[bioundgrd] 2010-11 Advanced Undergraduate Seminars
MacKenzie Outlund
moutlund at MIT.EDU
Mon Aug 23 14:21:06 EDT 2010
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 2010-2011 academic year: a set of 18 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, cancer biology, stem cells,
regenerative medicine, neurobiology, aging, systems biology, protein
engineering, biotechnology, drug discovery, biofuels, and human disease.
A student can take any number of these courses. The courses, which
generally involve four to eight students, are for 6 units, graded pass/fail,
and meet two hours each week. The focus is on reading and discussing the
primary research literature. Most courses have two short written
assignments. Some include field trips to MIT research laboratories or to
commercial sites using technologies discussed in the courses. The level of
each course will be tailored to the students who enroll. Because of the
small size of these courses, we expect students not to drop these courses
once they have begun.
These courses offer a number of special features: small class size,
a high degree of personal contact with the instructor, a focus on the
primary research literature, and an opportunity to discuss current problems
in biology interactively. I believe these courses greatly enrich an
undergraduate’s experience. There are limited alternative opportunities
available to undergraduates to interact closely with instructors who are
experienced full-time researchers; to learn to read, understand, and analyze
primary research papers; and to engage in the type of stimulating
discussions and debates that characterize how science is really done. Most
advanced MIT undergraduates (generally juniors and seniors) have been
sufficiently exposed to the basics of biology to be able to read the primary
literature and appreciate both methodologies and cutting-edge advances. These
courses have two goals: first, to expose students to the kind of thinking
that is central to contemporary biological research; and second, to impart
specific knowledge in particular areas of biology. These courses are
designed to be intellectually stimulating and also to provide excellent
preparation for a variety of future careers that require an understanding
both of what modern biology is and of how it is done. Students who have
taken Advanced Undergraduate Seminars in the past (different specific
courses, same general design) have been enormously enthusiastic about their
experiences.
I am writing to you before Registration Day to encourage you to
consider enrolling in one of these seminar courses. Please feel free to
contact any of the instructors to learn more about their courses.
To learn more about the Advanced Undergraduate Seminars to be
offered during both the Fall 2010 and Spring 2011 semesters, please check
our website (http://mit.edu/biology/www/undergrad/adv-ugsem.html) and/or
contact the instructors.
*Advanced Undergraduate Seminars*
*2010-2011*
* *
*Fall 2010*
* *
*7.340 Molecular Mechanisms of Learning and Memory *
Instructor: Sven Loebrich (loebrich at mit.edu, 8-5241; laboratory of Elly
Nedivi)
Fall 2010. Mondays, 1 – 3 pm. (Class time is flexible.) Room 68-151.
The mammalian brain significantly 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 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.
* *
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*7.341 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)
Fall 2010. Tuesdays, 1 pm – 3 pm. (Class time is flexible.) Room 68-151.
The goal of medicine is to prevent, ameliorate or cure disease. Despite
centuries of effort, modern medicine struggles against the same obstacles
today as it did in its early days: identifying the cause of 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 to difficulties posed by the large sizes
and instabilities of these macromolecules. What, then, is the next
therapeutic frontier? The answer might lie in RNA interference (RNAi), a
fundamental biological process discovered only a dozen years 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
protein synthesis. Since its discovery, RNAi has revolutionized basic
science research by allowing the dissection of cellular processes with
unprecedented specificity, thus providing an invaluable tool to identify the
bases of disease. More importantly, the race is now on to develop siRNAs as
therapeutic agents and to achieve a level of success in patients that has
eluded medicine thus far. In this course, we will discuss in detail the
therapeutic potential of RNAi. More generally, we will discuss its
discovery, functions in normal biological processes, utility as an
experimental tool, potential for therapeutic use, and pursuit by the
biotechnology industry.
* *
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*7.342 Systems and Synthetic Biology: How the Cell Solves
Problems*
Instructor: Hyun Youk (hyouk at mit.edu, 68-365, laboratory of
Alexander van
Oudenaarden)
Fall 2010. Wednesdays, 11 am – 1 pm. (Class time is flexible.) Rm
68-151.
