| Monday, November 2, 2009
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1:00 PM
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Atrogin-1 in Muscle Atrophy and Damage
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| Description: |
Stewart Lecker, Beth Israel Deaconess Medical Center
ROOM: 220, College of Health and Rehabilitation Sciences: Sargent College, Boston University, 635 Commonwealth Avenue
HOST: Dr. Susan Kandarian
Refreshments will be served
For more information on Dr. Lecker go to:
http://www.bidmc.org/Research/Departments/Medicine/Divisions/Nephrology/Investigators/Dr,-d-,StewartLecker.aspx
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| Contact: |
Danka Charland
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| Wednesday, November 4, 2009
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2:00 PM - 3:30 PM
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6:00 PM - 7:30 PM
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Perception in autism: Updating what means 'enhanced'
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| Description: |
Laurent Mottron, Université de Montréal Autism Center of Excellence (http://autism.mit.edu/mottron)
Room 3002 (auditorium), Building 46, MIT, 43 Vassar Street, Cambridge
Reception to follow
PLEASE RSVP TO LMAVROS@MITE.EDU
Supported by the Simons Initiative on Autism and the Brain at MIT (web.mit.edu/autism)
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| Contact: |
Lee Mavros
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| Thursday, November 5, 2009
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Noon - 1:00 PM
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IKK/NF-kB Signaling in Bone Diseases
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| Description: |
Speaker: Cun-Yu Wang, UCLA School of Dentistry
Location: The Forsyth Institute, Schulze Conference Room 2, 140 The Fenway, Boston
Summary: Nuclear factor kappa B (NF-kB) is a transcription factor which was originally found to play a critical role in inflammation and immune responses. The work from us and others has demonstrated that NF-kB controls apoptosis and oncogenesis. Recently, we have explored the role of NF-kB in chronic bone diseases. In my talk, I will discuss how NF-kB mediates cancer cell bone metastasis and promotes osteolytic bone destruction by activating osteoclasts. On the other hand, unexpected, we find that NF-kB is a negative regulator of bone formation. We will present our recent work on how NF-kB inhibits osteoblast function. According to our studies, targeting NF-kB may provide an important treatment strategy for bone metastasis, osteoporosis and other inflammatory bone diseases.
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| Contact: |
Pam Quattrocchi
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| Friday, November 6, 2009
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8:30 AM - 9:30 AM
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1:30 PM - 2:45 PM
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4:00 PM - 5:30 PM
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Probabilistic inference in neural circuits: from insects to humans.
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| Description: |
Speaker: Alexandre Pouget, University of Rochester
Room 3002, Building 46, MIT
A wide range of behaviors can be formalized as instances of probabilistic inferences. This includes odor recognition in insects, navigation in rodents, auditory localization in barn owls, decision making in primates and causal reasoning in humans, to name just a few. In all cases, the probabilistic inferences involve products of distributions and marginalization. We will show that, given the type of variability reported in neural responses, products of distributions can be implemented through linear operations over firing rates, while marginalization over Gaussian random variables requires a particular nonlinearity known as quadratic divisive normalization. Both operations are conspicuous in many neural circuits raising the possibility that seemingly unrelated behaviors could in fact rely on very similar neural mechanisms across different species. In addition, we will present experimental evidence that humans perception is akin to a sampling process, which supports the notion that humans also use sampling to solve complex Bayesian inferences.
