[bioundgrd] Biology Advanced Undergraduate Seminars-Spring 2011

[Nick Polizzi]

TO:     Biology Majors
FROM:    H. Robert Horvitz, Professor of Biology

        I am writing to inform you of the exciting Advanced Undergraduate Seminar courses being offered by the Department of Biology for the Spring 2011 term.  A complete list of the courses, instructors, and brief course descriptions are enclosed.  The topics are highly varied and encompass areas of biochemistry, molecular biology, microbiology, cancer biology, structural biology, stem cells, human disease, bioengineering, biofuels, biotechnology and therapeutics. A student can take any number of these courses.  The courses, which generally involve four to eight students, are for 6 units, graded pass/fail, and meet two hours each week.  The focus is on reading and discussing the primary research literature.  Most courses have two short written assignments.  Some include field trips to MIT research laboratories or to commercial sites using technologies discussed in the courses.  The level of each course will be tailored to the students who enroll.  Because of the small size of these courses, we expect students not to drop these courses once they have begun.

        These courses offer a number of special features:  small class size, a high degree of personal contact with the instructor, a focus on the primary research literature, and an opportunity to discuss current problems in biology interactively.  I believe these courses greatly enrich an undergraduate’s experience.  There are limited alternative opportunities available to undergraduates to interact closely with instructors who are experienced full-time researchers; to learn to read, understand, and analyze primary research papers; and to engage in the type of stimulating discussions and debates that characterize how science is really done.  Most advanced MIT undergraduates (generally juniors and seniors) have been sufficiently exposed to the basics of biology to be able to read the primary literature and appreciate both methodologies and cutting-edge advances.  These courses have two goals:  first, to expose students to the kind of thinking that is central to contemporary biological research; and second, to impart specific knowledge in particular areas of biology.  These courses are designed to be intellectually stimulating and also to provide excellent preparation for a variety of future careers that require an understanding both of what modern biology is and of how it is done.  Students who have taken Advanced Undergraduate Seminars in the past (different specific courses, same general design) have been enormously enthusiastic about their experiences.

         I am writing to you before Registration Day to encourage you to consider enrolling in one of these seminar courses.  Please feel free to contact any of the instructors to learn more about their courses. To learn more about the Advanced Undergraduate Seminars to be offered during the Spring  semester, please check our website (http://mit.edu/biology/www/undergrad/adv-ugsem.html) and/or contact the instructors.


Advanced Undergraduate Seminars
Spring 2011

7.340  Antibiotics, Toxins, and Protein Engineering: Science at the Interface of  Biology, Chemistry, Bioengineering, and Medicine

Instructor: Caroline Koehrer (koehrer at mit.edu<mailto:koehrer at mit.edu>, 3-1870; laboratory of Uttam L.   RajBhandary)Spring 2011.  Monday, 1 – 3 pm. (Day and time are flexible.)  Room 68-151.

The discovery of penicillin in the 1930s ushered in a new era in modern medicine and paved the way for the development of various antibiotics against disease-causing microbes. After decades of widespread use, however, many antibiotics are not as effective as they used to be. Resistance to commonly used antibiotics and the surfacing of multidrug-resistant microbes – so called superbugs – have become major clinical problems. Today, the Centers for Disease Control and Prevention call antibiotic resistance “one of the world’s most pressing public health problems.”  Did you know that many of the commonly used antibiotics – such as tetracyclines, aminoglycosides and macrolides – specifically target the cell’s translational apparatus and disrupt protein synthesis? In this course, we will discuss the structure and function of the ribosome and look into the most basic concepts of protein synthesis. We will explore the mechanisms of action of antibiotics and toxins targeting the translational machinery, their roles in everyday medicine, and the emergence and spread of drug resistance. We will also discuss the identification of new drug targets and how we can manipulate the cell’s protein synthesis machinery to provide powerful tools for protein engineering and potential new treatments for patients with devastating diseases, such as cystic fibrosis and muscular dystrophy.



7.341 Bench to Bedside: Molecularly Targeted Therapies in Blood Disorders and Malignancy

Instructors: Bill Wong (pwong at wi.mit.edu<mailto:pwong at wi.mit.edu>, 650-799-8364; laboratory of Harvey   Lodish)Spring 2011. Wednesdays, 3 – 5 pm.
(Class time is flexible.) Room 68-180.

