Genes and Social Behavior
What genes and regulatory sequences contribute to the organization and functioning of neural circuits and molecular pathways in the brain that support social behavior? How does social experience interact with information in the genome to modulate brain activity? Here, we address these questions by highlighting progress that has been made in identifying and understanding two key "vectors of influence" that link genes, the brain, and social behavior: (i) Social information alters gene expression in the brain to influence behavior, and (ii) genetic variation influences brain function and social behavior. We also discuss how evolutionary changes in genomic elements influence social behavior and outline prospects for a systems biology of social behavior.
Sources:
Genes and Social Behavior. Robinson et al. Science 7 November 2008, Vol. 322. no. 5903, pp. 896 - 900.
Nuclear Membrane Mechanics
In the fission yeast Schizosaccharomyces pombe, the nucleus is tethered to the cytoskeleton by KASH domain-containing proteins in the outer nuclear membrane and SUN domain-containing proteins in the inner nuclear membrane. By exerting force on these SUN-KASH complexes, the cytoskeleton controls the position of the nucleus within the cell. Centromeric DNA inside the nucleus has been observed to cluster near SUN-KASH complexes during interphase, raising the possibility that this association mediates a functional connection to the cytoskeleton. King et al. have identified an inner nuclear membrane protein (Ima1) in S. pombe that links DNA to SUN-KASH complexes. They show that Ima1 binds to centromeric DNA in vitro and colocalizes with the SUN domain-containing protein Sad1 at the inner nuclear membrane; in Ima1-deficient yeast, colocalization between centromeric DNA and Sad1 was disrupted, and nuclei were frequently deformed and asymmetric. The authors propose that these protein-protein interactions may therefore be required to maintain nuclear shape and integrity in the face of cytoplasmic tensioners and provide a means by which cytoskeletal forces contribute to organizing DNA within the nucleus
Sources:
Cell 134, 427 (2008)
Postdoctoral in Stem Cells and Neurodevelopment
A Postdoctoral position is available for research in the areas of STEM CELLS AND NEURODEVELOPMENT. The laboratory, headed by Dr. Alysson R. Muotri, make use of human ES and iPS cells, in combination with genetic, molecular, biochemical and computational
tools, to study early stages of brain development and the formation of neuronal networks.
Research currently focuses on two interconnected projects:
(1) Development of state-of-the-art human cellular models to study neurodevelopmental diseases, such as autism spectrum disorder;
(2) Study of neuronal complexity by the dynamics and regulation of mobile elements upon neuronal commitment.
Candidates should have a recent Ph.D. and solid experience in cell and molecular biology, genetics and/or computational biology, as demonstrated by record of publications. If interested, please send CV and two letters of recommendation via email to: Dr. Muotri,
muotri@salk.edu.
The UCSD stem cell initiative is a new interdisciplinary research program in the heart of La Jolla, California, focusing on several aspects of stem cell biology.
For more information please go to:
http://www.stemcells.ucsd.edu/
UCSD Stem Cell Program
9500 Gilman Drive, SAN DIEGO, CALIFORNIA 92093-0695 TEL (858)534-2412 FAX (858) 822-3249
Mitochondrial Dysfunction in Neurological Disease
Mitochondria are responsible for maintaining the energy balance of the cell and are also responsible for triggering apoptosis (programmed cell death) in response to oxidative stress. This one-day mini-symposium aims to highlight recent advances in our understanding of how these organelles function in the nervous system, and how mitochondrial dysfunction contributes to neurological disease.
Fondation IPSEN and Nature Publishing Group are proud to announce the sixth Emergence & Convergence mini-symposium. These one day meetings bring together leading international speakers to review both emerging information and its convergence with current understanding.
Join leaders in the field on December 5, 2008 in Washington Duke Inn and Golf Club In Durham, North Carolina, USA, to discuss Mitochondrial Dysfunction in Neurological Disease.
The panel of speakers includes:
Don Cleveland (University of California - San Diego, USA)
Mohanish Deshmukh (University of North Carolina - Chapel Hill, USA)
Tim Greenamyre (University of Pittsburgh, USA)
Peter Hollenbeck (Purdue University, USA)
Giovanni Manfredi (Weill Medical College of Cornell University, USA)
Carlos Moraes (University of Miami School of Medicine, USA)
Eric Shoubridge (McGill University, Canada)
Nicholas Wood (University College London, UK)
Deadline for application: October 10, 2008
Attendance at this meeting is free on acceptance of application.
To apply and for more information visit www.nature.com/natureconferences/eandc/mito
From the Organizers:
Kalyani Narasimhan (Nature Neuroscience, USA)
Alan Packer (Nature Genetics, USA)
Yves Christen (Fondation IPSEN, France)
Source:
Mitochondrial Dysfunction in Neurological Disease
Stem Cells and Amyotrophic Lateral Sclerosis
The generation of pluripotent stem cells from an individual patient would enable the large-scale production of the cell-types affected by that patient’s disease. These cells could in turn be used for disease modeling, drug discovery, and eventually autologous cell-replacement therapies. Although recent studies have demonstrated the reprogramming of human fibroblasts to a pluripotent state, it remains unclear whether these induced pluripotent stem (iPS) cells can be produced directly from elderly patients with chronic disease. We have generated iPS cells from an 82-year-old woman diagnosed with a familial form of amyotrophic lateral sclerosis (ALS). These patient-specific iPS cells possess properties of embryonic stem cells and were successfully directed to differentiate into motor neurons, the cell type destroyed in ALS.
Sources:
Induced Pluripotent Stem Cells Generated from Patients with ALS Can Be Differentiated into Motor Neurons