A millennial challenge in biology is to decipher how vast arrays of
molecular interactions inside the cell work in concert to produce a cellular
function. Systems biology, a new interdisciplinary field of science, brings
together biologists and physicists to tackle this grand challenge through
quantitative experiments and models. Molecular biology has provided us with
a detailed understanding of the components that make up a cell – including
the wealth of genes, RNAs, proteins and other macromolecules – as well as
specific intracellular biochemical interactions. The diversity among species
of specific cellular components in the context of broadly conserved chemical
classes is one aspect of the beauty and elegance of biology. Systems biology
is now revealing another elegant aspect of biology: when all these cellular
components are integrated into a network of interactions, we find that there
are common themes across a wide spectrum of organisms. There seems to be
unifying principles that all organisms use to perform cellular functions. In
this course, we will discuss what these principles are. We will begin by
considering several early papers in systems biology that identified key
challenges faced by a cell in both single and multi-cellular organisms. One
such challenge is that many intracellular processes, such as production of
specific proteins and RNA molecules, are stochastic in nature. In other
words, even within a population of cells that are genetically identical and
live in the same environment, there can be significant variation from one
cell to another in the level of individual gene products. This cell-to-cell
variability can lead to stark phenotypic variation within a genetically and
environmentally homogeneous population of cells. We will discuss how the
network of genes in a cell is wired to control for the amount of noise and
even take advantage of cell-to-cell variability for survival. Another
challenge that a cell has to meet is reliably measuring how many key
molecules are present in its surrounding environment so that it can respond
appropriately. We will discuss papers that revealed that there is an
ultimate limit to how accurately cells can ”count” the number of
extracellular molecules. We will then discuss how cells, from those in a
bacterium to those in the embryo of a fruit fly, meet this challenge.
Finally, we will discuss how researchers in the field of synthetic biology
are using the new knowledge gained from studying naturally-occurring
biological systems to create artificial gene networks capable of performing
new functions.
* *
*7.343 Vascular Development in Life, Disease and Cancer Medicine*
Instructor: Alexandra Naba (anaba at mit.edu, 2-2769; laboratory of Richard
Hynes)
Christopher Turner (turnercj at mit.edu, 3-6409; laboratory
of Richard Hynes)
Fall 2010. 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 inhibit the
pro-angiogenic vascular endothelial growth factor VEGF, that have been
approved by the Food and Drug Administration (FDA), 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 U.S.A.
* *
*7.344 p53: How the Guardian of our Genome Prevents Cancer*
Instructor: Wen Xue (wxue at mit.edu; 617-452-3821; laboratory of Tyler Jacks)
Fall 2010. Wednesday 3 - 5 pm. (Class time is flexible.) Room 68-151.
* *
Cancer is a leading cause of death worldwide. Cancer involves uncontrolled
cell growth, resistance to cell death, failure to differentiate into a
particular cell type and increased cellular motility. A family of
gate-keeper genes, known as tumor suppressor genes, plays important roles in
preventing the initiation and progression of cancer. Among these, p53 is the
most famous. More than 50% of human cancers harbor mutations in or deletion
of p53. p53 is induced by upstream signals, such as DNA damage and hyperactive
cell-growth signals. The p53 protein, functioning as a transcription factor,
binds to the promoters of many target genes involved in the cell cycle,
programmed cell death (apoptosis) and DNA repair. Because of its essential
role in maintaining genomic integrity, p53 is often called the guardian of
the genome. During this course, we will study how p53 serves as a pivotal
tumor suppressor gene in preventing cancer. We will examine the discovery of
the p53 protein, the spectrum of p53 mutations in human cancer and the role
of p53 as a transcription factor. The function of p53 in DNA damage, cell
death, cell cycle regulation and genome integrity will be discussed. We will
also consider some recent studies of p53 mutant mouse models and the
regulation by p53 of small RNA expression. We will discuss how future cancer
treatments might be achieved by therapies that restore p53 function to tumor
cells.
* *
*7.345 Survival in Extreme Conditions: The Bacterial Stress Response *
Instructor: Celeste Peterson (cnpeterso at gmail.com, 8-8684;
laboratory of Michael
Laub)
Fall 2010. Thursdays, 11 am - 1 pm. (Class time is flexible.) Room 68-151.