How are new drugs and treatments discovered? This course will take you from the discoveries of basic research to the customized design of drugs for treating patients with specific deadly blood disorders. Students will experience the scientific journey from the rationale of the scientists who started basic research projects to the clinicians who designed the trials to test the safety and efficacy of prospective drugs. We will consider the scientific discoveries that led to development of Gleevec, which is often referred as a miracle drug or silver bullet for a specific leukemia, chronic myelogenous leukemiz. Gleevec was developed based on the principle of molecularly targeting an aberrant kinase activity encoded by an oncogene and in this way killing leukemia cells while leaving normal cells alone. The following topics will be discussed: (1) identification of a bcr-abl chromosomal translocation and demonstration that this translocation generates an abnormal kinase activity that causes leukemia, (2) drug design and efficacy and toxicity testing in mice and humans, (3) mechanisms of drug resistance and finally, (4) uses of Gleevec in other diseases that also abnormally express the oncogenic abl kinase. We will also discuss other topics that demonstrate the process from “bench to bedside,” such as stem cell and gene therapy, the design of drugs based on RNA interference, and the reprogramming of somatic cells into stem cells for regenerative medicine.



7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases

Instructor:  Dan Ferullo (ferullo at mit.edu<mailto:ferullo at mit.edu>, 3-3745; laboratory of Graham Walker)  Wednesdays, 11 am – 1 pm.  (Class time flexible.)  Room 68-151.

Exactly how important is the mitochondrion, the “power house” of the cell?  Once a bacterial symbiote, the mitochondrion is an organelle that provides unique functions to nucleated eukaryotic cells.  Specifically, mitochondria produce the majority of cellular ATP, support aerobic respiration, and are key players in apoptosis (programmed cell death). An interesting feature of a mitochondrion is that it contains its own DNA, a relic of its bacterial ancestor.  The mitochondrial genome encodes some but not all of the proteins crucial for mitochondrial functions. Defects in mitochondrial functions have been found to cause or be associated with a variety of human diseases, including neurodegenerative and neuromuscular disorders and cancer as well as with aging. Accordingly, mitochondria have become attractive targets for developing therapies for disease.  In this course, we will discuss the biological roles of mitochondria and how mitochondria malfunction in human disease. We will learn about mitochondrial DNA (mtDNA) and how it is very easily damaged.  As such, we will discuss mechanisms that cells use to repair damaged mtDNA.  Importantly, we will examine how inadequate repair of mtDNA causes harmful mutations, compromises mitochondrial function, and is deleterious to the cell. We will examine how the problem of faulty mtDNA repair contributes to pathogenesis in disease. We will also discuss how mitochondria are key players in a normal process called “apoptosis” or “programmed cell death” designed to eliminate old or unhealthy cells in a controlled manner. However, mitochondrial defects can lead to improper apoptosis and in this way impact several diseases.  Lastly, we will discuss how mitochondria produce reactive oxygen species (ROS), which are potentially damaging molecules that can cause cellular injury when produced at high levels.  We will examine how elevated ROS production is caused by faulty mitochondria and is involved in disease and aging. By discussing studies using experimental systems ranging from yeast to human cancer cells, we will learn how defects in mitochondrial functions compromise cellular and organismic health.



7.343 Regenerative Medicine: from Bench to Bedside and Bedside to Bench

Instructor: Petra Simic (psimic at mit.edu<mailto:psimic at mit.edu>, 3-0809; laboratory of Leonard Guarente)  Wednesdays, 1 pm – 3 pm.  (Class time is flexible.)  Room 68-151.

Regenerative medicine involves the repair and regeneration of tissues for therapeutic purposes, such as replacing bone marrow in leukemia, cartilage in osteoarthritis or cells of the heart after a heart attack. Tissue regeneration has been of interest throughout history. There is even a Greek myth that describes liver regeneration: Prometheus was chained to a mountain, and his liver was eaten daily by an eagle, regenerated and then eaten again the next day. Today advances in basic and clinical research make tissue regeneration feasible. Tissue is normally generated during fetal development by the differentiation of embryonic stem cells or during postnatal life by a similar differentiation of adult stem cells. Regenerative medicine tries to mimic these processes. In this course, we will explore basic mechanisms of how cells differentiate into specific tissues in response to a variety of biologic signaling molecules. We will discuss the use of such factors for in vitro tissue production. For example, bone morphogenetic proteins can be used in vitro to drive the differentiation of adult stem cells towards bone and heart. We will also study the cellular mechanisms involved in the cloning of animals and how Scottish researchers produced the sheep Dolly using the nucleus of a mammary gland cell from an adult sheep. We will read papers describing organ production, such as the in vitro formation of beating heart cells. We will also consider the molecular bases of cellular and functional changes of different organs that occur in disease and treatments that cause tissue remodeling to correct these changes. We will discuss how studies of the developmental, cellular and molecular biology of regeneration have led to the discovery of new drugs. We will visit the Massachusetts General Hospital to see the patients with regenerated tissues.



