[bioundgrd] Biology Undergraduate Seminars Spring 2014

[Janice Chang]

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

        I am writing to inform you of an exciting course offering from the Department of Biology for this Spring, 2014:  a set of 7 very current seminar courses, 7.34x, Advanced Undergraduate Seminars.  These courses are similar in nature to the Advanced Undergraduate Seminars offered this past semester. A complete listing of the courses, instructors, and brief course descriptions is enclosed.  The spring topics are highly varied and encompass areas of genetics, genomics, biochemistry, molecular biology, cell biology, cancer biology, immunology, neurobiology, virology, epigenetics, stem cells, bioengineering, and human disease.

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 and in particular to discuss possible meeting days and times if those listed are not possible for you.

            To learn more about the Advanced Undergraduate Seminars to be offered during the Spring 2014 semester, please check our website (https://biology.mit.edu/undergraduate/course_listings/advanced_undergraduate_seminars) and/or contact the instructors.




Advanced Undergraduate Seminars

Spring 2014

7.341 Designer Immunity: Lessons in Engineering the Immune System
Instructors:   Gregory Szeto (gszeto at mit.edu<mailto:gszeto at mit.edu>, 617-253-0656; laboratories of Darrell Irvine and Douglas Lauffenburger)
            Talar Tokatlian (talar at mit.edu<mailto:talar at mit.edu>, 617-253-0656; laboratory of Darrell Irvine)
Spring 2014. Fridays 11 am – 1 pm. (Class time is flexible.) Room 68-150.

The immune system is one of the most complex and powerful of human body systems. It is highly dynamic and flexible, yet strictly regulates homeostasis and protects our bodies from both foreign and self-derived challenges. As basic understanding of immune function is growing, researchers are rapidly designing clever and diverse strategies to manipulate immunology to improve human health. In this course, we will explore important advances rooted in engineering principles to harness the power of the immune system, focusing on how engineering has fueled or inspired research concerning (1) vaccines, (2) immunotherapies, and (3) systems immunology. First we will discuss how engineering can improve the efficacy and efficiency of both delivery of vaccines to immune organs and vaccine-induced immunity. Next we will discuss engineered therapies to manipulate immunology in diseases such as cancer. Then we will focus on systems-based tools, including multivariate profiling and regulatory network analyses that have been developed to predict cell or patient immune responses to vaccines, therapies, and diseases. Many approaches to vaccine design and immunomodulation will be discussed, including therapeutics and prophylactics for influenza, hepatitis B, HIV/AIDS, malaria, cancer, and autoimmunity. Specific examples will include biomaterials as vaccine carriers that have been inspired by the natural biology of microbes and cell lines that have been engineered to use HIV antibodies as calcium signaling receptors to screen candidate HIV vaccines. Engineered therapies and immune system modeling are improving our understanding of immunology as well as our ability to manipulate immunological mechanisms for therapeutic purposes. A broad range of disciplines will be discussed, encompassing the fields of materials science and chemical, biomedical, electrical, and systems engineering. Each session will be driven by student-led discussions of important research articles. Emphasis will be placed on understanding the concepts, experimental techniques and experimental design utilized. Students should then be able to translate their reading of the primary research literature to the laboratory as well as to other real-world applications. We will visit an academic research laboratory or small biotechnology company currently engaged in immunoengineering.


7.342  Personal Genomics and Medicine: What’s in Your Genome?
Instructor: Zara Herskovits (aherskov at mit.edu<mailto:aherskov at mit.edu>; 3-4140; laboratory of Dr. Leonard Guarente)
Spring, 2014. Thursdays, 11 am – 1 pm. (Class time is flexible). Room 68-150.

Human genome sequencing has revolutionized our understanding of disease susceptibility, drug metabolism and human ancestry.   This course will explore how these advances have been made possible by revolutionary new sequencing methodologies that have decreased costs and increased throughput of genome analysis, making it possible to examine genetic correlates for a variety of biological processes and disorders.    Each student will have the opportunity  either to have the sequence of his/her own DNA determined or to explore publically available genome reference samples to understand what can be learned from examining genetic markers that can correlate with disease risk, carrier status and medication response.  We will discuss how an individual’s risk of developing a disease can be assessed based on small genetic changes in nucleotide sequence as well as on larger structural variations that affect entire regions of a chromosome.  We will also discuss how maternal ancestry, paternal lineage, and human populations can be analyzed by examining chromosomal or mitochondrial DNA.  We will read papers from the scientific literature to understand how genetic analysis is influencing treatment for patients who have cancers with specific mutations that can be targeted with tyrosine kinase inhibitors, such as individuals with chronic myelogenous leukemia who have the BCR-ABL fusion protein or patients with non-small cell lung cancer who have an EML4-ALK gene fusion.  Genomic analysis has also spurred the development of new drugs that might be helpful for patients in the general population, such as PCSK9 inhibitors for patients with hypercholesterolemia, an approach that was driven by the observation that people with a mutation in this gene have abnormally low LDL cholesterol. We will also debate social, legal and ethical aspects of genetic testing.  The course will combine discussions of primary scientific research papers with hands-on data analysis and small group presentations.  We will take a field trip to the Harvard Medical School Center for Personalized Genetic Medicine and Medical Genetics at the Brigham and Women’s Hospital to learn how genomic sequencing informs clinical decision making.