Bacteria survive in almost all environments on Earth, including some
considered extremely harsh. From the steaming hot springs of Yellowstone to
the frozen tundra of the arctic to the barren deserts of Chile, microbes
have been found, often thriving. Their tenacity to survive in such extreme
and varied conditions allows them to play fundamental roles in global
nutrient cycling. Microbes also cause a wide range of human diseases and
can survive inhospitable conditions found in the human body. In this course,
we will examine the molecular systems that bacteria use to adapt to changes
in their environment. What types of signal transduction pathways do bacteria
use to monitor their surroundings? How do they activate the appropriate
cellular response? Model systems such as the bacteria *E. coli* and *B.
subtilis* have been the tools for discovering many key concepts, and the
first part of the course will address how these organisms execute their
responses to changes in their environment. We will consider stresses
typically encountered, such as starvation, oxidative stress and heat shock,
with some focus on how the adaptive responses affect the evolution of the
bacteria. We will also examine how different signals integrate into signal
transduction pathways to determine whether the bacteria will deal with one
specific stress or enter a more general dormant state and “batten down the
hatches” until conditions improve. The second portion of the course will
address the far-reaching clinical and industrial applications of the stress
responses of environmentally and medically relevant organisms. How do
bacteria cope with toxic metal stresses caused by pollution? How does
mounting a general stress response affect antimicrobial drug activity? How
is the course of virulence in human disease affected by the stress response?
We will gain an appreciation of the power of bacterial genetics and how our
detailed understanding of the microbial stress response is key to our
ability to control bacteria in the wild and in disease.
* *
*7.346 Stem Cells: A cure or disease?*
Instructors: Grant Welstead (welstead at wi.mit.edu, 8-5205;
laboratory of Rudolf
Jaenisch)
Steve Bilodeau (bilodeau at wi.mit.edu , 8-5236;
laboratory of Richard
Young)
Fall 2010, Thursdays, 1-3 pm. (Class day and time is flexible.) Room 68-151.
Have you ever considered going to a pharmacy to order some new
cardiomyocytes (heart muscle cells) for your ailing heart? It might sound
crazy, but recent developments in stem cell science have made this concept
not so futuristic. In this course, we will explore the underlying biology
behind the idea of using stem cells to treat disease, specifically analyzing
the mechanisms that enable a single genome to encode multiple cell states
ranging from neurons to fibroblasts to T cells. We will study new
developments in the area of cellular reprogramming and transdifferentiation
and highlight how we have gained the power to control cell states in a Petri
dish. Specifically, this course will not only introduce important biological
concepts like pluripotency and epigenetics but also focus on key
technologies that are used to study them, such as genome-wide sequencing and
transcription-mediated reprogramming. We will also consider the potential
consequences and limitations of stem cell therapy, particularly the
connection between stem cells and cancer. Overall, we hope to provide a
comprehensive overview of this exciting new field of research and its
clinical relevance.
* *
* *
*7.347 Biological Networks: What Can Networks Teach Us about
Biology?*
Instructors: Igor Ulitsky (ulitskyi at gmail.com, 8-5990; laboratory
of David Bartel)
Muhammed Yildirim (yildirim at gmail.com, 4-1651;
laboratory of David
Bartel)
Fall 2010. Thursdays, 3 pm – 5 pm. (Class time is flexible.) Room 68-151.
What do Facebook, the human brain, the electricity grid and transcriptional
regulation in the cell have in common? One simple answer is that they can
all be represented as networks. In fact, studying the structures and
features of these networks can help us understand the principles of all of
these complex systems. Although networks from entirely different domains
share surprising similarities, biological networks also have their own
unique characteristics. Analysis of these networks involves using
established techniques from statistics, physics and computer science as well
as methods developed specifically for studying systems biology. In this
course we will introduce biological networks and how they are studied in the
context of general network theory. In addition, we will discover how
network-based approaches are advancing various areas of biomedical research.
We will begin by presenting the basic principles of network structures. We
will then cover many of the basic molecular interaction networks studied in
biology, including those of protein-protein interactions, transcriptional
regulation, microRNA targeting, genetic interactions, drug-target
interactions and others. We will see how these networks are constructed from
data, what kinds of models are used to study them and what such models can
teach us about the organizational principles of biological systems.
