[bioundgrd] Biology Advanced Undergraduate Seminars Spring 2016

Fri Dec 11 11:52:00 EST 2015

Please see the message below from Professor Horvitz regarding Advanced Undergraduate Seminars for the upcoming academic year. You can find course information here: https://biology.mit.edu/undergraduate/course_listings/advanced_undergraduate_seminars

TO:     MIT Biology Majors

FROM:   H. Robert Horvitz, Professor of Biology

DATE:  December 10, 2015

        I am writing to inform you of an exciting offering from the Department of Biology for the 2015-2016 academic year:  a set of eight very current seminar courses, 7.34x, Advanced Undergraduate Seminars.  A complete listing of the courses, instructors, and brief course descriptions is enclosed.  The topics are highly varied and encompass areas of genetics, genomics, biochemistry, molecular biology, microbiology, cell biology, developmental biology, cancer biology, immunology, neurobiology, reproductive biology, stem cells, bioengineering, biomaterials, biotechnology, pharmaceuticals 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 one short written assignment and one oral presentaton.  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(s), 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, analyze and critique 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 2015 semester, please check our website (https://biology.mit.edu/undergraduate/course_listings/advanced_undergraduate_seminars) and/or contact the instructors.

Advanced Undergraduate Seminars
2015-2016

Spring 2016

7.341  Treating Infertility – From Bench to Bedside and Bedside to Bench
Instructors: Michelle Carmell (carmell at wi.mit.edu<mailto:carmell at wi.mit.edu>, 617-258-5174; laboratory of David Page)
                  Jana Hersch (jckoubov at mit.edu<mailto:jckoubov at mit.edu>, 617-710-3496, Educational Coordinator, MIT Biology)
Spring 2016.  Tuesdays 1-3 pm. (Class day and time are flexible.)  Room 68-150.

In the western world, approximately 10-15% of couples suffer from subfertility. Consequently, over 5 million babies have been born thanks to assisted reproductive technologies, and more than half of those have been born in the past six years.  In some countries, 3-5% of births are achieved with assisted reproductive technologies, and this number is projected to grow as societies become increasingly interested in beating the biological clock.  This class will discuss the basic biology behind fertility and explore the etiology of infertility. We will cover the latest developments in reproductive science and consider the clinical challenges of translating research findings into medical treatments.  We will discuss recent studies of gonadal stem cells and their use for rejuvenation of fertility, oocyte and embryo cryopreservation studies and usage, current diagnostic tools for common causes of male infertility, and key mouse models with reproductive phenotypes.  This class will highlight open questions in reproductive biology, familiarize students with both tried-and-true and emerging reproductive technologies, and explore the advantages and pitfalls of each.  Students will have the opportunity to visit a Boston-area IVF (in vitro fertilization) clinic and speak with researchers who are on the front lines of reproductive technologies.

7.342  Pluripotent Stem Cells and Genome Engineering for Modeling Human Diseases

Instructors:Malkiel Cohen (malkiel at wi.mit.edu<mailto:malkiel at wi.mit.edu>, (617)852-5860, laboratory of Rudolf Jaenisch)

                    Katherine Wert (wert at wi.mit.edu<mailto:wert at wi.mit.edu>, (425)922-9055, laboratory of Rudolf Jaenisch)

MIT OpenCourseWare Website:

http://ocw.mit.edu/courses/biology/7-342-pluripotent-stem-cells-and-genome-engineering-for-modeling-human-diseases-spring-2015/index.htm

Spring 2016. Tuesdays, 3 pm – 5 pm. (Class day and time are flexible.) Room 68-150.