7.343  Biological Bases of Learning and Memory
Instructors:  Jai Subramanian (jai_sub at mit.edu<mailto:jai_sub at mit.edu>, 46-3225; laboratory of Elly Nedivi) and
                   Lauren Makuch (makuch at mit.edu<mailto:makuch at mit.edu>, 46-3225; laboratory of Elly Nedivi)
Spring 2014.  Thursdays, 3 pm – 5 pm. (Class time is flexible.)  Room 68-150.

The brain allows animals to have an incredible capacity to acquire information about the world and to encode, store, and later retrieve that knowledge. What are the biological bases of learning and memory? How does the brain come to learn whether a stimulus is annoying, rewarding or neutral, and how does remembering how to ride a bicycle differ from remembering scenes from a movie?  In this course, students will explore the concept that learning and memory have a physical basis that can be observed as biochemical, physiological and/or morphological changes to neural tissue. We will critically read and discuss primary research articles to become familiar with several different types of learning and memory and the experiments that have enabled them to be distinguished.  Newly learned information is encoded through changes in the strength of existing connections between neurons, called synapses (the junctions at which neurons communicate with each other), or by formation of new connections and/ or elimination of others. We will discuss the molecular and cellular mechanisms that mediate these changes by exploring concepts such as synapse formation and stabilization, synaptic transmission, synaptic plasticity, neuromodulation and experience-dependent circuit remodeling, among others. With this knowledge, we will discuss how scientists use cutting-edge technologies to introduce false memory in animals or tackle diseases affecting learning and memory, including Alzheimer’s disease and mental retardation. We will visit an MIT research laboratory that studies the biological bases of learning and memory or a pharmaceutical company that develops drugs to treat memory disorders.  Our goal will be to understand the strategies and techniques biologists use to search for memory traces , the “holy grail” of modern neuroscience.


7.344  Beyond the Code: Emerging Roles of Non-coding RNAs in the Regulation of Gene Expression
Instructors: Johanna Scheuermann (josch at mit.edu<mailto:josch at mit.edu>, 4-5094; laboratory of Laurie Boyer)
Jessica Hurt (hurt at mit.edu<mailto:hurt at mit.edu>, 3-6726; laboratory of Chris Burge)
Spring 2013. Wednesdays, 3 – 5 pm. (Class time is flexible.)  Room 68-150.

The central dogma of biology, “DNA makes RNA makes protein,” reflects the function of RNA primarily as a messenger molecule linking the storage of genetic information in DNA to its output as protein. However, recent groundbreaking research has revealed that only a small fraction of all mammalian RNA molecules is actually translated into protein.  Seeking the biological roles of this newly appreciated population of non-coding RNAs has quickly emerged as a novel horizon in the RNA field. We now know that many classes of non-coding RNAs, such as microRNAs and long non-coding RNAs, exist and play critical roles as regulatory molecules in the cell. Collectively, these RNA species are involved in every layer of the regulation of gene expression, often employing novel and unexpected molecular strategies. Numerous studies are underway with the goal of deciphering the many functions of non-coding RNAs in controlling differentiation, development, and tissue homeostasis. In this course we will discuss the classes of non-coding RNAs and differences between coding and non-coding transcripts. We will learn about mechanisms by which non-coding RNAs control gene expression, from the level of transcription and chromatin to the regulation of later steps in mRNA biogenesis, including transcription, splicing, polyadenylation and decay. For example, we will learn how microRNAs target specific mRNAs to inhibit protein synthesis and how incorrect expression of these RNAs can have dramatic consequences on cell differentiation and proliferation. We will also discuss how misregulation of non-coding RNAs has been linked to diseases such as cancer and Alzheimer’s disease and learn about exciting new therapeutic strategies involving non-coding RNAs, including for the treatment of muscular dystrophy. We are planning a field trip to an RNA laboratory with publications we will have studied in class, so that students will have an opportunity to discuss science directly with the authors and see in real life how the experiments were done. Classes will be based on interactive discussions of the primary research literature and will highlight open questions in the field, aspects of experimental design and data interpretation as well as the benefits and pitfalls of using different techniques to study non-coding RNAs. Students also will learn about current methodological and conceptual challenges in the RNA field.


7.345  Modulating DNA Damage Tolerance Pathways as an Approach to Novel Cancer Therapeutics
Instructor:  Kinrin Yamanaka (kinrin at mit.edu<mailto:kinrin at mit.edu>, 617-253-3745; laboratory of Graham Walker)
Spring 2014. Wednesdays, 11 - 1 pm. (Class time is flexible.) Room 68-150.