http://mit.edu/bcs/newsevents/colloquia.shtml
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| Contact: |
Kathleen Dickey
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| Monday, November 9, 2009
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Noon - 1:00 PM
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| Tuesday, November 10, 2009
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1:00 PM - 4:30 PM
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4:00 PM - 5:00 PM
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| Wednesday, November 11, 2009
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Noon - 1:00 PM
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| Thursday, November 12, 2009
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6:00 PM - 7:00 PM
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| Friday, November 13, 2009
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Noon - 1:00 PM
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Noon - 1:00 PM
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Teamwork in anaerobic metabolism: syntrophy and interspecies metabolic interactions
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| Description: |
Speaker: Michael J. McInerney, University of Oklahoma
Location: The Forsyth Institute, Schulze Conference Room 2, 140 The Fenway, Boston
Summary: Syntrophy is an essential intermediary step in the anaerobic conversion of organic matter to methane where metabolically distinct microorganisms are tightly linked by the need to maintain the exchanged metabolites at very low concentrations. Syntrophic metabolism is thermodynamically constrained and is probably a prime reason why it is difficult to culture microbes as these approaches disrupt consortia. Syntrophic metabolism proceeds at very low Gibbs’ free energy changes, close to the minimum free energy change needed to conserve energy biologically, which is the energy needed to transport one proton across the cytoplasmic membrane. Pathways for syntrophic degradation of fatty acids predict the net synthesis of about one-third of an ATP per round of catabolism, but it is not clear how net energy is conserved during syntrophic benzoate metabolism. Aromatic ring reduction by syntrophic metabolizers and strict anaerobes involves a novel benzoyl-CoA reductase not found in aerobes or facultative anaerobes. Syntrophic aromatic metabolism also involves the formation of alicyclic compounds such as cyclohexane carboxylate by unknown enzymes. Hydrogen and formate production during syntrophic metabolism require energy input by a process called reverse electron transfer. Comparative genomic analyses show that syntrophic metabolizers are metabolic specialists that have evolved a number of solutions to solve the problem of reverse electron transfer including soluble systems to produce hydrogen and possibly formate by a process called electron bifurcation and a novel, membrane-bound oxidoreductase uniquely made during syntrophic fatty and aromatic acid metabolism. While we have made great progress in delineating the genetic systems involved in syntrophic fatty and aromatic acid metabolism, we are less certain about what other gene systems may be needed for syntrophy.
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| Contact: |
Pam Quattrocchi
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1:30 PM - 2:45 PM
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4:00 PM - 5:30 PM
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Genes, brains, and spatial representation: Evidence from Williams syndrome
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| Description: |
Speaker: Barbara Landau, Johns Hopkins University
Room 3002, Building 46, MIT
Our experience of the spatial world is a unitary one?we perceive objects and layouts, we remember them and act on them, and we can even talk about them with ease. Despite this impression of seamlessness, spatial representations in human adults appear to be specialized in domain-dependent manner, engaging
different properties and computational mechanisms for different functions. In this talk, I will present evidence that this domain-specific specialization emerges early in development and is reflected in patterns of breakdown that occur under genetic defect. I will offer evidence from Williams syndrome?a relatively rare genetic syndrome that gives rise to an unusual profile of severely impaired
spatial representation together with spared language. Results from a variety of spatial domains ? including object representation, motion perception, action, navigation, and spatial language-- show a strikingly uneven profile of sparing and deficit within spatial representations, consistent with the idea that
specialization of function drives development and breakdown. These findings raise a crucial question: Can specific genes target specific aspects of cognitive structure? To answer this question, I will present a speculative hypothesis about the way that genes might affect the brain basis for specialization and how this might then guide patterns of both normal and abnormal development across spatial domains.
http://mit.edu/bcs/newsevents/colloquia.shtml
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| Contact: |
Kathleen Dickey
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| Tuesday, November 17, 2009
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Noon - 1:00 PM
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| Wednesday, November 18, 2009
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Noon - 1:00 PM
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Noon - 1:00 PM
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2:00 PM - 3:30 PM
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5:00 PM - 6:00 PM
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Recent Advances in Computational Structural Biology
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| Description: |
MICHAEL LEVITT, Stanford University
Room 110, Building 66, MIT
This talk covers two topics selected from many that occupy us in the Computational Structural Biology group at Stanford: Mesoscale Modeling of Macromolecular Machines and The Nature of the Protein Universe. Both topics are my own work. Mesoscale Modeling of Macromolecular Machines. Most of the central biological functions of living cells are performed by large complexes of individual protein domains, whose movement plays a crucial role in their biological function. I present a unique approach to this motion based on normal modes calculated in torsional angle space. Special problems arise because (1) systems are large mandating use of simplified representations; (2) modes must be calculated at an energy minimum mandating the use of accurate energy functions and convergent minimizers; (3) numerical accuracy mandates the use of complex step derivatives; (4) there are many independent molecules mandating combination of rigid body and internal degrees of freedom; and (5) resulting matrices are badly ill-conditioned mandating special eigenvalue methods.
