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<div style="margin:0px"><span style="font-size:12pt">Please see the message below from Professor Horvitz regarding Advanced Undergraduate Seminars for the upcoming academic year. You can find course information here: </span><a href="https://biology.mit.edu/undergraduate/course_listings/advanced_undergraduate_seminars" style="color:purple; font-size:12pt">https://biology.mit.edu/undergraduate/course_listings/advanced_undergraduate_seminars</a></div>
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<p class="x_MsoNormal"><span style="font-size:16px">TO: MIT Biology Majors</span></p>
<p class="x_MsoNormal"><span style="font-size:16px">FROM: H. Robert Horvitz, Professor of Biology</span></p>
<p class="x_MsoNormal"><span style="font-size:16px">DATE: December 10, 2015</span></p>
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<p class="x_MsoBodyText"><span lang="EN-GB" style="font-size:16px"> 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.</span></p>
<p class="x_MsoBodyText" style="text-indent:.5in"><span lang="EN-GB" style="font-size:16px">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.</span></p>
<p class="x_MsoBodyText"><span lang="EN-GB" style="font-size:16px"> 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.</span></p>
<p class="x_MsoNormal"><span style="font-size:16px"> 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.</span></p>
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<p class="x_MsoNormal"><span style="font-size:16px"> To learn more about the Advanced Undergraduate Seminars to be offered during the Spring 2015 semester, please check our website (<a href="https://biology.mit.edu/undergraduate/course_listings/advanced_undergraduate_seminars">https://biology.mit.edu/undergraduate/course_listings/advanced_undergraduate_seminars</a>)
and/or contact the instructors.</span></p>
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<b><font face="Helvetica" size="3">Advanced Undergraduate Seminars</font></b></div>
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<b><font face="Helvetica" size="3">2015-2016</font></b></div>
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<b style="font-size:12pt"><font face="Helvetica" size="3"><u>Spring 2016</u></font></b></div>
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<font face="Helvetica" size="3"><b>7.341 Treating Infertility – From Bench to Bedside and Bedside to Bench</b></font></div>
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<font face="Helvetica" size="3">Instructors: Michelle Carmell (<a href="mailto:carmell@wi.mit.edu" style="color:purple">carmell@wi.mit.edu</a>, 617-258-5174; laboratory of David Page)</font></div>
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<font face="Helvetica" size="3"> Jana Hersch (<a href="mailto:jckoubov@mit.edu" style="color:purple">jckoubov@mit.edu</a>, 617-710-3496, Educational Coordinator, MIT Biology)</font></div>
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<font face="Helvetica" size="3">Spring 2016. Tuesdays 1-3 pm. (Class day and time are flexible.) Room 68-150.</font></div>
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<font face="Helvetica" size="3">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 (<i>in vitro </i>fertilization)
clinic and speak with researchers who are on the front lines of reproductive technologies.</font></div>
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<b><font face="Helvetica" size="3">7.342 Pluripotent Stem Cells and Genome Engineering for Modeling Human Diseases</font></b></p>
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<font face="Helvetica" size="3">Instructors:<b></b>Malkiel Cohen (<a href="mailto:malkiel@wi.mit.edu" style="color:purple">malkiel@wi.mit.edu</a>, (617)852-5860, laboratory of Rudolf Jaenisch)</font></p>
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<b style="font-family:Helvetica"> </b><span style="font-family:Helvetica; font-size:14px">Katherine Wert (<a href="mailto:wert@wi.mit.edu" style="color:purple">wert@wi.mit.edu</a>, (425)922-9055, laboratory of Rudolf Jaenisch)</span></p>
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<font face="Helvetica" size="3">MIT OpenCourseWare Website: </font></p>
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<u><span style="color:blue"><font face="Helvetica" size="3"><a href="http://ocw.mit.edu/courses/biology/7-342-pluripotent-stem-cells-and-genome-engineering-for-modeling-human-diseases-spring-2015/index.htm" style="color:purple">http://ocw.mit.edu/courses/biology/7-342-pluripotent-stem-cells-and-genome-engineering-for-modeling-human-diseases-spring-2015/index.htm</a></font></span></u></p>
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<font face="Helvetica" size="3">Spring 2016. Tuesdays, 3 pm – 5 pm. (Class day and time are flexible.) Room 68-150.</font></p>
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<font face="Helvetica" size="3">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 20<sup>th</sup> 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.</font></p>
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<font face="Helvetica" size="3"><b>7.343 An RNA Safari: Exploring the Surprising Diversity of Mammalian Transcriptomes</b></font></div>
<div style="margin:0in 0in 0.0001pt; font-size:12pt; font-family:'Times New Roman'">
<font face="Helvetica" size="3">Instructors: Athma Pai (<a href="mailto:athma@mit.edu" style="color:purple">athma@mit.edu</a>, 3-7039, laboratory of Chris Burge) </font></div>
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<font face="Helvetica" size="3"> Matt Taliaferro (<a href="mailto:jmtali@mit.edu" style="color:purple">jmtali@mit.edu</a>, 3-6726, laboratory of Chris Burge)</font></div>
