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2006</title></head><body>
<div><font color="#000000">Hello,</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">This is a reminder about the Spring
Advanced Undergraduate Seminars in Biology. Descriptions of the
courses are included below.</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">There will be an informational session on
the seminars on Registration Day (Monday Feb. 6th) from 9am-4pm in the
Bldg. 68 lobby just outside the Biology Education Office, 68-120.
Refreshments will be provided.</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">--</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">December 12, 2005</font></div>
<div><font color="#000000"><br>
TO: MIT students</font></div>
<div><font color="#000000">FROM: H. Robert Horvitz,
Professor of Biology</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">I am writing to inform you of the exciting
Advanced Undergraduate Seminar courses being offering by the
Department of Biology for the Spring 2006 term. 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 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.</font></div>
<div><font color="#000000"><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 this Spring 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"><br></font></div>
<div><font color="#000000"><u><b>SPRING 2005-2006</b></u></font><br>
</div>
<div><font color="#000000"><u><b><br>
</b></u><b>7.340 Molecular Mechanism of Aging</b></font></div>
<div><font color="#000000">Instructors: Danica Chen
(</font><font color="#0000FF"><u>danicac@mit.edu</u></font><font
color="#000000">, 2-4140; laboratory of Lenny Guarente), Agnieszka
Czopik (</font><font
color="#0000FF"><u>czopik@mit.edu</u></font><font color="#000000">,
3-3567; laboratory of Lenny Guarente)<br>
Spring 2006. Thursdays, 1-3 pm. Room 68-151.</font></div>
<div><font color="#000000"><br>
Aging is a degenerative process that results in decreased viability
and increased susceptibility to diseases. This course will focus on
molecules and molecular pathways that regulate the aging process, such
as the insulin-signaling pathway and members of the Sir2 gene family.
We will discuss the molecular mechanism of calorie restriction, the
only known dietary regimen that extends the lifespans of a variety of
organisms. Other topics will include the human premature aging
disorders Werner's Syndrome and Hutchinson-Gilford Progeria, the role
of oxidative damage and the mitochondria in aging, and the effects of
metabolism on aging. We will explore the reciprocal effects of aging
and immunity at the cellular and molecular levels and the ways these
effects may be relevant to human biology. The class will be concluded
with tours of a research laboratory at MIT and a biotech company both
focused on aging.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.342 The RNA Revolution</b></font></div>
<div><font color="#000000">Instructors: Rickard Sandberg
(sandberg@mit.edu, 3-7039; laboratory of Chris Burge), Michael Stadler
(stadler@mit.edu, 3-7039; laboratory of Chris Burge)<br>
Spring 2006. Thursdays, 3-5 pm. Room 68-151.</font><br>
</div>
<div><font color="#000000">Recent findings have revolutionized our
view of the roles of RNA in biology. For example, short non-coding
RNAs (microRNAs and short interfering RNAs) play key roles in
development and cancer by regulating gene expression. The biology of
short non-coding RNAs and their importance in these processes will be
topics for this course. In addition, the mechanism of alternative
splicing explains in part how humans can express 500,000 different
proteins with only 25,000 genes. Alternative splicing, the process by
which exons are joined in different combinations to generate multiple
variants of a gene, is estimated to affect about 75% of all human
genes. We will discuss how alternative splicing diversifies the human
protein repertoire, influences sex determination and courtship
behavior in fruit flies and when disrupted can cause diseases such as
spinal muscular atrophy. Attention will also be given to catalytic
RNAs that act in the ribosome during protein synthesis. In each
session we will critically evaluate both the experimental and the
computational techniques used in the primary literature to foster an
understanding of their strengths and limitations. This course will
give you an overview of the exciting newly emerging roles for RNA.<br>
<br>
<b> <br>
7.343 Takin' Out the Trash: Quality Control in Cellular
Processes</b></font></div>
<div><font color="#000000">Instructors: Peter Chien (</font><font
color="#0000FF"><u>pchien@mit.edu</u></font><font color="#000000">;
laboratory of Tania Baker), Eric Spear (</font><font
color="#0000FF"><u>espear@mit.edu</u></font><font color="#000000">;
laboratory of Chris Kaiser)</font></div>
<div><font color="#000000">Spring 2006. Wednesdays, 3-5 pm. Room
68-151. </font><br>
</div>
<div><font color="#000000">Messenger RNAs are synthesized from a DNA
blueprint, the proteins resulting from these messages are produced
using the complex machinery of the ribosome, and finally these