The Nature of the Protein Universe. After a decade of serious structure-determination and sequencing efforts there are over 50,000 structures and over 6 million protein sequences; an overview of the set of all proteins of all organisms is becoming an essential roadmap. Here I analyze the protein universe in terms of sequence families that have single or multi-domain architectures, with or without known structures. Growth of single domain families has saturated: almost all growth comes from multi-domain architectures that are combinations of about 25,000 domains. Multi-domain architectures, which are specific to the major groups of organisms, account for species diversity. There are known structures for a quarter of the single domain families and half of all sequences can be partially modeled due to their membership in these families.
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| Contact: |
Patrice Macaluso
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6:00 PM - 7:30 PM
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| Thursday, November 19, 2009
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9:00 AM - 6:00 PM
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The Sixth IABMR Annual Meeting: Scientific Symposium Theme - Knockdown Strategies in Biomedicine: RNAi and Beyond
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| Description: |
Location: Conference Center (3rd Floor), The Forsyth Institute, M. Barbara Schulze, 140 The Fenway, Boston
Registration: IABMR members: Free (Annual Membership Fee: $20)
Forsyth Employees: Free
Non-members: $20
Register Online at http://www.iabmr.org
MEETING SCHEDULE
9:00 – 10:00 Registration and Coffee
10:00 – 12:30 Poster Sessions I & II
11:00 – 1:30 Vendor Exhibition & Luncheon Reception
1:15 – 1:30 Welcome and Introduction
Tsute Chen, President of IABMR
Opening Remarks
Philip Stashenko, President and CEO, The Forsyth Institute
1:30 – 4:40 Scientific Symposium
1:30 – 2:10 Delivery is in the Details
Catherine Pachuk, Pfizer Research Technology Center
2:10 – 2:50 Lost in translation: mechanisms and tumor suppressive activity of microRNAs
Carl Novina, Dana-Farber Cancer Institute
2:50 – 3:20 Coffee Break
3:20 – 4:00 MicroRNA in gliomas: small regulators of a big problem
Anna Krichevsky, Brigham and Woman’s Hospital
4:00 – 4:40 Genome wide RNAi screens in Drosophila: A journey from pre-RNAi to RNAi days
Norbert Perrimon, Harvard Medical School
4:40 – 6:00 Poster Awards Ceremony
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| Contact: |
Catherine O'Hara
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4:30 PM - 5:30 PM
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| Friday, November 20, 2009
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8:30 AM - 9:30 AM
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Microbiology of Cultural Heritage Materials
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| Description: |
MSI Chalktalk: Nick Konkol (SEAS)
Please join us for pastries at 8:30 AM in the Harvard Center for the Environment Geological Museum, 24 Oxford St, 3rd Floor, Rm 310.
