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<div><font color="#000000"><br></font></div>
<div><font color="#000000">TO: Biology
Majors<br>
<br>
FROM: H. Robert Horvitz, Professor of Biology<br>
<br>
<br>
I am writing to inform you
of an exciting course offering from the Department of Biology for the
2003-2004 academic year: a set of 13 new and very current
seminar courses, 7.340-7.346, 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, genomics, biochemistry, proteomics,
bioinformatics, molecular biology, cell biology, immunology, cancer
biology, neurobiology, evolution, 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.<br>
<br>
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.<br>
<br>
I am writing to you
before Registration Day to encourage you to consider enrolling for one
of these seminar courses. Please feel free to contact any of the
instructors to learn more about their courses.</font><br>
</div>
<div><font
color="#000000"><x-tab>
</x-tab>To learn more about the Advanced Undergraduate Seminars to be
offered during both the Fall 2003 and Spring 2004 semesters, please
join the instructors at a poster session on Registration Day
(September 2, 2003) from 10 am to 2 pm in room W35-199, just across
from Registration.</font></div>
<div><font color="#000000"><br>
<b>FALL, 2003</b></font></div>
<div><font color="#000000"><b><br>
7.340 Animal Models of Human Disease<br>
</b>Fall, 2003. Thursdays, 1-3 pm. Room 68-151.<br>
Instructors:<x-tab> </x-tab>Joe Kissil
(<u>jkissil@mit.edu</u>, 3-0264; laboratory of Tyler Jacks)<br>
Kevin Haigis (<u>kmhaigis@mit.edu</u>, 3-0264; laboratory of Tyler
Jacks)<br>
<br>
Animal models of human disease are essential tools in basic science
and medicine. Such models have proven indispensable to the
understanding of molecular mechanisms underlying disease and in the
development of therapeutics. In the past, most animal models
have relied on experimentally or pharmacologically altered wild-type
animals as well as on naturally-occurring mutant strains. More
recently, the genetic basis of numerous human diseases has been
elucidated, and emerging technologies involving mutagenesis,
transgenic animals (in which specific altered genes have been
introduced into animals), and gene knockouts (in which specific
endogenous genes have been inactivated) have led to the creation of
rationally designed animal models. In this course we will
consider different approaches to generating models for a variety of
human diseases, including cancer and autoimmune and neurodegenerative
diseases. The strengths, limitations and medical implications of
these models will be addressed. The ethics of using animal
models and the potential of biochemical or cellular rather than animal
model systems will also be discussed.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.341 Age and the Malleable Brain: Biological and
Clinical Perspectives on the Loss of Adaptability by the Maturing
Brain <br>
</b>Fall, 2003. Tuesdays, 11 am - 1 pm. Room 68-151.<br>
Instructor: Matt Colonnese (<u>colonnese@wi.mit.edu</u>; 8-5252;
laboratory of Alan Jasanoff)<br>
<br>
Can you teach an old brain new tricks? For most of the last 100
years, the answer has been no. The brain was thought to be like
plastic: easy to mold at first, but once set no longer
malleable. After a certain age, it was thought, new neurons are
not born, neural processes do not grow, and new synapses are no longer
made. However, neurobiological research over the last 20 years
has shown that much of this thinking is untrue. What has
changed? In this class we will ask why we once thought that the
brain does not change in adulthood, and why we now think it does.