Genomic DNA is constantly under attack by a wide variety of DNA-damaging agents. Although cells possess multiple DNA repair mechanisms, DNA lesions can escape repair. As a consequence, DNA synthesis can be blocked and single-stranded DNA gaps can be generated. Translesion DNA synthesis (TLS) is a mechanism that helps cells tolerate unrepaired DNA lesions and is carried out by TLS DNA polymerases. The outcome of the lesion bypass can be either accurate or mutagenic, depending on the identity of the TLS polymerase involved and the type of DNA lesion. Thus, on the one hand TLS polymerases can prevent cancer from being triggered by catalyzing accurate replication bypass of specific DNA lesions and performing DNA repair synthesis. For example, polymerase  (pol ) accurately bypasses thymine dimers, the major ultraviolet UV light-induced DNA lesions, and deficiency in this polymerase causes Xeroderma Pigmentosum Variant XP-V, a disorder associated with a high incidence of skin cancer in humans. However, on the other hand, TLS polymerases upon encountering different DNA substrates also can promote carcinogenesis and resistance to chemotherapy by introducing mutations in crucial genes during error-prone TLS or performing TLS past DNA lesions induced by chemotherapeutic agents. In this case, pol  can facilitate cellular resistance to commonly used chemotherapeutic agents, such as cisplatin, by catalyzing replication bypass of cisplatin-induced lesions. In this course, we will discuss the basics of DNA damage repair and tolerance pathways. We will then turn to the TLS pathway and review the functions of each TLS polymerase and how defects in and/or dysregulation of the functions of TLS polymerases can promote tumorigenesis and chemoresistance. Additionally, we will learn about emerging cancer therapies that target TLS pathways and will explore what other therapies targeting this pathway might be designed to improve current cancer therapeutic strategies. We will focus on the primary research literature, so students will learn how to read and critique research papers. Additionally, we will visit a pharmaceutical company laboratory that is developing anti-cancer drugs.


7.346   The Battle Within - How the Innate Immune System Fights Infection
Instructor: Ana Camejo (acamejo at mit.edu<mailto:acamejo at mit.edu>, 5-4031; laboratory of Jeroen Saeij)
Spring 2014. Wednesdays, 1 pm – 3 pm. (Class day and time are flexible.) Room 68-150.

It is one of nature's fiercest battles, in many cases a matter of life and death. Humans are exposed to millions of potential pathogens daily, through contact, ingestion, and inhalation. Infectious diseases have the potential to decimate millions of people and can emerge naturally as outbreaks or pandemics, or deliberately through bioterrorism. The innate immune system comprises cells and mechanisms that defend the host from infection in a non-specific manner, without conferring protective long-lasting immunity to the host. Innate immune responses depend on a group of proteins and phagocytic cells that recognize conserved features of pathogens and become quickly activated to help destroy invaders. Innate immune responses have been found among both vertebrate and invertebrate animals, as well as in plants. In this course students will learn how to design and critique experiments through the discussion of primary research articles that explore the molecular basis of innate immunity. We will include studies that use vertebrate, invertebrate and plant models. We will discuss a variety of investigative approaches at the forefront of scientific discovery, including genetics, biochemistry, cell biology, and genomics/proteomics. Together, we will understand why the inflammasome is setting our cells on fire and unravel Nobel Prize winning topics, such as Toll-like receptors, the complement system and phagocytosis.


7.347  Epigenetic Regulation of Stem Cells
Instructors: Eric Williams (eow1 at mit.edu<mailto:eow1 at mit.edu>, 607-351 2831; laboratory of Leonard Guarente)
                 Joe Wamstad (jwamstad at mit.edu<mailto:jwamstad at mit.edu>, 617-324-5094; laboratory of Laurie Boyer)
Spring 2014. Thursdays, 1 pm - 3 pm. (Class time is flexible.) Room 68-150.

During development a single totipotent cell gives rise to the vast array of cell types present in the adult human body, yet each cell has essentially the same DNA sequence.  As cells differentiate, distinct sets of genes must be coordinately activated and repressed, ultimately leading to a cell-type specific pattern of gene expression and a particular cell fate. In eukaryotic organisms, DNA is packaged in a complex protein super structure known as chromatin. Modification and reorganization of chromatin plays a critical role in coordinating the cell-type specific gene expression programs that are required as a cell transitions from a pluripotent stem cell to a fully differentiated cell type.  Epigenetics refers to such heritable changes that occur in chromatin without altering the primary DNA sequence.  The ability to study the epigenome (the chromatin-associated proteins and RNAs that organize and coordinate access to DNA) on a grand scale has only recently become feasible with the advent of methods for genome-wide analyses and high-throughput sequencing technologies. For example, we are now able to map essentially any epigenetic modification that occurs to either the DNA itself and or to the chromatin protein scaffold around which the DNA is organized.  We can even decipher the 3-dimensional structure of chromatin within the nucleus during different epigenetic states. These advances have led to an explosion of data and a comprehensive picture of the epigenome and the factors that regulate it. In this class we will discuss the various mechanisms of epigenetic regulation, including DNA methylation and post-translational modification of histones, and the roles of chromatin-assembly modifying complexes, non-coding RNAs and nuclear organization. We will read papers from the primary research literature and discuss both the scientific discoveries and the new technologies that have made these discoveries possible. This class will focus on the role of epigenetic regulation with respect to developmental fate and also consider the fact that the epigenetic mechanisms discussed have broad implications, including how seemingly normal cells can be transformed into cancerous cells.







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