Furthermore, we will discuss specific questions that can be answered by
understanding networks: what is the best way to perturb a biological network
to escape from a disease? what does the position of a gene in a network tell
us about its function? how can we use networks to identify drugs that share
a mode of action? The course will not require any expert knowledge in
biology, computer science or statistics and is open to students from any
relevant department.
* *
* *
*7.348 Biology of Aging and Age-Related Diseases*
Instructors: Michael S. Bonkowski (mbonkows at mit.edu, 3-4768, laboratory of
Lenny Guarente)
Sergiy Libert (libert at mit.edu, 3-4768, laboratory of
Lenny Guarente)
Fall 2010. Fridays, 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 experience diseases like osteoporosis, stroke,
and neurodegenerative disorders? Is aging itself a disease? What changes
happen at the molecular and cellular levels to cause the changes that we
associate with old age? Can changing the nutrient balance of the human diet
extend lifespan and diminish negative features of the aging process? 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 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, which might 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.
* *
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*Spring 2011*
* *
*7.340 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 2011. Monday, 1 – 3 pm. (Day and time are flexible.) Room 68-151.
The discovery of penicillin in the 1930s ushered in a new era in modern
medicine and paved the way for the development of various antibiotics
against disease-causing microbes. After decades of widespread use, however,
many antibiotics are not as effective as they used to be. Resistance to
commonly used antibiotics and the surfacing of multidrug-resistant microbes
– so called *superbugs* – have become major clinical problems. Today, the
Centers for Disease Control and Prevention call antibiotic resistance “one
of the world’s most pressing public health problems.” Did you know that
many of the commonly used antibiotics – such as tetracyclines,
aminoglycosides and macrolides – specifically target the cell’s
translational apparatus and disrupt protein synthesis? In this course, we
will discuss the structure and function of the ribosome and look into the
most basic concepts of protein synthesis. We will explore the mechanisms of
action of antibiotics and toxins targeting the translational machinery,
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 cell’s 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.
* *
* *
*7.341 Bench to Bedside: Molecularly Targeted Therapies in Blood
Disorders and Malignancy *
Instructors: Bill Wong (pwong at wi.mit.edu, 650-799-8364; laboratory of
Harvey
Lodish)
Spring 2011. Wednesdays, 3 – 5 pm. (Class time is flexible.) Room 68-151.
How are new drugs and treatments discovered? This course will take you from
the discoveries of basic research to the customized design of drugs for
treating patients with specific deadly blood disorders. Students will
experience the scientific journey from the rationale of the scientists who
started basic research projects to the clinicians who designed the trials to
test the safety and efficacy of prospective drugs. We will consider the
scientific discoveries that led to development of Gleevec, which is often
referred as a miracle drug or silver bullet for a specific leukemia, chronic
myelogenous leukemiz. Gleevec was developed based on the principle of
molecularly targeting an aberrant kinase activity encoded by an oncogene and
in this way killing leukemia cells while leaving normal cells alone. The
following topics will be discussed: (1) identification of a bcr-abl
chromosomal translocation and demonstration that this translocation
generates an abnormal kinase activity that causes leukemia, (2) drug design
and efficacy and toxicity testing in mice and humans, (3) mechanisms of drug
resistance and finally, (4) uses of Gleevec in other diseases that also
abnormally express the oncogenic abl kinase. We will also discuss other
topics that demonstrate the process from “bench to bedside,” such as stem
cell and gene therapy, the design of drugs based on RNA interference, and
the reprogramming of somatic cells into stem cells for regenerative
medicine.
* *
*7.342 Powerhouse Rules: The Role of Mitochondria in Human
Diseases*
Instructor: Dan Ferullo (ferullo at mit.edu, 3-3745; laboratory of
Graham Walker)
Spring 2011. Wednesdays, 11 am – 1 pm. (Class time flexible.) Room
68-151.