One of the major priorities in biomedical research is understanding the molecular events that establish the complex processes involved in human development and the relationships of these processes to human disease and disease progression. The role of stem cells as a tool to help reveal these processes has long been appreciated.  During the 20th century, Mario Capecchi, Martin Evans, and Olivier Smithies made ground-breaking discoveries using mouse embryonic stem cells for gene targeting in mammals. Their efforts made it possible to modify DNA of specific genes within the genomes of living and fertile mice, allowing scientists to determine the roles of individual genes in health and disease. This approach of genome engineering has produced numerous non-human vertebrate models of human disorders, including diabetes, cancer, cardiovascular and neurodegenerative diseases. For their discoveries, Capecchi, Evans, and Smithies shared the 2007 Nobel Prize in Physiology and Medicine. In 2012, the Nobel Prize in Physiology and Medicine was received by Shinya Yamanaka and John Gurdon for their discovery that cells of mature humans and other animals can be reprogrammed to an early embryonic stage, known as pluripotency, and then differentiate into various cell types of the adult body. This work and many other studies have stimulated the stem cell field into generating pluripotent stem cells from human patients, and these patient-specific stem cells have been used to better model human diseases by reflecting those disorders in a cell culture system. Scientists can now cause such patient-specific stem cells to differentiate into the cell type that is affected by the disease, allowing the study of the diseased cells and an understanding of the mechanisms underlying disease progression; these cells can be further used to test potential treatment options. In this class, we will explore the field of stem cell biology and the way in which this field has developed and shaped our ability to study complex human disease. We will introduce the topics of stem cell biology and genome engineering through critical reading of both the classical and newest primary research literature. This course will focus on the methods behind the generation of embryonic and induced pluripotent stem cells, genome editing to create transgenic animal models of human diseases, regenerative medicine (such as the transplantation of stem cell-derived cell types to replace diseased tissues), and current hot topics in genome engineering such as CRISPR/cas9, a novel method that can be used to delete or insert genes of interest in cultured cells and intact organisms. In addition, this course will discuss specific disease model systems and their benefits/limitations for understanding the disease and treating human patients. Students will obtain a deep understanding of the main concepts and questions concerning stem cell biology, become familiar with current research techniques to model complex human diseases, and learn to critically evaluate the experimental design and claims in this field.

7.343  An RNA Safari: Exploring the Surprising Diversity of Mammalian Transcriptomes
Instructors: Athma Pai (athma at mit.edu<mailto:athma at mit.edu>, 3-7039, laboratory of Chris Burge)
                   Matt Taliaferro (jmtali at mit.edu<mailto:jmtali at mit.edu>, 3-6726, laboratory of Chris Burge)
Spring 2016. Wednesdays, 11 am-1 pm. (Class day and time are flexible.) Room 68-150.

One of the most fascinating aspects of mammalian biology is the use of a single DNA blueprint to create a myriad of RNA molecules that define each differentiated cell type. For many years, it was thought that RNA exists solely to do the bidding of DNA by relaying instructions for protein synthesis to the cytoplasm and aiding in translational processes. However, recent research into RNA biology has shown that RNA exists in the cell in many varied forms, each with a distinct set of cellular responsibilities. We now understand that RNAs are dynamic molecules capable of participating in a wide range of chemical reactions, from guiding the modification and processing of other RNA molecules to directing protein complex formation or silencing unwanted transposon expression. Many newly discovered RNA classes have unique capabilities and reveal surprising complexity in their compositions, lengths, and even shapes. The aim of this class is introduce the exciting and often underappreciated discoveries in RNA biology by exploring the diversity of RNAs – encompassing classical molecules such as ribosomal RNAs (rRNAs), transfer RNAs (tRNAs) and messenger RNAs (mRNAs) as well as newer species, such as microRNAs (miRNAs), long-noncoding RNAs (lncRNAs), and circular RNAs (circRNAs). For each class of RNA we will discuss its role as a critical component of cellular machinery, its function in the context of disease, and/or its adaptation as a powerful tool in molecular biology. We will discuss the seminal studies that led to the discovery of each class of RNA, beginning with classic experiments that first identified the mRNAs, rRNAs and tRNAs as key regulators of gene expression. Given this historical perspective, we will move forward by discussing a new class of RNAs each week. As we progress, we will consider advances in techniques and equipment that have that facilitated the discovery, annotation, and analysis of new RNA molecules, with a particular focus on high-throughput sequencing and novel genomic methods. In line with this approach, we will visit a research platform at the Broad Institute of MIT and Harvard to better understand the impact of these techniques and to meet scientists helping to further discoveries in RNA biology. Class sessions will be highly interactive and focus on the critical reading of the primary research literature to introduce important concepts in RNA biology, experimental approaches, and as-yet-unanswered questions in the field. For each new class of RNA, we will evaluate the evidence for its existence as well as for its proposed function. Students will develop both a deep understanding of the field of RNA biology and the ability to critically assess new papers in this fast-paced field.

