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Seminars</title></head><body>
<div><font color="#000000">TO: Biology
Majors<br>
FROM: H. Robert Horvitz, Professor of Biology<br>
<br>
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, microbiology, cell biology, immunology, 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 this Spring to encourage you to consider
enrolling for one of these seminar courses. To learn more about
the Advanced Undergraduate Seminars, please check our website
(</font><font
color="#0000FF"><u>http://mit.edu/biology/www/undergrad/adv-ugsem.html</u
></font><font color="#000000">) and/or contact the
instructors</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000"><u><b>Spring 2006-2007<br>
<br>
</b></u><b>7.340 Under the Radar Screen: How Bugs Trick Our
Immune Defenses<br>
</b>Instructors: Marie-Eve Paquet (</font><font
color="#0000FF"><u>paquet@wi.mit.edu</u></font><font color="#000000">;
4-1734; laboratory of Hidde Ploegh)<br>
Gijsbert Grotenbreg (</font><font
color="#0000FF"><u>grotenbreg@wi.mit.edu</u></font><font
color="#000000">; 4-2081; laboratory of Hidde Ploegh)<br>
Spring 2007. Thursdays, 1-3 pm. Room 68-151.<br>
<br>
Why are infectious diseases such as HIV, mycobacterium tuberculosis,
malaria or influenza thriving today and killing millions of people
each year? These diseases are threats because our immune system
sometimes fails. Although we are equipped to effectively counter most
attacks from the microbial world, some pathogens have developed ways
to evade both our innate and adaptive immune barriers to ensure their
own survival. The strategies used by these viruses, bacteria or
parasites are numerous, but all target specific branches and pathways
of our immune defenses. In this course, we will explore the specific
ways by which microbes defeat our immune system and the molecular
mechanisms that are under attack (phagocytosis, the
ubiquitin/proteasome pathway, MHC I/II antigen presentation). Through
our discussion and dissection of the primary research
literature, we will explore aspects of host-pathogen interactions. We
will particularly emphasize the experimental techniques used in the
field and how to read and understand research data. Technological
advances in the fight against microbes will also be discussed, with
specific examples. These sessions will highlight the interplay among
different disciplines of biology and the fact that much can be learned
about the fundamental properties of our immune system through the
study of immune evasion.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.341 Sex, Chromosomes, and Disease<br>
</b>Instructors:<x-tab>
</x-tab>Dena Cohen (</font><font
color="#0000FF"><u>greendna@mit.edu</u></font><font color="#000000">,
3-3567; laboratory of Leonard Guarente)<br>
<x-tab>
</x-tab><x-tab>
</x-tab>Sheryl Krevsky Elkin (</font><font
color="#0000FF"><u>skelkin@mit.edu</u></font><font color="#000000">,
4-1963; laboratory of Angelika Amon)<br>
Spring 2007. Wednesdays, 3-5 pm. Room 68-151.</font><br>
</div>
<div><font color="#000000">Organisms as diverse as the papaya and the
platypus use sexual reproduction to generate genetic diversity.
How does an organism with two copies of each chromosome create a
gamete with only one set of chromosomes? What are the genetic
determinants of gender, and how did these elements evolve? In
this course we will examine meiosis, the specialized cell division
through which diploid organisms generate haploid gametes such as sperm
and eggs. During meiosis, cells undergo DNA replication,
followed by two nuclear divisions, and the chromosomes must be
properly segregated, one copy to each daughter cell. Improper
chromosome segregation during meiosis is the leading cause of
miscarriage and can also result in a variety of disorders, such as
Down's Syndrome (three copies of chromosome 21) and Klinefelter
syndrome (men have an extra copy of the X chromosome, i.e. are XXY
instead of XY). We will talk about what makes the X and Y
chromosomes different and how those chromosomes can cause individuals
to be male (XY) or female (XX). We will also think about how sex
chromosomes have evolved and discuss special mechanisms, such as
X-chromosome inactivation, that have evolved to help organisms cope
with the fact that females have twice as many copies of the X
chromosome as do males.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.342 G-Protein Coupled Receptors: Vision and Disease<br>
</b>Instructor: Parvathi Kota (</font><font
color="#0000FF"><u>pkota@mit.edu</u></font><font color="#000000">,
3-1866; laboratory of Gobind Khorana)<br>
Spring 2007. Thursdays, 3-5 pm. Room 68-151.<br>
<br>
How do we communicate with the outside world? How are our senses
of vision, smell, taste and pain controlled at the cellular and
molecular levels? What causes medical conditions like allergies,
hypertension, depression, obesity and various central nervous system
disorders? G-protein coupled receptors (GPCRs) provide a
major part of the answer to all of these questions. GPCRs
constitute the largest family of cell-surface receptors and in humans
are encoded by more than 1,000 genes. GPCRs convert
extracellular messages into intracellular responses and are involved
in essentially all physiological processes. GPCR dysfunction
results in numerous human disorders, and over 50% of all prescription
drugs on the market today directly or indirectly target GPCRs.