Exactly how important is the mitochondrion, the “power house” of the
cell? Once
a bacterial symbiote, the mitochondrion is an organelle that provides unique
functions to nucleated eukaryotic cells. Specifically, mitochondria produce
the majority of cellular ATP, support aerobic respiration, and are key
players in apoptosis (programmed cell death). An interesting feature of a
mitochondrion is that it contains its own DNA, a relic of its bacterial
ancestor. The mitochondrial genome encodes some but not all of the proteins
crucial for mitochondrial functions. Defects in mitochondrial functions have
been found to cause or be associated with a variety of human diseases,
including neurodegenerative and neuromuscular disorders and cancer as well
as with aging. Accordingly, mitochondria have become attractive targets for
developing therapies for disease. In this course, we will discuss the
biological roles of mitochondria and how mitochondria malfunction in human
disease. We will learn about mitochondrial DNA (mtDNA) and how it is very
easily damaged. As such, we will discuss mechanisms that cells use to
repair damaged mtDNA. Importantly, we will examine how inadequate repair of
mtDNA causes harmful mutations, compromises mitochondrial function, and is
deleterious to the cell. We will examine how the problem of faulty mtDNA
repair contributes to pathogenesis in disease. We will also discuss how
mitochondria are key players in a normal process called “apoptosis” or
“programmed cell death” designed to eliminate old or unhealthy cells in a
controlled manner. However, mitochondrial defects can lead to improper
apoptosis and in this way impact several diseases. Lastly, we will discuss
how mitochondria produce reactive oxygen species (ROS), which are
potentially damaging molecules that can cause cellular injury when produced
at high levels. We will examine how elevated ROS production is caused by
faulty mitochondria and is involved in disease and aging. By discussing
studies using experimental systems ranging from yeast to human cancer cells,
we will learn how defects in mitochondrial functions compromise cellular and
organismic health.
* *
* *
*7.343 Regenerative Medicine: from Bench to Bedside and Bedside
to Bench*
Instructor: Petra Simic (psimic at mit.edu, 3-0809; laboratory of Leonard
Guarente)
Spring 2011. 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.
* *
*7.344 Taking Snapshots of Protein Complexes in Action*
Instructor: Nozomi Ando (nando at mit.edu, 617-715-4891; laboratory
of Catherine
Drennan)
Edward Brignole (brignole at mit.edu, 617-715-4891;
laboratory of
Catherine Drennan)
Spring 2011. Wednesdays 3-5 pm. (Class time is flexible.) Room 68-151.
In 1958, John Kendrew and his co-workers used X-ray crystallography to solve
the world’s first structure of a protein at atomic resolution. This
technological breakthrough was one of the defining moments in modern
biology. Today, structure determination is an integral part of biology. More
than 66,000 structures have been solved to date, allowing us to understand
the chemistry, folding, and binding of proteins and other biomacromolecules.
Inside a cell, however, many thousands of different proteins are working on
a vast array of functions through their interactions with each other. So,
now that we know what many proteins look like, how can we visualize them at
work? Some protein complexes are too large and complicated to be easily
crystallized, and some protein interactions are too weak or dynamic to be
properly captured by crystallography. In this course, we will discuss the
usage of two structural techniques, small-angle X-ray scattering (SAXS) and
electron microscopy (EM), that help to fill the gap between atomic-level
structure determination and cellular-level imaging. We will discuss the
history of the now standard methods of biological structure determination,
with emphasis on how SAXS and EM have been used to visualize complicated
protein complexes such as viruses, DNA replication and repair machinery, and
metabolic enzymes and how they have contributed to a dynamic view of the
protein structure-function relationship. Students will learn about exciting
protein structure-function research and current technologies used in this
field.
* *
*7.345 Cancer and Its (Micro)environment – from Basic Science to
Therapy*
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 2011. Tuesdays, 2-4 pm. (Class time is flexible.) Room 68-151.
Despite major 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.
*7.346 Metastasis: The Deadly Spread of Cancer *
Instructors: John Lamar (lamarj at mit.edu, 452-2769; laboratory of
Richard Hynes)
Amy McMahon (mcmahona at mit.edu, 452-2769; laboratory
of Richard
Hynes)
Spring 2011. Thursdays, 1-3 pm. (Class time is flexible.) Room 68-151.
Cancer is a devastating disease that kills millions of people every year.
Greater then 90% of these deaths result from metastasis, the spread of
cancerous cells from the initial tumor to other organs in the body.
Metastasis is a complex cascade involving several essential cellular
processes, including migration, invasion, intravasation and extravasation
(entering and exiting the bloodstream, respectively), survival, and growth.
