<!doctype html public "-//W3C//DTD W3 HTML//EN">
<html><head><style type="text/css"><!--
blockquote, dl, ul, ol, li { padding-top: 0 ; padding-bottom: 0 }
--></style><title>Biology Advanced Undergraduate
Seminars</title></head><body>
<div><font color="#000000">Dear Biology undergraduates:</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">Please take note of the following
information from Prof. Horvitz on the Biology Advanced Undergraduate
Seminars.</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">Best wishes,</font></div>
<div><font color="#000000">Janice</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">*******</font></div>
<div><font color="#000000"><br>
TO: Biology Majors</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"><x-tab>
</x-tab>I am writing to inform you of an exciting course offering from
the Department of Biology for the 2006-2007 academic year: a set
of ten new and very current seminar courses, 7.340-7.344, 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, chemical biology, cell biology, stem
cells, immunology, neurobiology, evolution and human
disease.</font></div>
<div><font color="#000000"><br></font></div>
<div><font
color="#000000"><x-tab>
</x-tab>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></font></div>
<div><font
color="#000000"><x-tab>
</x-tab>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></div>
<div><font color="#000000"><br></font></div>
<div><font
color="#000000"><x-tab>
</x-tab>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.</font></div>
<div><font color="#000000"><br></font></div>
<div><font
color="#000000"><x-tab>
</x-tab>To learn more about the Advanced Undergraduate Seminars to be
offered during both the Fall 2006 and Spring 2007 semesters, 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><br></div>
<div><br></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000"><u><b>Fall 2006-2007<br>
<br>
</b></u><b>7.340 Avoiding Genomic Instability: DNA Replication,
the Cell Cycle, and Cancer<br>
</b>Instructors: John Randell (jrandell@mit.edu, 8-7352, laboratory of
Steve Bell)<br>
Robyn Tanny (ret@mit.edu, 3-1979, HHMI Education Group postdoctoral
associate)<br>
Fall 2006. Wednesdays, 11 am - 1 pm. Room 68-151.<br>
<br>
Every time a cell divides, it must faithfully duplicate its genetic
material once and only once. At the same time, the cell must
ensure that this process does not introduce errors that could lead to
either cell death or tumorigenesis. In fact, mutations in genes
that control DNA replication can be found in a wide variety of tumors.
In this class we will learn about how the process of DNA replication
is regulated throughout the cell cycle and what happens when DNA
replication goes awry. How does the cell know when and where to
begin replicating its DNA? How does a cell prevent its DNA from
being replicated more than once? How does damaged DNA cause the
cell to arrest DNA replication until that damage has been repaired?
And how is the duplication of the genome coordinated with other
essential processes? We will examine both classical and current papers
from the scientific literature to provide answers to these questions
and to gain insights into how biologists have approached such
problems. We will also learn how the misregulation of DNA
replication contributes to tumor formation and how some anti-cancer
drugs target proliferating cells by disrupting DNA replication.
Finally, we will see how viruses overcome the cellular controls on DNA
replication to promote their own multiplication and cause
disease.</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000"><b>7.341 Brightening Up Life:
Harnessing The Power of Fluorescence Imaging to Observe Biology in
Action<br>
</b>Instructors: Anthony Leung (akleung@mit.edu 3-0265;
laboratory of Phillip Sharp)<br>
<x-tab> </x-tab> Mark
Howarth (mhowarth@mit.edu, 8-0218; laboratory of Alice Ting)<br>
Fall 2006. Tuesdays, 11 am - 1 pm. Room 68-151.</font><br>
</div>
<div><font color="#000000">One summer in the 1960s a young Japanese
researcher, with the help of a few high school students, chopped up
10,000 jellyfish. As a by-product of this harvest, they isolated
a green fluorescent protein (GFP). Since then, GFP has triggered
a revolution in our understanding of gene expression and signaling in
live cells. In this seminar, we will examine how this small
protein generates fluorescence, i.e. absorbs light of one wavelength
and emits light of a longer wavelength. We will discuss how the
color palette has been extended from green to blue, red and many other
colors, based on protein engineering of GFP and the study of vividly