We will explore the differential abilities of the young and mature
brain to recover from injury. For example, an infant can have
half of his or her cerebral cortex removed and behave apparently
normally, an impossibility for an adult. What is the
neurobiological basis of this difference? How exactly does a
young brain differ from a mature one, and can we use this knowledge to
promote recovery from brain or other nervous system damage? We
will answer these questions by examining both studies of humans with
brain damage and of animals subjected to experimental manipulations
that have helped reveal the biological mechanisms
involved. <br>
<br>
<br>
<b>7.342 Evolution of the Immune System<br>
</b>Fall, 2003. Tuesdays, 1 - 3 pm. Room 68-151.<br>
Instructors:<x-tab> </x-tab>Susann Beetz
(<u>sbeetz@mit.edu</u>; 3-6705; laboratory of Lisa Steiner)<br>
Nadia Danilova (<u>ndanilov@mit.edu</u>; 3-6705; laboratory of Lisa
Steiner)<br>
<br>
>From very early in evolution, organisms encountered the problem of
protecting themselves from invading pathogens. Such protection
requires the ability to discriminate self from non-self. In
response to this problem, a complex and sophisticated immune system
capable of detecting and destroying pathogens, as well as of similarly
responding to cancer cells, has evolved. Even prokaryotes have
self-protective mechanisms, including restriction endonucleases,
antimicrobial peptides, and RNA-interference. In multicellular
organisms, specialized immune cells have evolved, with the ability to
recognize and engulf foreign cells. Such defensive mechanisms
are based upon germline-encoded receptors and are said to constitute a
system of innate immunity. In jawed vertebrates, innate immunity
is supplemented with a second system, known as adaptive immunity,
which involves a specialized network of immune cells and organs.
Adaptive immunity, in contrast to innate immunity, is based on
diversification of immune receptors and distinct immunological
memories in each individual. In this course, we will analyze
evolutionary pathways that have led to the development of innate and
adaptive immunity, trace both the conserved and unique features of the
immune response from bacteria to higher vertebrates, and identify
factors, such as adaptive changes in pathogens, that shaped the
evolution of immune system.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.343 RNA Interference, a Revolutionary Technology Based on
an Ancient Gene-Silencing Pathway<br>
</b>Fall, 2003. Thursdays, 3 - 5 pm. Room 68-151.<br>
Instructors:<x-tab>
</x-tab>Michael McManus (<u>mmcmanus@mit.edu</u>; 3-6458; laboratory
of Phil Sharp)<br>
Alla Grishok (<u>agrishok@mit.edu</u>; 3-0265 laboratory of Phil
Sharp)<br>
<br>
Now that the sequence of the entire human genome is known and the
number of predicted genes is estimated, the next challenge is to
assign biological function to each of the genes. A new and very
powerful way for exploring gene function is offered by RNA
interference (RNAi). In this method, the introduction of
double-stranded RNA identical in sequence to that of the gene of
interest inactivates the gene or, more precisely, "interferes"
with its function. Initially discovered in worms, this method
was viewed as a "magic wand" for shutting down genes, with little
understanding about how it worked. With the efforts of many
scientists the magic of RNAi began to unfold from being a curiosity in
worms to being an ancient gene-silencing mechanism common to plants,
fungi, and animals. Researchers have discovered that specific
genes are required for RNAi to occur and that these genes constitute
an evolutionarily conserved pathway that uses endogenous cellular
dsRNA to silence developmentally important genes in a precise manner.
Although the field of RNAi has emerged only recently, it has already
made a profound impact in biology. This course will discuss the
discovery of RNAi, its mechanisms, and applications in uncovering gene
function and curing human disease.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.344 Genomics and Bioinformatics of Gene Expression<br>
</b>Fall, 2003. Wednesdays 1-3 pm. Room 68-151.<br>
Instructors:<x-tab> </x-tab>Uwe Ohler
(<u>ohler@mit.edu</u>; 3-7039; laboratory of Chris Burge)<br>
Gabriel Kreiman (<u>kreiman@mit.edu</u>; 3-0547; E25-201B; laboratory
of <br>
<span
></span
> <span
></span> Tommy
Poggio)<b><br>
<br>
</b>A large number of both normal and disease biological processes
depend on specific spatial and temporal patterns of the expression of
particular genes or groups of genes. The recent availability of
DNA sequence information (from humans and other organisms) as well as
high-throughput methods for the analysis of gene expression data
(e.g., from microarrays) allow us to use computational algorithms to
study gene expression (transcription). In this seminar we will
focus on transcriptional initiation, regulation, and networks and on
how expression levels are measured using high-throughput techniques.
