[bioundgrd] Biology Advanced Undergraduate Seminars 2009-2010

Nick Polizzi npolizzi at MIT.EDU
Mon Aug 24 14:17:50 EDT 2009


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 the 2009-2010 academic year:  a set of 11 very current  
seminar courses,
7.34x, Advanced Undergraduate Seminars.  A complete list of the  
courses, instructors,
and brief course descriptions are enclosed.  The topics are highly  
varied and
encompass areas of genetics, biochemistry, molecular biology, cell  
biology,
developmental biology, cancer biology, stem cells, regenerative  
medicine, neurobiology,
aging, evolution, biotechnology, protein engineering 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 undergraduateʼs 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
both the Fall 2009 and Spring 2010 semesters, please check our website
(http://mit.edu/biology/www/undergrad/adv-ugsem.html) and/or contact  
the instructors.


Advanced Undergraduate Seminars

2009-2010


Fall 2009

7.340            Learning and Memory:  The Activity of the Nervous  
System Controls Gene
Expression To Shape the Biology of the Brain
Instructor: Sven Loebrich (loebrich at mit.edu, 8-5241; laboratory of  
Elly Nedivi)
Fall 2009.  Mondays, 1 – 3 pm. (Class time is flexible.) Room 68-151.

The mammalian brain easily outperforms any man-made supercomputer with  
respect to computing time and process complexity. The brain adapts and  
changes constantly in response to external stimuli. Most importantly,  
the brain enables us to continuously learn and remember new things. A  
single experience, such as touching a hot plate, witnessing a tragedy,  
or experiencing the shocking taste of durian fruit can be remembered  
for life. What are the molecular mechanisms that lead to learning and  
memory? How do nerve cells, inter-neural connections (synapses) and  
brain circuits change over time to store information? Electrical  
activity in the nervous system controls the expression of a set of  
genes that can affect neuronal function. What are the cellular roles  
that activity-regulated gene products play to implement changes in the  
brain? We will discuss the molecular mechanisms of such neuronal  
plasticity at the synaptic, neuronal and circuit levels. We will  
consider fundamental neurobiological processes, such as (1) synapse  
formation, (2) synaptic growth and stabilization, (3) synaptic  
transmission, (4) axonal and dendritic outgrowth, and (5) circuit  
formation, with some focus on the visual system. We will learn about  
the roles of some activity-regulated genes in these processes, and we  
will study their functions in various experimental systems, such as  
dissociated neuronal cultures, cultured brain slices, and the living  
brain. In addition, we will learn about the tools and techniques  
employed in modern neuroscience research. Our goal will be to  
understand molecular mechanisms the brain employs to bring about the  
complex phenomena of learning and memory.

7.341  Bench to Bedside: Molecularly Targeted Therapies in Blood  
Disorders and Malignancy
Instructors:   Johan Flygare (flygare at wi.mit.edu, 2-5227; laboratory  
of Harvey Lodish)
                      Bill Wong (pwong at wi.mit.edu, 650-799-8364;  
laboratory of Harvey
                      Lodish)
Fall 2009. Wednesdays, 3 – 5 pm.  (Class time is flexible.) Room  
68-151.

Where do new drugs and treatments come from?  This class will take you  
from the test tubes and mice of the laboratory to the treatment of  
patients with deadly blood disorders. Students will learn how to think  
as a scientist by discussing primary research papers describing the  
discoveries of several novel treatments from the perspectives of a  
basic scientist, the pharmaceutical industry and a practicing  
clinician.  Topics such as gene therapy, the potential of drugs based  
on RNA interference and the reprogramming of somatic cells into stem  
cells for regenerative medicine will be discussed. We will consider in  
depth the leukemia drug Gleevec, which is often referred to as a  
miracle drug or silver bullet. This drug is used to treat chronic  
myelogenous leukemia (CML) and kills leukemic cells while normal cells  
are left alone by targeting an oncogenic protein that exists in only  
the leukemic cells. The unprecedented success of this drug’s  
achieving 90% efficacy in patients depended strongly on basic  
research: first an abnormal chromosome was discovered, then the exact  
genetic defect -- bcr-abl chromosomal translocation -- was identified,  
the abnormal kinase activity encoded by the bcr-abl fusion genes was  
shown to be the cause of the leukemia and then a specific inhibitor of  
this kinase was developed.  This striking success increased the  
rationale for bringing ‘bench’ discoveries to the ‘bedside.’ We  
will discuss issues involved in drug development, such as lead  
compound discovery, modification through medicinal chemistry and  
efficacy and toxicity testing in vitro, in animal models and  
eventually in humans in large-scale clinical trials. Just as bacteria  
can develop resistance to antibiotics, leukemic cells similarly can  
evolve mechanisms to evade the therapeutic effects of Gleevec.    
Strategies will be discussed to attack Gleevec-resistant leukemic  
cells.  Finally, we will explore the uses of Gleevec in diseases other  
than CML that constitutively express the oncogenic Abl kinase or other  
kinases that have proven also to be inhibited by Gleevec