http://www.msi.harvard.edu/fridays.html
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| Contact: |
Andrea Lenco
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Noon - 1:00 PM
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Biofilm-associated genes in clinical isolates of Streptococcus mutans, and establishment of in vivo new model for oral infection
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| Description: |
Speaker: Hidenobu Senpuku, National Institute of Infectious Diseases Japan
Location: The Forsyth Institute, Schulze Conference Room #2
140 The Fenway, Boston
Summary: Streptococcus mutans is a pioneering organism that plays an important role in biofilm formation and is a primary causative agent of dental caries. In the previous reports, the several associated genes with S. mutans biofilm formation were found and their roles were investigated, however, little is known biofilm-associated genes in clinical isolates. There is a possible that clinical isolates have more number of genes for biofilm formation than laboratory stains to survive in sever surrounding. Therefore, using clinical isolates, we investigated to identify new genes for biofilm formation. Using microarray analysis and real time-PCR, various associated genes with biofilm morphology of S. mutans were identified (Appl Environ Microbiol. 2006; 72:6277-87). In some of them, the three genes (sunL; ORF482, hypothetical protein; ORF1507, pqq; ORF1508) were found as an associated gene with biofilm formation by comparison analyses between biofilm and planktonic cells of clinical isolates. We constructed each mutant of the three genes {DsunL, Dhypothetical protein and Dpqq} in both clinical isolates (FSM-5 and -6) and laboratory stains (UA159 and GS5). The biofilm volumes of FSM-5 and -6.DsunL and Dpqq decreased significantly in comparison with wild types. On the other hand, in UA159 and GS5, there were not significant differences between mutants and wild types. Therefore, sunL and pqq are biofilm-associated genes in clinical isolates but not laboratory strains. The contribution of SunL and pqq for biofilm formation may be lost by many times of subculture.
In various our studies using genetic recombination and target gene mutation in mice, NOD/SCID.E2f1-/- mice were established. The mutant mice showed a decreased volume of saliva and lost acquired immune reactivity, and increased susceptibility for oral infection. Therefore, we considered that NOD/SCID.E2f1-/- mouse was a useful animal model for initial adhesion and biofilm formation of oral microbe.
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| Contact: |
Pam Quattrocchi
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1:30 PM - 2:45 PM
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| Monday, November 23, 2009
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Noon - 1:00 PM
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Sjögren's Syndrome: Many Questions, Few Answers
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| Description: |
Speaker: Seunghee Cha, College of Dentistry, University of Florida
Location: The Forsyth Institute, Schulze Conference Room 2
140 The Fenway, Boston
Summary: Autoimmune Sjögren’s syndrome (SjS) targets the exocrine glands, such as the salivary and lacrimal glands, of mostly female individuals, leading to severe secretory dysfunction and its complications. Our research goal is to understand SjS pathogenesis and to develop SjS-specific diagnostics and therapeutics for SjS patients. The focuses of the presentation will include but are not limited to: 1) Aberrant MicroRNA expression and its potential implication in autoimmune SjS: MicroRNAs (miRNAs) are small noncoding RNAs that negatively regulate gene expression via degradation/translational repression of their targeted mRNAs. Our latest observation indicates that miR-146a and miR-155 exhibit increased expression compared to healthy controls in human SjS patient PBMCs. Functional assays in human THP-1 monocytes are being utilized to determine possible implications of these miRNA in innate immune immunity. 2) Underlying mechanisms of secretory dysfunction in SjS: Our studies have proven that the degree of dryness are not correlated with lymphocytic focus score but, rather, associated with the presence of anti-muscarinic type 3 receptor (M3R) autoantibodies. These antibodies are able to interfere with M3R-mediated secretory pathway by binding to the receptor. Since one or more vital pathways associated with fluid secretion are affected by the changes in intracellular calcium signaling, we are currently investigating the trafficking of GFP-Aquaporin5(AQP-5) using a real-time confocal imaging system to determine if altered intracellular calcium release by binding of autoantibodies to the receptor blocks the translocation of AQP-5 to the plasma membrane, thus leading to loss of secretion in SjS. 3) Receptor-mediated siRNA delivery: Our studies utilizing animal models indicate disrupted glandular homeostasis such as increased apoptosis of epithelial cells in the salivary glands precedes SjS-like disease onset, subjecting the salivary glands to immune cell infiltration and subsequently loss of secretory function. Based on our expertise on M3R, we are currently testing if a MR agonist, carbachol, can deliver caspase-3 siRNA as a carbachol: caspase-3 siRNA conjugate via receptor-mediated endocytosis in vitro. This is ultimately to alter epithelial cell responses to external cues such as pro-inflammatory or death signals by delivering secretagogues: siRNA conjugates that are specific for MR, resulting in acinar cell preservation in the salivary glands of SjS patients.