7.344 Taking Snapshots of Protein Complexes in Action

Instructor: Nozomi Ando (nando at mit.edu<mailto:nando at mit.edu>, 617-715-4891; laboratory of Catherine Drennan)  Edward Brignole (brignole at mit.edu<mailto:brignole at mit.edu>, 617-715-4891; laboratory of   Catherine Drennan) Wednesdays 3-5 pm. (Class time is flexible.) Room 68-151.

In 1958, John Kendrew and his co-workers used X-ray crystallography to solve the world’s first structure of a protein at atomic resolution. This technological breakthrough was one of the defining moments in modern biology. Today, structure determination is an integral part of biology. More than 66,000 structures have been solved to date, allowing us to understand the chemistry, folding, and binding of proteins and other biomacromolecules. Inside a cell, however, many thousands of different proteins are working on a vast array of functions through their interactions with each other. So, now that we know what many proteins look like, how can we visualize them at work? Some protein complexes are too large and complicated to be easily crystallized, and some protein interactions are too weak or dynamic to be properly captured by crystallography. In this course, we will discuss the usage of two structural techniques, small-angle X-ray scattering (SAXS) and electron microscopy (EM), that help to fill the gap between atomic-level structure determination and cellular-level imaging. We will discuss the history of the now standard methods of biological structure determination, with emphasis on how SAXS and EM have been used to visualize complicated protein complexes such as viruses, DNA replication and repair machinery, and metabolic enzymes and how they have contributed to a dynamic view of the protein structure-function relationship. Students will learn about exciting protein structure-function research and current technologies used in this field.



7.345 Cancer and Its (Micro)environment – from Basic Science to Therapy

Instructors: Julia Rastelli (rastelli at wi.mit.edu<mailto:rastelli at wi.mit.edu>, 8-5173; laboratory of Bob Weinberg) Asaf Spiegel (spiegel at wi.mit.edu<mailto:spiegel at wi.mit.edu>, 8-5173; laboratory of Bob Weinberg) Tuesdays, 2-4 pm. (Class time is flexible.) Room 68-151.

Despite major advances in cancer research, the treatment of most cancers remains insufficient, rendering the disease a leading cause of death in the western world. Tumors are complex tissues that consist not only of malignant cells but also of a variety of non-malignant stromal cells, such as blood vessel cells, immune cells, and fibroblasts. What is the role of stromal cells in the tumor, and what is the normal physiological role of such cells in the human body? Where do stromal cells come from, and what triggers their recruitment into tumors? How do stromal cells affect the fundamental steps of tumor progression, such as angiogenesis (blood vessel formation) and metastasis (spreading of tumor cells to distant tissues)? In this course we will discuss and critically evaluate scientific papers that attempt to answer these questions in one of the most exciting and rapidly evolving fields in cancer research – the tumor (micro)environment. We will also discuss how non-malignant tumor cells might be used as new targets for cancer therapy as a complement to conventional therapy based on targeting only the malignant cells.



7.346 Metastasis: The Deadly Spread of Cancer

Instructors:  John Lamar (lamarj at mit.edu<mailto:lamarj at mit.edu>, 452-2769; laboratory of Richard Hynes)  Amy McMahon (mcmahona at mit.edu<mailto:mcmahona at mit.edu>, 452- 2769; laboratory of Richard   Hynes)Spring 2011. Thursdays, 1-3 pm. (Class time is flexible.) Room 68-151.

Cancer is a devastating disease that kills millions of people every year. Greater then 90% of these deaths result from metastasis, the spread of cancerous cells from the initial tumor to other organs in the body. Metastasis is a complex cascade involving several essential cellular processes, including migration, invasion, intravasation and extravasation (entering and exiting the bloodstream, respectively), survival, and growth. It is still unclear what is occurring at the molecular level inside tumor cells to promote cancer progression, making metastasis an important area of research in cancer biology. In this course we will discuss current theories about how cancer cells gain the ability to metastasize as well as how several of the critical processes involved in metastatic dissemination are regulated at a cellular level. We will investigate how metastasis can be influenced by the interaction of tumor cells with other cells in the body, including non-malignant cells present in the tumor, the bloodstream, and distant organs to which tumor cells metastasize. We will learn about existing therapies that target metastatic dissemination and explore how new therapies could be designed to target the processes and interactions discussed throughout the course. We will visit a research facility and have the optional opportunity to attend research seminars presented by prominent scientists in the field.



7.347 Fueling Sustainability: Engineering Microbial Systems for Biofuel Production

Instructor:  Michelle O’Malley (momalley at mit.edu<mailto:momalley at mit.edu>, 3-9838; laboratory of Chris   Kaiser) Thursdays, 3 pm – 5 pm. (Class time is flexible.) Room 68-151.