7.344  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 2016. Wednesdays, 1 pm – 3 pm. (Class day and time are flexible.) Room 68-150.

Genomic DNA is constantly under attack by a wide variety of DNA-damaging agents, and DNA mutations can cause cancer. Although cells possess multiple DNA repair mechanisms, DNA lesions can escape repair, and DNA synthesis can be blocked as a consequence. Translesion DNA synthesis (TLS) is a mechanism that helps cells tolerate unrepaired DNA lesions through replication of damaged DNA 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 by catalyzing accurate replication bypass of specific DNA lesions and performing DNA repair synthesis. For example, TLS polymerase  accurately bypasses thymine dimers, the major ultraviolet 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 chemoresistance by introducing mutations in genes during error-prone TLS or when performing TLS past DNA lesions induced by chemotherapeutic agents. In this case, TLS polymerase  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 first discuss the basic mechanisms of tumorigenesis and chemoresistance. We will then turn our focus to TLS pathways and review the functions of TLS polymerases and discuss how defects in and/or dysregulation of the functions of TLS polymerases can promote tumorigenesis and chemoresistance. Additionally, we will learn about the emerging cancer therapies that target TLS pathways. Toward the end of the course, we will discuss the roles TLS polymerases play outside TLS and how these previously unknown functions of TLS polymerases relate to tumorigenesis and chemoresistance. We will discuss the primary research literature to allow students to learn how to read and critique research papers. There will also be an opportunity to visit a local pharmaceutical company that is developing cancer therapeutics.

7.345  Are There Inherent Limits to Our Understanding in Biology? A Challenge and Exploration Based on Diseases of the Nervous System
Instructor: Sepehr Ehsani (ehsani at csail.mit.edu<mailto:ehsani at csail.mit.edu>; 617-797-8940; laboratory of Bonnie Berger)
Spring 2016. Wednesdays 3 pm ‒ 5 pm. (Class day and time are flexible.) Room 68-150.

Molecular biology over the past two decades has experienced significant changes in both methods and understanding, with major technical innovations facilitating diverse breakthroughs. For example, high-throughput techniques and genome sequencing, introduced in the 1990s, have generated vast quantities of data and valuable insights concerning the workings of the cell under normal and disease conditions. The impact of these findings in the context of human disease has been greatest in the case of single-gene disorders (e.g., cystic fibrosis), which in general are relatively rare. However, most common human diseases, ranging from solid tumors (e.g., sarcomas and carcinomas) to cardiovascular, neurodegenerative and neuropsychiatric pathologies, have remained refractory to non-symptomatic therapeutic interventions, mostly because researchers have been unable to identify simple causative mechanisms. In other words, most common diseases have proved to be both heterogeneous in origin and mechanistically complex. Why is this the case, and what is preventing us from reaching an understanding of the pathologies of these disorders -- a scientific understanding that is not merely descriptive but rather founded on mechanism? This course aims to examine current challenges in the field of pathobiology (the study of the molecular and physiological mechanisms of disease). Students will discuss, through detailed analysis of the primary research literature, whether these challenges possess an underlying commonality. For example, have ultimate causes of many diseases remained elusive because of (i) limitations in experimental or computational methodology, (ii) limitations in our ability to interpret complex data, and/or (iii) some unknown facet of the diseases themselves? Can we identify a common thread in the answers to these questions for multiple diseases? In our efforts to answer such questions, might we discover some inherent limitation to human understanding -- a cognitive limitation similar to that which a rodent faces when fruitlessly attempting to learn to navigate a prime-number maze? If the answer is yes, can we do anything to overcome that limitation? If the answer is no, does that mean that there are no upper limits to what science can reveal and to what we can comprehend, e.g., concerning the etiology of a disease? We will focus on disorders of the nervous system, such as neurodegenerative diseases and cancers of the central nervous system. Our discussions will be framed by two general themes: (i) the quantification and meaning of uncertainty in experimental biology and (ii) a potential limit to scientific understanding. The primary goals of this course are for students to enhance their skills in critically evaluating the primary research literature and to think about the relationship between objective realities as typified by experimental data and human cognitive abilities and limits. The course will include a field trip to a computational/theoretical biology laboratory focused on the structures of proteins to observe how theoretical studies of protein structures can help reveal novel facets of pathological protein-protein interactions in neurodegenerative disorders.

