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Biology</title></head><body>
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<div><font face="Helvetica" size="+2"
color="#000000">TO: Biology Majors<br>
<br>
FROM: H. Robert Horvitz, Professor of Biology</font><br>
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I am writing to inform you
of the exciting Advanced Undergraduate Seminars courses being offered
by the Department of Biology for the Spring 2004 term. 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.</font><br>
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<div><font face="Helvetica" size="+2"
color="#000000"> 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></div>
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<div><font face="Helvetica" size="+2" color="#000000"><b>SPRING
2004</b></font></div>
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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>
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<b>7.341 The Molecular Basis of Aging<br>
</b>Spring, 2004. Tuesdays 3-5 pm. Room
68-151.</font></div>
<div><font face="Helvetica" size="+2" color="#000000">Instructors:
Gil Blander (<u>gblander@mit.edu</u>; 3-6717; laboratory of Lenny
Guarente),</font></div>
<div><font face="Helvetica" size="+2"
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</x-tab>Marcia Haigis (<u>mchaigis@mit.edu</u>; 3-3567; laboratory of
Lenny Guarente)</font></div>
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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.</font><br>
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<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.</font><br>
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<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><br>
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<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>
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<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><br>
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<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)</font><br>
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<div><font face="Helvetica" size="+2" color="#000000">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.</font></div>
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<div>-- <br>
Stuart Dietz<br>
Biology Education Office, Rm. 68-120<br>
Massachusetts Institute of Technology<br>
77 Massachusetts Ave.<br>
Cambridge, MA 02139<br>
<br>
Phone (617) 252-1783<br>
Fax (617) 258-9329<br>
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