It is still unclear what is occurring at the molecular level inside tumor
cells to promote cancer progression, making metastasis an important area of
research in cancer biology. In this course we will discuss current theories
about how cancer cells gain the ability to metastasize as well as how
several of the critical processes involved in metastatic dissemination are
regulated at a cellular level. We will investigate how metastasis can be
influenced by the interaction of tumor cells with other cells in the body,
including non-malignant cells present in the tumor, the bloodstream, and
distant organs to which tumor cells metastasize. We will learn about
existing therapies that target metastatic dissemination and explore how new
therapies could be designed to target the processes and interactions
discussed throughout the course. We will visit a research facility and have
the optional opportunity to attend research seminars presented by prominent
scientists in the field.
* *
*7.347 Fueling Sustainability: Engineering Microbial Systems for
Biofuel Production*
Instructor: Michelle O’Malley (momalley at mit.edu, 3-9838;
laboratory of Chris
Kaiser)
Spring 2011. Thursdays, 3 pm – 5 pm. (Class time is flexible.) Room 68-151.
The need to identify sustainable forms of energy as an alternative to our
dependence on depleting worldwide oil reserves is one of the grand
challenges of our time. The energy from the sun converted into plant
biomass is the most promising renewable resource available to humanity. Almost
all of this energy is contained within cellulose, the natural yet difficult
to digest polymer of sugars that make up plant cell walls. How can we
unlock the energy within cellulose and convert it to more useful forms of
energy? Fortunately, nature has evolved several enzymes that work together
to break down cellulose. These enzymes are found within bacteria and fungi
that thrive in cellulose-rich environments (*e.g.*, the digestive tracts of
grazing animals, compost piles, and soil). Sugars released from cellulose
hydrolysis can later be fermented into biofuels like ethanol. We will
examine each of the critical steps along the pathway towards the conversion
of plant biomass into ethanol. We will focus on the biology behind
enzymatic cellulose breakdown, the different types of enzymes required, and
how these enzymes form complexes in nature that improve their catalytic
performance. State-of-the-art methods currently in use to identify new
cellulolytic enzymes with novel properties as well as metabolic engineering
strategies to introduce these enzymes into yeast will be discussed. We will
further examine issues associated with industrial-scale production and
catalytic performance of cellulolytic enzymes; such issues have limited the
economic feasibility of cellulosic biofuels. By the end of the course,
students will have a broader knowledge regarding the biology behind
cellulose breakdown, the challenges associated with industrial biofuel
production, and new opportunities to further its development.
* *
*7.348 Bacterial Communities: Group Behavior through Chemical
Signals*
Instructors: Carla Bonilla (cbonilla at mit.edu, 3-6702; laboratory of
Alan Grossman)
Houra Merrikh (merrikh at mit.edu, 3-6702; laboratory
of Alan Grossman)
Spring 2011. Fridays ,11 - 1 pm. (Class time is flexible.) Room 68-151.
Bacteria are everywhere, living in the soil, the oceans and on and in our
bodies. Bacteria help us stay healthy by aiding us in nutrient absorption
and vitamin production as well as by guarding our bodies against virulent
species. But bacteria can also threaten our health by causing deadly
infections. Although they are single-celled organisms, much of what
bacteria do, “good” or “bad,” originates from their ability to perform
complex communal behaviors that allow them to act as multicellular entities.
How can such single-celled organisms function in multicellular communities?
How do bacteria “talk” to each other? In this course, we will learn about
conserved chemical languages that bacteria use to communicate with other
bacteria of the same or different species. We will study group behaviors of
bacteria, including the roles of such group behaviors in allowing bacteria
to colonize a host, to defend themselves from predatory bacterial species or
from antibiotics, and simply to live in harmony in large multicellular
communities, such as in biofilms. We will learn about the chemical signals
used by different bacteria, including certain pathogenic species, such
as *Pseudomonas
aeruginosa* and *Vibrio cholera*, and how these signals are sensed and
interpreted through different genetic and molecular pathways. Understanding
the language that bacteria use to communicate is important not only as a
basic aspect of the extensive microbial world but also because of
implications for developing new treatments for infections caused by
pathogenic bacteria. Current antibiotics kill bacteria directly and
consequently select for resistant individuals. With drugs designed to
silence bacterial communication, on the other hand, there is no selective
pressure to survive, and therefore such treatments might offer a way to
circumvent the development of drug resistance, a major clinical problem
today.
* *
* *
* *
* *
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