We will discuss recent advances in the methods of genomics and
bioinformatics available to a biologist interested in this area of
research. Many of these tools also have applications in other
areas of biological research.<br>
<br>
<br>
<b>7.345 The Chemistry and Biology of Carbohydrates, Key
Molecules of Life<br>
</b>Fall 2003. Wednesdays, 3-5 pm. Room 68-151.<br>
Instructor: Kuberan Balagurunathan (<u>kuby@mit.edu</u>, 3-8803;
laboratory of Robert Rosenberg)<br>
<br>
Carbohydrates differ from other biological polymers, such as nucleic
acids and proteins, in many ways. Most importantly, they have
different functional groups that provide almost unlimited variations
in their structures. Carbohydrates that are conjugated to
proteins or lipids are termed glycoconjugates. They decorate the
outer surface of mammalian cells. Their strategic location
enables them to regulate many important biological processes,
including fertilization, cell growth, cell-cell adhesion, cell-cell
communication, development, immune defense, viral and parasitic
infection, degradation of blood clots, inflammation etc.
Furthermore, alterations in the synthesis or catabolism of
cell-surface carbohydrates are associated with various pathological
conditions, including malignant transformations and congenital and
neurological disorders. Deciphering the enigmatic structures of
carbohydrates and understanding their biosynthetic/catabolic pathways
are critical for the development of carbohydrate-based therapeutics.
In this course, we will discuss the tools available to characterize
carbohydrate structures, methods to synthesize carbohydrates, the
biosynthesis and catabolism of carbohydrates, and the role of
carbohydrates in human diseases and developmental disorders such as
cancer, congenital defects, and Sanfilippo disease.</font></div>
<div><font color="#000000"><br>
<br>
<b>SPRING, 2004<br>
<br>
7.340 Immune Evasion: How Sneaky Pathogens Avoid Host
Surveillance<br>
</b>Spring, 2004. Thursdays, 1 - 3 pm. Room 68-151.<br>
Instructor: Dina Gould Halme (<u>dghalme@mit.edu</u>; 2-2557;
HHMI Education Group postdoctoral associate)<br>
<br>
Every infection consists of a battle between the invading pathogen and
the resisting host. To be successful, a pathogen must escape the
many defenses of the host's immune system until it can replicate and
spread to another host. Therefore, a pathogen must prevent at
least one of three stages of immune function: detection, activation,
or effector function. Human Cytomegalovirus (HCMV) has at least
three genes that act to prevent the detection of virally-infected
cells, helping it to infect 90% of people living in urban settings.
Human Immunodeficiency Virus (HIV), which causes AIDS, produces
a protein that prevents the activation of immune cells. Many
gastric, colorectal and pancreatic cancers bear surface receptors that
prevent the tumors from being lysed by the immune system. In
this course, we will discuss these examples and many other mechanisms
used by pathogens to prevail over their hosts' immune systems and
cause disease. We will consider what these host-pathogen
interactions reveal not only about the causes of persistent disease
but also about the normal function of the immune system and basic cell
biological processes, such as protein maturation and
degradation.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.341 The Molecular Basis of Aging<br>
</b>Spring, 2004. Tuesdays 3-5 pm. Room 68-151.<br>
Instructors:<x-tab> </x-tab>Gil Blander
(<u>gblander@mit.edu</u>; 3-6717; laboratory of Lenny Guarente)<br>
Marcia Haigis (<u>mchaigis@mit.edu</u>; 3-3567; laboratory of Lenny
Guarente)<br>
<br>
Aging is a basic feature of the biology of humans and other
organisms. Research has shown that in certain experimental
organisms aging can be postponed or accelerated. This course
will explore key pathways that regulate aging. Recent
experiments in which the lifespans of simple organisms have been
extended will be discussed. We will also consider the molecular
mechanisms responsible for the human premature aging disorders
Werner's Syndrome and Hutchinson-Gilford Progeria. We will
discuss the effect of caloric restriction, insulin-signaling, and the
Sir2 gene on lifespan extension. In addition, we will explore
the role of oxidative damage and the mitochondria in aging. To
allow students to see aging research first-hand, we will visit
laboratories at MIT and in industrial settings.<br>
<br>
<br>
<b>7.342 Obesity, a Big Fat Problem: from the Transcriptional
Control of Adipogenesis and Energy Balance to a Worldwide Epidemic<br>
</b>Spring, 2004. Tuesdays 1-3 pm. Room 68-151.<br>
Instructor: Frederic Picard (<u>picard@mit.edu</u>; 3-6717;
68-289; laboratory of Lenny Guarente)<br>
<br>
Maintaining a healthy body weight has been recognized worldwide as a
primary goal by national health agencies. Recent increases in
the frequency of obesity have been alarming. In the last two decades,
our understanding of the transcriptional pathways regulating the
differentiation of fat cells, or adipogenesis, has grown remarkably.