proteins must attain their proper mature folded state. Although this
process is extraordinarily accurate, care must be taken by the cell to
cope with the inevitable mistakes that occur along this long and
complicated pipeline. To this end, the cell has evolved a broad
range of mechanisms to ensure the quality of the final protein
product. For example, improperly folded proteins are often
recognized as aberrant and subsequently degraded, relieving the cell
of the potentially detrimental effects of a non-functional and
abnormal protein. In this class, we will discuss some of the
many mechanisms used for cellular quality control. We will consider
the stresses that can generate such aberrant protein products and how
the cell continuously fights these challenges. The recognition
of misfolded proteins and how these proteins are targeted to the
degradative machinery will also be discussed. We will consider
both prokaryotic and eukaryotic quality control, drawing attention to
the similarities between these two systems as well as highlighting
differences between them. The importance of these quality
control mechanisms will be emphasized throughout the course by
discussing a number of relevant human diseases, including cystic
fibrosis, Huntington's Disease, and certain types of
cancer.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.344 Toxins, Antibiotics, Protein Engineering and the
Ribosome</b></font></div>
<div><font color="#000000">Instructors: Caroline Koehrer
(</font><font color="#0000FF"><u>koehrer@mit.edu</u></font><font
color="#000000">, 3-1870; laboratory of Uttam RajBhandary), Mandana
Sassanfar (</font><font
color="#0000FF"><u>mandana@mit.edu</u></font><font color="#000000">,
452-4371; Education Office)<br>
Spring 2006. Tuesdays, 1-3 pm. Room 68-151.<br>
<br>
What do the lethal poison Ricin,<i> Diphtheria</i> toxin, and the
widely used antibiotic tetracycline have in common? They all inhibit
protein synthesis by targeting the cell's translation machinery. Why
is Ricin such a powerful toxin? How does it work? If<i> Diphtheria</i>
toxin and tetracycline also inhibit translation, why do they have such
different consequences? How does resistance to antibiotics like
tetracycline arise? In this course, we will explore the mechanisms of
action of toxins and antibiotics that specifically target components
of the translational apparatus leading to the disruption of protein
synthesis. We will discuss the roles of these antibiotics and toxins
in everyday medicine, the emergence and spread of drug resistance, and
how we might overcome this increasing problem by identifying new drug
targets and designing new drugs. We will also discuss how the detailed
understanding of the structure of the ribosome and the translation
machinery has led to new technologies in protein engineering and
promising applications for human therapy. </font></div>
<div><font color="#000000"><b><br></b></font></div>
<div><font color="#000000"><b><br></b></font></div>
<div><font color="#000000"><b>7.346 How Abnormal Protein Folding
Causes Alzheimer's, Parkinson's, Mad Cow and Other Neurodegenerative
Diseases<br>
</b>Instructor: Atta Ahmad (</font><font
color="#0000FF"><u>giftee6@mit.edu</u></font><font color="#000000">,
3-3707; laboratory of Vernon Ingram)<br>
Spring 2006. Thursdays, 11 am - 1 pm. Room
68-151.</font><br>
</div>
<div><font color="#000000">The cause of both Alzheimer's Disease (AD)
and Parkinson's Disease (PD) is abnormal deposition of proteins in
brain cells. In addition, there are 20 other neurological diseases
caused by similar protein deposition. Millions of people suffer from
these diseases. The latest research shows that these diseases arise as
a consequence of a specific series of molecular events. First, a
protein assumes a non-native sticky "misfolded state." Two
or more such sticky proteins associate together to generate a multi
protein "oligomeric state." These oligomers can associate
with each other or can recruit newly formed sticky proteins, thereby
growing into bigger thread-like structures called "amyloid
fibrils." These fibrils can deposit either inside or outside
brain cells, disrupting normal biological functions and resulting in
neuronal cell death. Depending on the region of the brain affected,
this cell death leads to visible symptoms, such as memory loss, loss
of cognitive ability, abnormal muscular movements, involuntary shaking
and, in many cases, death. In this course, we will discuss the
processes that trigger protein aggregation (such as, mutations and
environmental effects) with an emphasis on Alzheimer's Disease,
Parkinson's Disease and Mad Cow Disease. The methods used to study the
processes of aggregation (<i>e.g.</i>, fluorescence spectroscopy,
circular dichroism, infrared spectroscopy, transmission electron
microscopy, confocal microscopy) will be discussed. We will consider
the consequences of the aberrant proteins on cellular processes. We
will also discuss potential targets for intervening with these
processes and approaches that could lead to possible treatments for
these disorders.</font></div>
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