The Salk Institute for Biological Studies is an independent, non-profit, scientific research institute located in La Jolla, California. It was founded in 1960 by Jonas Salk, the developer of the polio vaccine; among the founding consultants were Jacob Bronowski and Francis Crick. Building did not start until spring of 1962. The institute consistently ranks among the top institutions in the US in terms of research output and quality in the life science. In 2004, the Times Higher Education Supplement ranked Salk as the world's top biomedicine research institute, and in 2009 it was ranked number one globally by ScienceWatch in the neuroscience and behavior areas.The institute employs 850 researchers in 60 research groups and focuses its research in three areas: Molecular Biology and Genetics; Neuroscience; and Plant Biology. Research topics include cancer, diabetes, birth defects, Alzheimer's disease, Parkinson's disease, AIDS, and the neurobiology of American Sign Language. The March of Dimes provided the initial funding and continues to support the institute. Current research is funded by a variety of organizations, such as the NIH, the HHMI and private organizations such as Paris-based Ipsen and the Waitt Family Foundation. In addition, the internally administered Innovation Grants Program encourages cutting-edge high-risk research. The institute appointed genome biologist Eric Lander and stem cell biologist Irving Weissman as non-resident fellows in November 2009.The campus was designed by Louis Kahn. Salk had sought to make a beautiful campus in order to draw the best researchers in the world. Salk and Kahn having both descended from Russian Jewish parents that had immigrated to the United States had a deeper connection than just mere partners on an architectural project. The results of their connection is seen in the design that resulted from their collaboration. The original buildings of the Salk Institute were designated as a historical landmark in 1991. The entire 27-acre site was deemed eligible by the California Historical Resources Commission in 2006 for listing on the National Register of Historic Places. Wikipedia.
Allen N.J.,Salk Institute for Biological Studies
Annual review of cell and developmental biology | Year: 2014
Astrocytes regulate multiple aspects of neuronal and synaptic function from development through to adulthood. Instead of addressing each function independently, this review provides a comprehensive overview of the different ways astrocytes modulate neuronal synaptic function throughout life, with a particular focus on recent findings in each area. It includes the emerging functions of astrocytes, such as a role in synapse formation, as well as more established roles, including the uptake and recycling of neurotransmitters. This broad approach covers the many ways astrocytes and neurons constantly interact to maintain the correct functioning of the brain. It is important to consider all of these diverse functions of astrocytes when investigating how astrocyte-neuron interactions regulate synaptic behavior to appreciate the complexity of these ongoing interactions.
Lundblad V.,Salk Institute for Biological Studies
Genes and Development | Year: 2012
Most human cells lack telomerase, the enzyme that elongates telomeres. The resulting telomere erosion eventually limits cell proliferation and tissue renewal, thereby impacting age-dependent pathologies. In this issue of Genes & Development, a technical tour-de-force by Chow and colleagues (pp. 1167-1178) reveals a highly choreographed sequence of events that processes newly replicated chromosome ends into mature telomeres. This sheds new light on an underappreciated contribution to telomere dynamics that may be as important as telomerase in dictating the correlation between life span and telomere length. © 2012 by Cold Spring Harbor Laboratory Press.
Taylor R.C.,Salk Institute for Biological Studies
Cold Spring Harbor perspectives in biology | Year: 2011
Aging cells accumulate damaged and misfolded proteins through a functional decline in their protein homeostasis (proteostasis) machinery, leading to reduced cellular viability and the development of protein misfolding diseases such as Alzheimer's and Huntington's. Metabolic signaling pathways that regulate the aging process, mediated by insulin/IGF-1 signaling, dietary restriction, and reduced mitochondrial function, can modulate the proteostasis machinery in many ways to maintain a youthful proteome for longer and prevent the onset of age-associated diseases. These mechanisms therefore represent potential therapeutic targets in the prevention and treatment of such pathologies.
Xia Y.,Salk Institute for Biological Studies
Nature cell biology | Year: 2013
Diseases affecting the kidney constitute a major health issue worldwide. Their incidence and poor prognosis affirm the urgent need for the development of new therapeutic strategies. Recently, differentiation of pluripotent cells to somatic lineages has emerged as a promising approach for disease modelling and cell transplantation. Unfortunately, differentiation of pluripotent cells into renal lineages has demonstrated limited success. Here we report on the differentiation of human pluripotent cells into ureteric-bud-committed renal progenitor-like cells. The generated cells demonstrated rapid and specific expression of renal progenitor markers on 4-day exposure to defined media conditions. Further maturation into ureteric bud structures was accomplished on establishment of a three-dimensional culture system in which differentiated human cells assembled and integrated alongside murine cells for the formation of chimeric ureteric buds. Altogether, our results provide a new platform for the study of kidney diseases and lineage commitment, and open new avenues for the future application of regenerative strategies in the clinic.
Osakada F.,Salk Institute for Biological Studies
Nature protocols | Year: 2013
Rabies viruses, negative-strand RNA viruses, infect neurons through axon terminals and spread trans-synaptically in a retrograde direction between neurons. Rabies viruses whose glycoprotein (G) gene is deleted from the genome cannot spread across synapses. Complementation of G in trans, however, enables trans-synaptic spreading of G-deleted rabies viruses to directly connected, presynaptic neurons. Recombinant rabies viruses can encode genes of interest for labeling cells, controlling gene expression and monitoring or manipulating neural activity. Cre-dependent or bridge protein-mediated transduction and single-cell electroporation via the EnvA-TVA or EnvB-TVB (envelope glycoprotein and its specific receptor for avian sarcoma leukosis virus subgroup A or B) system allow cell type-specific or single cell-specific targeting. These rabies virus-based approaches permit the linking of connectivity to cell morphology and circuit function for particular cell types or single cells. Here we describe methods for construction of rabies viral vectors, recovery of G-deleted rabies viruses from cDNA, amplification of the viruses, pseudotyping them with EnvA or EnvB and concentration and titration of the viruses. The entire protocol takes 6-8 weeks.