10261/17120/1/Tesis%20Sheila%20Ros.pdf

Saturday, November 21, 2009

Epigenetic Silencing in Friedreich Ataxia Is Associated with Depletion of CTCF (CCCTC-Binding Factor) and Antisense Transcription

OPEN ACCESS


PLoS ONE 4(11): e7914. doi:10.1371/journal.pone.0007914
Irene De Biase1#, Yogesh K. Chutake1#, Paul M. Rindler1, Sanjay I. Bidichandani1,2*
1 Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America, 2 Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America

Abstract

 

Background

Over 15 inherited diseases are caused by expansion of triplet-repeats. Friedreich ataxia (FRDA) patients are homozygous for an expanded GAA triplet-repeat sequence in intron 1 of the FXN gene. The expanded GAA triplet-repeat results in deficiency of FXN gene transcription, which is reversed via administration of histone deacetylase inhibitors indicating that transcriptional silencing is at least partially due to an epigenetic abnormality.

Methodology/Principal Findings

We found a severe depletion of the chromatin insulator protein CTCF (CCCTC-binding factor) in the 5′UTR of the FXN gene in FRDA, and coincident heterochromatin formation involving the +1 nucleosome via enrichment of H3K9me3 and recruitment of heterochromatin protein 1. We identified FAST-1 (FXN Antisense Transcript – 1), a novel antisense transcript that overlaps the CTCF binding site in the 5′UTR, which was expressed at higher levels in FRDA. The reciprocal relationship of deficient FXN transcript and higher levels of FAST-1 seen in FRDA was reproduced in normal cells via knockdown of CTCF.

Conclusions/Significance

CTCF depletion constitutes an epigenetic switch that results in increased antisense transcription, heterochromatin formation and transcriptional deficiency in FRDA. These findings provide a mechanistic basis for the transcriptional silencing of the FXN gene in FRDA, and broaden our understanding of disease pathogenesis in triplet-repeat diseases.

 Full text (pdf) http://www.plosone.org/article/fetchObjectAttachment.action;jsessionid=F09024199E18C3B55BF5F22C106E7255?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0007914&representation=PDF