7.342  The X in Sex: A Genetic, Medical, and Evolutionary View of the  
X Chromosome
Instructor:  Jacob Mueller (jmueller at wi.mit.edu, 254-8420; laboratory  
of David Page)
Fall 2009.  Thursdays, 1-3 pm.  (Class time is flexible.)  Room 68-151.

What do colorblindness, Queen Victoria, and ligers (hybrids generated  
by male lions and female tigers) have to do with the X chromosome?   
This course will explore a diverse collection of striking biological  
phenomena associated with the X chromosome.  The X chromosome is the  
most intensively studied chromosome in medical genetics; genes for  
over 300 diseases have been mapped to it.  We will examine the genetic  
basis and significance of several X-linked mutations (e.g. the  
mutation proving the chromosome theory of inheritance and mutations  
that cause sex reversal).  We will also discuss why men are more  
likely than women to display X-linked traits.  This X-inequality  
between the sexes (XY males, XX females) raises an important  
biological question: how do males, with their single X chromosome per  
cell, and females, with two, balance their relative levels of X-linked  
gene expression?  We will look at the different mechanisms by which X  
chromosome gene expression is equalized in mammals, flies, and worms  
and how these mechanisms can yield unusual phenotypes, such as calico  
cats, almost all of which are female.  We will also discuss the  
evolutionary history of the X chromosome, considering questions such  
as: how did the X and Y chromosomes evolve from an ordinary pair of  
autosomes?  what role do X-linked genes play in the male sterility of  
hybrid organisms, such as ligers, mules or zorses?  and what can the X  
chromosome tell us about the speciation of humans?  Throughout our  
discussions of the X chromosome we will use both recent and classic  
primary research papers to learn about this chromosome’s fascinating  
biology.


7.343   When Development Goes Crazy: How Cancer Co-opts Mechanisms of  
Embryogenesis
Instructors:  Trudy Oliver (tgo at mit.edu; 8-6789; laboratory of Tyler  
Jacks)
          Etienne Meylan (emeylan at mit.edu; 2-3821; laboratory of Tyler  
Jacks)

Fall 2009.  Thursdays, 3 – 5 pm.  (Class time is flexible.)  Room  
68-151.


Cancer is a leading cause of death worldwide.  Few treatment options  
exist, most of which rely on a single characteristic of cancer cells— 
their increased proliferation rate.  Treatment with traditional  
therapies, such as radiation or chemotherapy, can be highly toxic, and  
patients often experience relapse as cancers acquire mutations that  
confer drug resistance.  More effective cancer therapies are very much  
needed.  Such therapies are now being developed based upon an  
understanding of cancer biology, which in many ways involves  
dysregulation of the normal biology of development.  During human  
embryonic development, a single cell—the fertilized egg—divides and  
its descendants grow, differentiate, and assemble to generate a highly  
complex human being.  Throughout these developmental processes, cells  
communicate with each other via complex signaling networks composed of  
proteins interacting with other proteins.  Signaling pathways that  
drive development have been identified, and, strikingly, many of them  
are altered in cancer.  Cancer involves uncontrolled cell growth,  
failure to differentiate into a particular cell type, resistance to  
cell death, increased cellular motility, and formation of new blood  
vessels.  All of these processes are utilized during development, and  
all are misused in cancer.

During this course, we will study the similarities between cancer and  
normal development to understand how tumors co-opt developmental  
processes to facilitate cancer initiation, maintenance and  
progression.  We will examine critical signaling pathways that govern  
these processes and, importantly, how some of these pathways hold  
promise as therapeutic targets for cancer treatment.  We will discuss  
how future treatments might be personalized to target cancer cells in  
specific patients.  We will also consider examples of newly-approved  
drugs that have dramatically helped patients combat this devastating  
disease.


