[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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