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<font face="Helvetica" size="3">Spring 2016. Wednesdays, 11 am-1 pm. (Class day and time are flexible.) Room 68-150.</font></div>
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<font face="Helvetica" size="3">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.</font></div>
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<b><font face="Helvetica" size="3">7.344 Modulating DNA Damage Tolerance Pathways as an Approach to Novel Cancer Therapeutics</font></b></div>
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<font face="Helvetica" size="3">Instructor: Kinrin Yamanaka (<a href="mailto:kinrin@mit.edu" style="color:purple">kinrin@mit.edu</a> 617-253-3745; laboratory of Graham Walker)</font></div>
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<font face="Helvetica" size="3">Spring 2016. Wednesdays, 1 pm – 3 pm. (Class day and time are flexible.) Room 68-150.</font></div>
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<font face="Helvetica" size="3">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. </font></div>
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<b><font face="Helvetica" size="3">7.345 Are There Inherent Limits to Our Understanding in Biology? A Challenge and Exploration Based on Diseases of the Nervous System</font></b></div>
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<font face="Helvetica" size="3">Instructor: Sepehr Ehsani (<a href="mailto:ehsani@csail.mit.edu" style="color:purple">ehsani@csail.mit.edu</a>; 617-797-8940; laboratory of Bonnie Berger)</font></div>
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<font face="Helvetica" size="3">Spring 2016. Wednesdays 3 pm ‒ 5 pm. (Class day and time are flexible.) Room 68-150.</font></div>
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<font face="Helvetica" size="3">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.</font></div>
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<b><font face="Helvetica" size="3">7.346 Engineering Immune Responses through Biomaterial Design</font></b></div>
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<font face="Helvetica" size="3">Instructors: Tyson Moyer (<a href="mailto:tmoyer@mit.edu" style="color:purple">tmoyer@mit.edu</a>, 3-0656, laboratory of Darrell Irvine)</font></div>
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<font face="Helvetica" size="3"> Kavya Rakhra (<a href="mailto:kavyarakhra@gmail.com" style="color:purple">kavyarakhra@gmail.com</a>, 3-0656, laboratory of Darrell Irvine)</font></div>
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<font face="Helvetica" size="3">Spring 2016. Thursdays, 11 am – 1 pm. (Class day and time are flexible.) Room 68-150.</font></div>
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<font face="Helvetica" size="3">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.</font></div>
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<div style="margin:0in 0in 0.0001pt; font-size:12pt; font-family:'Times New Roman'">
<b><font face="Helvetica" size="3">7.347 Peptides as Biological Signaling Molecules and Novel Drugs</font></b></div>
<div style="margin:0in 0in 0.0001pt; font-size:12pt; font-family:'Times New Roman'">
<font face="Helvetica" size="3">Instructor: Mohammed Shabab (<a href="mailto:shabab@mit.edu" style="color:purple">shabab@mit.edu</a>, 617-253-3745, laboratory of Graham Walker)</font></div>
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<font face="Helvetica" size="3">Spring 2016. Thursdays, 1 pm - 3 pm. (Class day and time are flexible.) Room 68-150.</font></div>
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<font face="Helvetica" size="3">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 <i>Staphylococcus aureus</i>. Infections with these pathogenic bacteria are untreatable with known antibiotics like <span lang="EN">gentamicin, streptomycin and kanamycin<b>. </b>Some antimicrobial
peptides can kill methicillin</span>-resistant <i>S. aureus</i> strains, making these <span lang="EN">promising drugs or drug leads.</span> 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.</font></div>
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<div style="margin:0in 0in 0.0001pt; font-size:12pt; font-family:'Times New Roman'">
<b><font face="Helvetica" size="3">7.348 An Evolutionary Arms Race: Molecular and Immunological Mechanisms Underlying the Causes of Infectious Diseases</font></b></div>
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<font face="Helvetica" size="3">Instructors: Jasdave Chahal (<a href="mailto:chahal@wi.mit.edu" style="color:purple"><span style="color:windowtext; text-decoration:none">chahal@wi.mit.edu</span></a>, 609-613-1129, laboratory of Hidde Ploegh)</font></div>
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<font face="Helvetica" size="3"> Florian Schmidt (<a href="mailto:fschmidt@wi.mit.edu" style="color:purple">fschmidt@wi.mit.edu</a>, 857-313-9456, laboratory of Hidde Ploegh)</font></div>
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<font face="Helvetica" size="3">Spring 2016. Thursdays, 3 pm – 5 pm. (Class day and time are flexible.) Room 68-150.</font></p>
<div style="margin:0in 0in 0.0001pt; font-size:12pt; font-family:'Times New Roman'">
<font face="Helvetica" size="3"> </font></div>
<div style="margin:0in 0in 0.0001pt; font-size:12pt; font-family:'Times New Roman'">
<font face="Helvetica" size="3">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 19<sup>th</sup> 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.</font></div>
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<div>Joyce Roberge<br>
Undergraduate Program<br>
Biology Education Office 68-120<br>
Massachusetts Institute of Technology<br>
31 Ames Street<br>
Cambridge, MA 02139<br>
617-253-4718<br>
fax: 617-258-9329<br>
email: <a href="mailto:roberge@mit.edu">roberge@mit.edu</a></div>
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