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| Contact: |
Pam Quattrocchi
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4:00 PM - 5:00 PM
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Natural Product Antibiotic Biosynthesis: Two New Roles for Diiron Monooxygenases
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| Description: |
John D. Lipscomb, University of Minnesota
Room 114, Building 56, MIT
Refreshments 3:45 pm
Natural product non-ribosomal peptide assembly lines invoke tailoring enzymes to provide the rich structural diversity and bioactivity of the products. Some of these enzymes introduce hydroxyl groups wherein the oxygen derives from O2. This is the case for the chloramphenicol biosynthetic pathway in which two steps involve oxygenase catalysis: beta-hydroxylation of the p-aminophenylalanine precursor, and subsequent N-oxygenation of the amino function to yield a rare nitro analog. Previously, only cytochrome P450 and alpha-ketoglutarate-linked oxygenases have been shown to contribute to natural product biosynthesis. Here, we will discuss two new enzymatic strategies for the oxygenation steps in the biosynthesis of chloramphenicol that are likely to be broadly relevant to natural product pathways.
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| Contact: |
Betty Lou McClanahan
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| Tuesday, November 24, 2009
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Noon - 1:00 PM
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1. Mechanism of excision and integration of the Bacteroides conjugative transposon CTnDOT and 2. Regulation of excision and transfer of the Bacteroides conjugative transposon CTnDOT
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| Description: |
Speakers: Jeffrey Gardner, University of Illinois
Abigail Saylers, University of Illinois
Location: The Forsyth Institute, Schulze Conference Room 2
140 The Fenway, Boston
Summary 1. CTnDOT is a Bacteroides conjugative transposon that has facilitated the spread of antibiotic resistance in the human gut in recent years. The integrase (IntDOT) encoded by CTnDOT is a member of the tyrosine family of recombinases. It is unusual in that it recombines sites that contain short regions of non-identical base pairs. We have used a genetic approach to perform a structure-function study of IntDOT. We have found mutants that are deficient in specific steps in the recombination pathway. We have also developed in vitro systems to study the integration and excision reactions catalyzed by IntDOT. Integration requires a supercoiled substrate containing the CTnDOT attachment site (attDOT), the bacterial attachment site (attB), and IntDOT and a host factor encoded by Bacteroides. The excision reaction is complex and requires excision substrates (attL and attR), at least three CTnDOT encoded proteins (Orf2c, Orf2d, and Exc), a host factor and IntDOT. The roles of the Orf2c, Orf2d, Exc and the host factor in the excision reaction will be discussed.
Summary 2. Both excision and transfer of CTnDOT are stimulated by tetracycline. This stimulation has proven to be a complex process. Initial steps in the regulatory cascade involve a two component system, RteA and RteB. Production of RteA and RteB is affected not only by translational attenuation but also by a growth phase associated mechanism. RteB activates expression of a third gene, rteC. RteC protein in turn activates expression of an operon that contains the excision genes, genes that encode the proteins that participate with the integrase to catalyze excision. Surprisingly, these same excision proteins also act as regulatory proteins. They are required to activate expression of the transfer genes, which encode proteins that form the mating apparatus through which the single stranded copy of CTnDOT is transferred. Finally, a small RNA, rteR, is responsible for repression of transfer gene expression. This complex cascade will be described, with special emphasis on the last steps of the cascade. The complex regulatory circuit may explain why CTnDOT is so stably maintained in the absence of selection.