  7.344            The Biology and Diseases of Aging
Instructors:            Michael Bonkowski (mbonkows at mit.edu, 68-295;  
laboratory of
Lenny Guarente)

                                 Dena Cohen (greendna at mit.edu, 68-294;  
laboratory of Lenny Guarente)
Fall 2009.            Thursdays, 11 am – 1 pm.  (Class time is  
flexible.)  Room 68-151.

Aging is a familiar yet mysterious aspect of human biology.  Why are  
older people so much more likely to develop diseases like  
osteoporosis, stroke, and neurodegenerative disorders?  Is aging  
itself a disease? What changes happen at the molecular and cellular  
levels that cause the changes that we associate with old age?  Can  
changing the nutrient balance of the human diet extend lifespan?  To  
this day, the specific molecular causes of aging remain poorly  
defined.  Common laboratory organisms such as yeast, the roundworm C.  
elegans, and mice undergo aging, and scientists have studied these  
organisms to try to unlock the mysteries of the aging process.  For  
all of these organisms, mutations have been identified that slow  
aging, allowing the organism to live up to ten times as long as  
normal.  The finding that aging can be controlled by individual genes  
has led to the exciting idea that drugs might be developed to  
intervene with the actions of such genes, slow the aging process and  
delay the onset of all of the diseases of aging in humans.  In this  
course, we will explore the scientific discoveries that have led to  
various theories of the molecular basis of aging.  We will study the  
shared genetic pathways that control lifespan in organisms as  
different from each other as yeast and mice. We will also discuss the  
first tests of drugs such as resveratrol, a small molecule found in  
red wine, that may target aging pathways in mammals.  We will  
participate in a field trip to a meeting of the Boston Area Aging Data  
Club, where we will meet the authors of some of the papers that we  
have covered in class and hear a presentation by a researcher actively  
working on a hot topic in the aging field.

7.345  Vascular Development in Life, Disease and Cancer Medicine
Instructor: Alexandra Naba (anaba at mit.edu, 3-6424; laboratory of  
Richard Hynes)
                   Christopher Turner (turnercj at mit.edu, 3-6409;  
laboratory of Richard Hynes)
Fall 2009. Wednesdays, 1-3 pm. (Class time flexible.)  Room 68-151.

The growth of blood vessels, a process known as angiogenesis, is one  
of the earliest events in mammalian development and is regulated by a  
sensitive interplay of growth factors and other molecules.  Abnormal  
or excessive angiogenesis occurs in diseases that include cancer,  
diabetes and atherosclerosis, whereas insufficient angiogenesis or  
vessel regression can lead to Alzheimer’s disease, ischemic heart  
disease and impaired wound healing.  For this reason, more than $4  
billion dollars has been invested in research and development to  
identify medicines that either promote or reduce the growth of new  
blood vessels, making angiogenesis one of the most exciting and  
heavily funded research areas in biomedicine today.  In this course,  
we will discuss the key molecular regulators of blood vessel  
development as well as the techniques and experimental systems that  
have been utilized by vascular biologists.  Emphasis will be given to  
the recent progress made in the microscopic visualization of blood  
vessels and live cell and intravital imaging used for diagnosis in the  
clinic.  We will also examine the success of several anti-angiogenic  
treatments that have been approved by the Food and Drug Administration  
(FDA), that inhibit the pro-angiogenic vascular endothelial growth  
factor, VEGF, and that are now being used to treat age-related macular  
degeneration.  Finally, we will explore how during the course of  
cancer progression, establishment of a blood supply into a tumor can  
lead to the growth and spread of cancer cells to secondary sites.  We  
will discuss the caveats and potential pitfalls of targeting tumor  
blood vessels to starve cancer cells and prevent the spread of cancer,  
which remains one of the leading causes of death in the USA.

Spring 2010

7.346  RNAi: A Revolution in Biology and Therapeutics
Instructors:             Allan Gurtan (gurtan at mit.edu, 3-6458;  
laboratory of Phillip Sharp)
                         Michael Goldberg (michaelg at mit.edu, 3-6457;  
laboratory of Phillip                                     Sharp)
Spring 2010. Thursdays, 3 pm – 5 pm. (Class time is flexible.) Room  
68-151.