7.346  Engineering Immune Responses through Biomaterial Design
Instructors: Tyson Moyer (tmoyer at mit.edu<mailto:tmoyer at mit.edu>, 3-0656, laboratory of Darrell Irvine)
                   Kavya Rakhra (kavyarakhra at gmail.com<mailto:kavyarakhra at gmail.com>, 3-0656, laboratory of Darrell Irvine)
Spring 2016. Thursdays, 11 am – 1 pm. (Class day and time are flexible.) Room 68-150.

Vaccines are combinations of antigens (substances that stimulates an adaptive immune response) and adjuvants (substances that accelerate, prolong or enhance an antigen-specific immune response) that can elicit a robust, long-lasting immune response. Vaccines have been used to eradicate diseases like small pox and polio. Other diseases, including HIV, cancer, and various autoimmune disorders, have not been able to be effectively treated using vaccines. In this course we will focus on bioengineering approaches to better understand the mechanisms of immune responses and to create novel therapeutics. Based upon the recent primary research literature, we will discuss approaches to understand and enhance the interactions of synthetic biomaterials with the immune system to program immune cells to perform specific tasks, such as the production of HIV-neutralizing antibodies by B cells or the elimination of cancer cells by enhancing the activity of cytotoxic T cells. Specifically, we will discuss parameters that affect the behaviors of different materials, such as particle size, shape, and chemical structure, in the contexts of vaccines. We will also consider other immunotherapies, such as the engineering and delivery of anti-tumor antigen specific T-cells. For effective vaccine design, antigens and specific immune-cell targeting molecules (e.g. antibodies specific to surface receptors on immune cells) must be displayed on the surface of larger particulates or scaffolds. Additionally, immunostimulatory danger signals that indicate the presence of pathogens to and trigger responses from the innate immune system must be hidden and encapsulated into the interior of the material scaffold. The effects of materials properties on vaccine performance will be discussed in the context of the route of administration, the trafficking of particles within the body, and the release of antigens. We will critically examine the functioning of the immune system in normal and diseased states such as cancer, autoimmune disorders and HIV/AIDS as well as other infectious diseases. We will discuss strategies to optimize biomaterials vaccine design through controlled release of antigens and adjuvants using different materials platforms (polymers, lipids, metals). We will visit a biotechnology company that focuses on the synthesis of lipid-based materials to design therapeutic vaccines to treat human papilloma virus (HPV) induced cancers.  Students will gain an understanding of the biological and synthetic parameters that are important in materials design for the modulation of the immune system as well as the ability to evaluate and design well-controlled experiments to test scientific hypotheses.

7.347  Peptides as Biological Signaling Molecules and Novel Drugs
Instructor: Mohammed Shabab (shabab at mit.edu<mailto:shabab at mit.edu>, 617-253-3745, laboratory of Graham Walker)
Spring 2016. Thursdays, 1 pm - 3 pm. (Class day and time are flexible.) Room 68-150.