In this course, we will discuss GPCR-mediated signal transduction
pathways, GPCR oligomerization and the diseases caused by GPCR
dysfunction. We will study the structure and function of
rhodopsin, a dim-light photoreceptor and a well-studied GPCR that
converts light into electric impulses sent to the brain and leads to
vision. We will also discuss how mutations in rhodopsin cause
retinal degeneration and congenital night blindness.<br>
<br>
<br>
<b>7.343 Neuron-glial Cell Interactions in Biology and
Disease<br>
</b>Instructor: Bikem Akten (</font><font
color="#0000FF"><u>bikem@mit.edu</u></font><font color="#000000">,
2-2726, 46-3251, Supervisor: Dr. Troy Littleton) Spring 2007.
Thursdays, 11 am - 1 pm. Room 68-151.<br>
<br>
Glia (Greek for "glue"), the non-neuronal elements of the nervous
system, were first identified in 1846 by the anatomist Rudolph
Virchow. Since then, glial cells have been regarded as passive
nervous system components that provide insulation and tropic support
for neurons. This view has been challenged in the last few
years, and we now know that glial cells actively control synapse
formation, synapse function and synaptic plasticity. In the
mammalian nervous system, glial cells outnumber neurons by a factor of
ten, reflecting the importance of these cells. Thus, it seems
essential that we understand the functions of these cells and rethink
our view of the nervous system as we learn more about the dynamic
connections among neuronal and glial cells. The main goal of
this seminar will be to study the nervous system from the perspective
of neuron-glia interactions. In each class, we will focus on one
type of glial cell and discuss its origin, classification and function
within the nervous system. Current findings concerning
diseases associated with each type of glial cell will be discussed.
Topics will include the behavior of glial cells in diseases such as
Multiple Sclerosis (MS), glioblastoma multiforme (GBM), HIV-associated
dementia (HAD), Alzheimer's Disease (AD), ischemia, hypoxia and
epilepsy. We will also discuss the role of glial cells as neural
stem cells in the adult brain and their importance in the effective
rebuilding of damaged brains after injury or disease-associated
neurodegeneration. The class will include a field trip to a
medical school to observe clinical research concerning glial
disorders. </font></div>
<div><font color="#000000"><br>
<br>
<br>
<br>
<br>
<b>7.344 Antibiotics, Toxins, and Protein Engineering<br>
</b>Instructors:<x-tab>
</x-tab>Caroline Koehrer (</font><font
color="#0000FF"><u>koehrer@mit.edu</u></font><font color="#000000">,
3-1870; laboratory of Uttam RajBhandary)<br>
Mandana Sassanfar (</font><font
color="#0000FF"><u>mandana@mit.edu</u></font><font color="#000000">,
452-4371; Education Office)<br>
Spring 2007. Tuesdays, 1-3 pm. Room 68-151.</font><br>
<font color="#000000"></font></div>
<div><font color="#000000">The lethal poison Ricin (best known as a
weapon of bioterrorism),<i> Diphtheria</i> toxin (the causative agent
of a highly contagious bacterial disease), and the widely used
antibiotic tetracycline 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.</font></div>
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