This course will review the molecular biology and function of fat
cells (adipocytes), how new adipocytes are made, the regulatory
pathways of energy balance and current and potential therapeutic
targets to treat obesity.<br>
<br>
<br>
<b>7.343 Tagged for Destruction: How Ubiquitin Controls Our
Lives<br>
</b>Spring, 2004. Wednesdays, 3 - 5 pm. Room 68-151.<br>
Instructor: Marta Rubio (<u>mrubiotx@mit.edu</u>; 3-9838;
68-541; laboratory of Chris Kaiser)<br>
<br>
The proper functioning of cells depends not only on the activation but
also on the inactivation of cellular proteins. Many proteins are
targeted for degradation in a highly regulated fashion.
Post-translational mechanisms have evolved to generate signals that
target proteins for degradation. Tagging proteins to be
destroyed by the attachment of special molecules enables specific
cellular machinery, the "proteasome," to recognize those proteins
as substrates. Ubiquitin is a small protein used as such a label
to target proteins for degradation. The aim of this course is to
discuss the mechanisms of the ubiquitin-conjugation system and its
importance in the functioning of eukaryotic cells. We will study
how ubiquitination is key for the global control of many cellular
pathways. We will learn about how dysfunctions in ubiquitination
can lead to the development of a variety of human diseases, including
neurodegenerative disease (such as Alzheimer's, Huntington's and
Parkinson's), disorders associated with acute cellular injury
(ischemia), immune disorders (e.g., in antigen presentation),
disorders caused by abnormalities in the regulation of the cell cycle,
signal transduction, or programmed cell death (cancer, muscular
atrophy). We will also see how viruses like HIV, human papilloma
virus, and other infectious agents deceive their cellular hosts by
hijacking cellular machinery that acts in regulatory steps involving
ubiquitination. Finally, we will consider how our increasing
knowledge of the ubiquitin system offers the possibility of designing
new pharmacological agents to battle disease.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.344 Biological Computing-at the Crossroads of Engineering
and Science<br>
</b>Spring 2004. Wednesdays, 11 am-1 pm. Room 68-151.<br>
Instructor: Julia Khodor (<u>jkhodor@mit.edu</u>; 324-0055; HHMI
Education Group postdoctoral associate)<br>
<br>
Imagine you are a salesman needing to visit 100 cities connected by a
set of roads. Can you do it while stopping in each city only
once? Even a supercomputer working at 1 trillion operations per
second would take longer than the age of the universe to find a
solution by considering each possibility in turn. In 1994,
Leonard Adleman published a paper in which he described using the
tools of molecular biology - including nucleic acids, enzymes, and
affinity purification with a biotin-avidin magnetic bead system -- to
solve a smaller 7-city example of this problem. His paper
generated enormous scientific and public interest, and kick-started
the field of Biological Computing. Mathematicians, computer
scientists, chemists, biologists, and engineers came together to
create a new field in which contributions from each are critical for
the success of the whole. Currently Biological Computing
encompasses many areas of active research. For example,
three-dimensional self-assembly of molecules can be used to create
stereometrical shapes or to effect computation. Molecule-based
string rewrite systems aim to emulate various mathematical models of
computation using DNA as rewritable tape. Work in the area of
exquisite detection focuses on lowering the number of solution
molecules that can be detected, while whole-cell computing focuses on
hijacking normal cellular processes for computation. We will
discuss how the engineering point of view differs from the scientific
perspective, and how each colors one's thinking and approach to
research. We will analyze the Adleman paper, as well as papers
that came before and after it, and critically examine them with an eye
to identifying engineering and scientific aspects of each paper and
the interplay between the two. Non-Biology majors welcome.