All living cells possess the machinery for peptide synthesis, secretion, and posttranslational modifications. An enormous structural and functional diversity of peptides is generated by use of this cellular machinery. Peptides are broadly used as signal molecules for intercellular communication by prokaryotes, plants, fungi, and animals. Peptide signals in animals include vast numbers of peptide hormones, growth factors and neuropeptides. Some of the best known examples are enkephalins (which help us sense pain), somatotropin (which helps us grow), and insulin and glucagon (both of which regulate our blood glucose levels). Similarly in plants, peptide signals such as CLAVATA3 play important roles in development. Peptides are also used by living organisms as components of their host defense systems. What determines the functional specificity of each peptide? How do these small polymers of amino acids survive hostile protein-digesting enzymes? How are peptides able to communicate with their specific peptide receptors and other interacting proteins for proper function? In this course, we will learn about molecular bases of peptide signaling. In addition, peptides potentially can be used as potent broad-spectrum antibiotics and hence might define novel therapeutic agents. For example, antimicrobial peptides (AMPs) are low molecular weight proteins with broad spectrum antimicrobial activity against bacteria, viruses, and fungi and are found among all lifeforms. The ability of AMPSs to kill multidrug-resistant microorganisms has gained them considerable attention and clinical interest, since multidrug-resistant microorganisms have developed resistance to multiple antimicrobial agents and are difficult to treat with available antibiotics. One of the most notorious examples is MRSA, deadly strains of methicillin-resistant Staphylococcus aureus. Infections with these pathogenic bacteria are untreatable with known antibiotics like gentamicin, streptomycin and kanamycin. Some antimicrobial peptides can kill methicillin-resistant S. aureus strains, making these promising drugs or drug leads. In this class, we will discuss signaling and antimicrobial peptides, their biological functions, mechanisms of action, and applicability as therapeutic agents. Students will learn about various human defense peptides, such as defensins, neuropeptides and about plant peptides involved in symbiosis, such as nodule-specific cysteine-rich peptides. We will consider techniques to detect, quantify and modify peptides. We will also discuss experimental methods, such as high-performance liquid chromatography (HPLC) and liquid chromatography coupled with mass spectroscopy (LC-MS), used for quantification of peptides and other small molecules. We will focus on the primary research literature, and students will learn how to read and critique research papers. Additionally, we will visit Aileron Therapeutics, a pharmaceutical company based in Cambridge, MA, which is developing peptide inhibitors of p53 pathways for treatment of solid and hematological malignancies.

7.348  An Evolutionary Arms Race: Molecular and Immunological Mechanisms Underlying the Causes of Infectious Diseases
Instructors: Jasdave Chahal (chahal at wi.mit.edu<mailto:chahal at wi.mit.edu>, 609-613-1129, laboratory of Hidde Ploegh)
                   Florian Schmidt (fschmidt at wi.mit.edu<mailto:fschmidt at wi.mit.edu>, 857-313-9456, laboratory of Hidde Ploegh)

Spring 2016. Thursdays, 3 pm – 5 pm. (Class day and time are flexible.) Room 68-150.

Infectious diseases were the leading cause of human death until just this past century, and continue to be so in low-income countries. The surge forward in the biological understanding of pathogens that began in the late 19th century led, with impressive speed, to the near eradication of the most deadly bacterial, viral, and parasitic afflictions in developed nations. Nevertheless, new infectious agents, such as HIV and SARS coronavirus, adapt to humans on a regular basis and challenge both our immune and healthcare systems. Modern tools now allow us to dissect in exquisite detail the mechanisms exploited by infectious agents that contribute to their propagation and, ultimately, to their morbidity and mortality in human populations. Understanding how pathogens invade a host, replicate by hijacking the host’s cells, and evade the immune system requires an understanding of basic molecular and cell biology and the ability to apply the concepts of modern biology to new problems. In fact, studying host-pathogen interactions and using pathogens as biological probes have led to fundamental discoveries in the field of cell biology. In this course, students will learn to critically analyze the primary research literature and to understand, critique, interpret, and design scientific experiments in the field of host-pathogen interactions. The strategies used by the most successful human pathogens will be examined, with an emphasis on the molecular details of the pathogen life cycles that lead to morbidity and the countermeasures employed both by the immune system and by medical treatments to combat them. We will discuss well-studied pathogens for which effective treatments have long been available as well as emerging diseases that have only begun to be fully understood. The goals of this course are to challenge students to apply their basic knowledge about biology to the pathology of human infectious diseases and to attain a perspective concerning the challenges of addressing the substantial burden of infectious disease in less developed parts of the world. Students will visit a local academic laboratory focused on the elucidation of novel interactions between a human pathogen and host cells.

Joyce Roberge
Undergraduate Program
Biology Education Office 68-120
Massachusetts Institute of Technology
31 Ames Street
Cambridge, MA 02139
617-253-4718
fax: 617-258-9329
email: roberge at mit.edu<mailto:roberge at mit.edu>

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