The goal of medicine is to cure disease.  Despite centuries of effort,  
however, modern medicine struggles against the same obstacles today as  
medicine did in its early days: identifying the cause of a disease and  
treating it specifically without inducing side effects.  While  
significant advances in medicinal chemistry have been made over many  
decades, traditional small molecule therapeutics remain unpredictable,  
often because of a lack of specificity.  Similarly, the recent advent  
of recombinant DNA technology, though ushering in an era of protein- 
based therapeutics, has achieved only limited success, owing in part  
to difficulties posed by the large sizes of these macromolecules.   
What, then, is the next therapeutic frontier?  The answer may lie in  
RNA interference (RNAi), a fundamental biological process discovered  
only a decade ago and recognized soon afterwards with the 2006 Nobel  
Prize in Physiology or Medicine.  RNAi is mediated by small  
interfering RNAs (siRNAs), which direct the efficient degradation of  
specific messenger RNAs, thereby inhibiting the synthesis of specific  
proteins.  Since its discovery, RNAi has revolutionized basic science  
research by allowing analyses of the genes and proteins required for  
cellular processes.  RNAi can be used to test candidate disease target  
genes in cellular and animal models of human disease.  Additionally,  
the race is now on to develop siRNAs as a class of therapeutic  
agents.  In principle, any gene known to play an essential role in a  
disease pathway can be targeted by RNAi.  In this course, we will  
discuss the studies that have led to the current excitement concerning  
the therapeutic potential of this new field.  Specifically, we will  
consider various aspects of RNAi: its discovery, how it functions in  
normal biological processes, its utility as an experimental tool, its  
potential for therapeutic use, and how RNAi therapeutics are being  
pursued by the biotechnology industry.

7.347  Antibiotics, Toxins, and Protein Engineering: Science at the  
Interface of Biology, Chemistry, Bioengineering, and Medicine
Instructor:  Caroline Koehrer (koehrer at mit.edu, 3-1870; laboratory of  
Uttam L.
                    RajBhandary)
Spring 2010. Thursdays, 1 – 3 pm. (Class time is flexible.)  Room  
68-151.


The lethal poison Ricin, best known as a weapon of bioterrorism;  
Diphtheria toxin, the causative agent of a highly contagious bacterial  
disease; and the widely used antibiotic tetracycline – all three have  
one thing in common: they specifically target the cell’s  
translational apparatus and disrupt protein synthesis. In this course,  
we will explore the mechanisms of action of toxins and antibiotics,  
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 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.


7.348  Non-malignant Tumor Cells – A Broader Approach to Cancer  
Research

Instructors: Julia Rastelli (rastelli at wi.mit.edu, 8-5173; laboratory  
of Bob Weinberg)

        Asaf Spiegel (spiegel at wi.mit.edu, 8-5173; laboratory of Bob  
Weinberg)

Spring 2009. Wednesdays, 3-5 pm. (Class time is flexible.) Room 68-151.



Despite 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.


7.349  From Molecules to Behavior:  Synaptic Neurophysiology
Instructor:  Alex Chubykin (chubykin at mit.edu; 46-3301; laboratory of  
Mark Bear)
Spring 2010. Wednesdays, 11 am – 1 pm. (Class time is flexible.)   
Room 68-151.

The brain is the most sophisticated computational machine known.  
Vastly different from conventional man-made computers, the brain is  
massively parallel, self-organizing, and plastic - it can change its  
own components and rewire itself to a new configuration necessary for  
a new task. Synapses, the connections between nerve cells, are the  
fundamental computational units of the brain. Like transistors in a  
computer, synapses perform complex computations and connect the  
brain’s non-linear processing elements (neurons) into a functional  
circuit. Understanding the role of synapses in neuronal computation is  
essential to understanding how the brain works. In this course  
students will be introduced to cutting-edge research in the field of  
synaptic neurophysiology. The course will cover such topics as synapse  
formation, synaptic function, synaptic plasticity, the roles of  
synapses in higher cognitive processes and how synaptic dysfunction  
can lead to disease. This research requires a wide range of  
techniques, including molecular genetics, biochemistry,  
electrophysiology and optical imaging, and examines mechanisms  
involved in the development, physiology, and pathophysiology of the  
nervous system. We will read both classical research papers addressing  
the basics of synaptic physiology and the latest research papers  
addressing the role of synapses in the function of neuronal circuits.  
Students will learn to critically analyze scientific papers, to apply  
the scientific method in neuroscience research, to evaluate and  
interpret data and to design experiments.


7.340 Regenerative Medicine: from Bench to Bedside

Instructor: Petra Simic (psimic at mit.edu, 3-0809; laboratory of Lenny  
Guarente)

Spring 2010.  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 and the Genzyme drug production  
facility to see how drugs are produced for human use.








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