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| Contact: |
Pam Quattrocchi
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12:30 PM - 1:30 PM
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| Tuesday, December 1, 2009
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4:00 PM - 5:00 PM
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Retinoblastoma: Bridging Developmental Neurobiology and Cancer Genetics
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| Description: |
Speaker: Michael Dyer, St. Jude Children’s Research Hospital
Enders Auditorium, John F. Enders Research Bldg., Children's Hospital Boston, 320 Longwood Ave.
Cardiovascular Seminar Series
Department of Cardiology | Children’s Hospital Boston
This conference is supported by the Faye and Karen Sinclair
Research Fund for Congenital Heart Disease
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| Contact: |
Michelle Merry
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| Wednesday, December 2, 2009
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2:00 PM - 3:30 PM
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6:00 PM - 7:30 PM
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| Thursday, December 3, 2009
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Noon - 1:00 PM
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MICROBIAL DORMANCY: ROLE IN DISEASE AND "UNCULTIVABILITY"
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| Description: |
Speaker: Kim Lewis, Northeastern University
Location: The Forsyth Institute, Schulze Conference Rm. 2
140 The Fenway, Boston
Summary: Pathogen populations produce persister cells, specialized survivor cells that are dormant and highly tolerant to all known antibiotics. Molecular mechanisms of persister formation will be discussed, as well as their role in disease, such as biofilm infections of catheters, cystic fibrosis, and oropharyngeal candidiasis. Dormancy may also be an underlying cause of bacterial “uncultivability”. Growth factors produced by neighboring species are essential for growth of a considerable number of environmental organisms, and are likely to play a role in the human host, including the oral environment.
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| Contact: |
Pam Quattrocchi
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6:00 PM - 7:00 PM
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Host/Candida Interactions During Health and Disease
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| Description: |
Speaker: Carol Kumamoto, Tufts University Dept. of Microbiology
Location: Room 310, 3rd Floor, Geological Museum, Harvard Center for the Environment, 24 Oxford Street
MSI monthly seminar series. Please join us for a wine & cheese reception at 5:30pm.
http://www.msi.harvard.edu/thursdays.html
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| Contact: |
Andrea Lenco
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| Friday, December 4, 2009
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1:30 PM - 2:45 PM
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4:00 PM - 5:30 PM
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Hans-Lukas Teuber Lecture Internally generated cell assembly sequences in the service of cognition
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| Description: |
György Buzsáki, Rutgers, The State University of New Jersey
Singleton Auditorium, Room 3002, Building 46, MIT
Abstract:
How does the brain orchestrate perceptions, thoughts and memories from the spiking activity of its neurons? A long-standing conjecture in neuroscience is that aspects of cognition depend on the brain's ability to self-generate sequential neuronal activity. Large-scale recordings from neuronal ensembles now offer opportunities for testing these ideas. I will show that even in the absence of changing environmental or body inputs, the hippocampus can generate perpetually changing assembly sequences. In a task which required rats to alternate between the left and right turns and wait between the choices in order to receive a reward, a unique assembly sequence (“neural trajectory”) was generated several seconds before the animal entered the left arm and a different unique sequence was observed before the animal entered the right arm. Such neural trajectories may represent the brain's internal mechanism for planning routes on the basis of past experience. The temporal dynamics of internally generated sequences were similar to those observed while the rat navigated in the maze and environmental cues affected neuronal patterns. I hypothesize that the neural algorithm that evolved for assisting navigation in small-brain animals (i.e., measuring and using first and higher order distances in the physical world) is identical with the algorithm that allows us to navigate in “cognitive space”. The assembly-based approach can provide an insight into centrally-organized (cognitive) events without reference to introspection.
G. Buzsaki. Rhythms of the Brain. Oxford University Press, 2006.
E. Pastalkova, V. Itskov, A. Amarasingham, and G. Buzsaki. Internally generated cell assembly sequences in the rat hippocampus. Science 321, 5894:1322-7, 2008.
http://mit.edu/bcs/newsevents/colloquia.shtml
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| Contact: |
Kathleen Dickey
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Month of November 2009