The need to identify sustainable forms of energy as an alternative to our dependence on depleting worldwide oil reserves is one of the grand challenges of our time.  The energy from the sun converted into plant biomass is the most promising renewable resource available to humanity.  Almost all of this energy is contained within cellulose, the natural yet difficult to digest polymer of sugars that make up plant cell walls.  How can we unlock the energy within cellulose and convert it to more useful forms of energy?  Fortunately, nature has evolved several enzymes that work together to break down cellulose.  These enzymes are found within bacteria and fungi that thrive in cellulose-rich environments (e.g., the digestive tracts of grazing animals, compost piles, and soil).  Sugars released from cellulose hydrolysis can later be fermented into biofuels like ethanol.  We will examine each of the critical steps along the pathway towards the conversion of plant biomass into ethanol.  We will focus on the biology behind enzymatic cellulose breakdown, the different types of enzymes required, and how these enzymes form complexes in nature that improve their catalytic performance.  State-of-the-art methods currently in use to identify new cellulolytic enzymes with novel properties as well as metabolic engineering strategies to introduce these enzymes into yeast will be discussed.  We will further examine issues associated with industrial-scale production and catalytic performance of cellulolytic enzymes; such issues have limited the economic feasibility of cellulosic biofuels.  By the end of the course, students will have a broader knowledge regarding the biology behind cellulose breakdown, the challenges associated with industrial biofuel production, and new opportunities to further its development.



7.348 Bacterial Communities: Group Behavior through Chemical Signals

Instructors: Carla Bonilla (cbonilla at mit.edu<mailto:cbonilla at mit.edu>, 3-6702; laboratory of Alan Grossman) Fridays ,11 - 1 pm. (Class time is flexible.) Room 68-151.

Bacteria are everywhere, living in the soil, the oceans and on and in our bodies. Bacteria help us stay healthy by aiding us in nutrient absorption and vitamin production as well as by guarding our bodies against virulent species. But bacteria can also threaten our health by causing deadly infections.  Although they are single-celled organisms, much of what bacteria do, “good” or “bad,” originates from their ability to perform complex communal behaviors that allow them to act as multicellular entities. How can such single-celled organisms function in multicellular communities? How do bacteria “talk” to each other? In this course, we will learn about conserved chemical languages that bacteria use to communicate with other bacteria of the same or different species. We will study group behaviors of bacteria, including the roles of such group behaviors in allowing bacteria to colonize a host, to defend themselves from predatory bacterial species or from antibiotics, and simply to live in harmony in large multicellular communities, such as in biofilms. We will learn about the chemical signals used by different bacteria, including certain pathogenic species, such as Pseudomonas aeruginosa and Vibrio cholera, and how these signals are sensed and interpreted through different genetic and molecular pathways. Understanding the language that bacteria use to communicate is important not only as a basic aspect of the extensive microbial world but also because of implications for developing new treatments for infections caused by pathogenic bacteria. Current antibiotics kill bacteria directly and consequently select for resistant individuals. With drugs designed to silence bacterial communication, on the other hand, there is no selective pressure to survive, and therefore such treatments might offer a way to circumvent the development of drug resistance, a major clinical problem today.



7.349   Stem Cells: A cure or disease?

Instructors:   Grant Welstead (welstead at wi.mit.edu<mailto:welstead at wi.mit.edu>, 8-5205; laboratory of Rudolf Jaenisch)
Steve Bilodeau (bilodeau at wi.mit.edu<mailto:bilodeau at wi.mit.edu> , 8-5236; laboratory of Richard Young) Thursdays, 1-3 pm. (Class day and time is flexible.) Room 68-121.

Have you ever considered going to a pharmacy to order some new cardiomyocytes (heart muscle cells) for your ailing heart?  It might sound crazy, but recent developments in stem cell science have made this concept not so futuristic. In this course, we will explore the underlying biology behind the idea of using stem cells to treat disease, specifically analyzing the mechanisms that enable a single genome to encode multiple cell states ranging from neurons to fibroblasts to T cells. We will study new developments in the area of cellular reprogramming and transdifferentiation and highlight how we have gained the power to control cell states in a Petri dish. Specifically, this course will not only introduce important biological concepts like pluripotency and epigenetics but also focus on key technologies that are used to study them, such as genome-wide sequencing and transcription-mediated reprogramming. We will also consider the potential consequences and limitations of stem cell therapy, particularly the connection between stem cells and cancer. Overall, we hope to provide a comprehensive overview of this exciting new field of research and its clinical relevance.











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