Care will be taken to fill in any knowledge gaps for both scientists
and engineers.</font></div>
<div><font color="#000000"><br>
<br>
<br>
<br>
<b>7.345 Microarray Analysis: From Functional Genomics to the
Clinic<br>
</b>Spring, 2004. Thursdays, 3 - 5 pm. Room 68-151.<br>
Instructor: Bérengère Bouzou (<u>bbouzou@mit.edu</u>;
2-3851; laboratory of Robert Rosenberg)<br>
<br>
Gene expression analysis has reached a new dimension with the
development of microarray chip technologies. Microarrays exploit
the preferential binding of complementary single-stranded nucleic acid
sequences. A microarray is typically a glass slide, on to which
DNA molecules are attached at fixed locations (spots). There may
be tens of thousands of spots on an array, each containing a huge
number of identical fragments of DNA molecules, of lengths from 20 to
hundreds of nucleotides. A typical dimension of such an array is
about 1 inch or less, the spot diameter is of the order of 0.1 mm, and
for some microarrays even smaller. These potentially powerful
methods can allow the screening of millions of genes with a single
small array chip and perhaps one day will allow the screening of the
whole genome with one chip. This technology promises a
revolution in clinical diagnosis, as apparently similar diseases with
different prognoses and requiring different treatments can be
distinguished by their molecular fingerprints. Microarray
analysis requires first the extraction of quantitative information
from the images resulting from the readout of fluorescent or
radioactive hybridizations and then the collection of these data into
a database that supports both mathematical analysis and a connection
to available information about the structure and function of the
individual genes. The goal of this course is to explore how gene
expression can be analyzed using microarrays based upon the primary
research literature. We will examine the variability of patterns
in gene expression among different mouse and human organs, tissue and
cell types (e.g., brain, endothelium, cardiac muscle cells). We
will discuss how the screening of gene expression in human cancers
before and after treatment with anticancer drugs has helped define
distinct types of breast cancers and lymphomas. We will consider
the techniques employed to generate the biological samples used in
microarray analysis, the types of available microarrays, and the
bioinformatics and statistical tools commonly used to extract
biological significance from microarray data.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.346 The Role of DNA Repair in the Prevention of Human
Disease<br>
</b>Spring 2004. Wednesdays ,1-3 pm. Room 68-151.<br>
Instructor: Penny Beuning (beuning@mit.edu, 3-3745, laboratory
of Graham<br>
Walker)<br>
<br>
The accurate maintenance and transmission of genetic information is of
supreme importance to all organisms. Although some mutations may
give rise to useful properties and drive evolution, many mutations are
harmful to the organism. Mutations can arise from assaults on
the genome either from the external environment or from inside the
cell. Mutations can also occur as a consequence of errors in DNA
replication or DNA repair. In prokaryotes loss of replicative
fidelity can lead to mutations in and the death of a single cell.
In humans defects in DNA repair can lead to disease. Such human
diseases include premature aging syndromes, e.g., Werner's and Bloom's
syndromes, and Xeroderma pigmentosum (XP), the main phenotype of which
is severe UV light sensitivity leading to skin cancer. In this
course we will discuss mechanisms that have evolved to maintain
accurate replication and transmission of genetic information, and the
consequences of the loss of this accuracy. We will focus on the
roles of DNA repair enzymes, considering both structural and
mechanistic viewpoints. We will also discuss how the loss of
specific DNA repair functions can lead to human disease.<br>
</font></div>
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