colorful coral reefs. We will then investigate how these
fluorescent proteins can be used to track the motion of DNA, RNA and
protein in living cells, as well as to see waves of signaling
molecules propagate across a cell. GFP is also a powerful tool
for fluorescent imaging of whole organisms, from worms to mice, and we
will see how it has been used in tracking the spread of cancer cells,
controlling malaria and in understanding how neuronal connections
form. In this seminar, we will explore this wonderful protein as
well as other important methods of and reagents for fluorescent
imaging.<br>
<br>
<br>
<br>
<b>7.342 Reading the Blueprint of Life: Transcription,
Stem Cells and Differentiation<br>
</b>Instructors: Matt Guenther (</font><font
color="#0000FF"><u>guenther@wi.mit.edu</u></font><font
color="#000000">; 258-7822; laboratory of Rick Young)<br>
<x-tab> </x-tab>
Roshan Kumar (</font><font
color="#0000FF"><u>roshan@wi.mit.edu</u></font><font color="#000000">;
258-7822; laboratory of Rick Young)<br>
Fall 2006. Thursdays, 3-5 pm. Room 68-151.<br>
<br>
Stem cells have the unique ability to give rise to all human tissues
and hold great potential for tissue regeneration and treating human
disease. Realizing this potential will require an understanding
of the fundamental mechanisms that allow stem cells to generate
descendants that have a variety of fates and that lock in the
specialized states and distinctive RNA and protein expression patterns
of differentiated cells. Transcriptional regulation is believed to
account for a large part of the specialized gene expression programs
of cells. In this course, we will address how transcriptional
regulators both prohibit and drive differentiation during the course
of development. How does a stem cell know when to remain a stem
cell and when to become a specific cell type? Are there global
differences in the way the genome is read in multipotent and
terminally differentiated cells? We will explore how stem cell
pluripotency is preserved, how master regulators of cell-fate
decisions execute developmental programs, and how chromatin regulators
control undifferentiated versus differentiated states.
Additionally, we will discuss how aberrant regulation of
transcriptional regulators produces disorders such as developmental
defects and cancer.<br>
<br>
<br>
<b>7.343 Photosynthesis: Life from Light<br>
</b>Instructors:<x-tab> </x-tab>Yongting
Wang (ytwang@mit.edu, 2-1876; laboratory of Jon King)<br>
<x-tab>
</x-tab><x-tab>
</x-tab>Peter Weigele (pweigele@mit.edu, 3-3545; laboratory of Jon
King)<br>
Fall 2006. Wednesdays, 3-5 pm. Room 68-151.<br>
<br>
The biological conversion of solar energy to chemical energy forms the
basis of life as we know it. Knowledge of this fundamental
process is critical to our understanding of the biogeochemical cycles
that mitigate global warming. In this course, you will journey
through the web of physical, chemical, and biological reactions that
collectively constitute photosynthesis. We will begin with light
harvesting and follow photons to the sites of primary photochemistry:
the photoreaction centers. A molecular-scale view will show in
atomic detail how these protein complexes capture and energize
electrons. Then we will follow the multiple pathways electrons
take as they carry out their work. Consequent reactions, such as
the synthesis of ATP and the reduction of CO2 during the synthesis of
carbohydrates, will also be discussed in structural detail.
Lastly, we will delve into the evolution of these systems and also
discuss other photosynthetic strategies, such as light-driven proton
pumps and anoxygenic photosynthesis. The course will include a
visit to an electron microscope to allow students to directly observe
proteins involved in photosynthesis.</font></div>
<div><font color="#000000"><br>
<br>
<b> <br>
7.344 Diabetes and Obesity: Energy Balance and Disease<br>
</b>Instructor: Kelly Wong (kwong@wi.mit.edu, 8-0377; Laboratory
of Harvey Lodish)<br>
Fall 2006. Thursdays, 1-3 pm; Room 68-151.<br>
<br>
Do you know how your eating behavior is controlled at the molecular
and cellular levels? How do the cells in your body determine how
much energy they need? What are the mechanisms your body
activates to burn fat? Importantly, what happens when these
processes go wrong? Diabetes and obesity constitute one of the
fastest growing epidemics in the United States. According to the
Center for Disease Control, over the last 10 years there has been an
alarming increase in the number of patients diagnosed with diabetes
and a startling increase in obesity across the United States.
The burden on the U.S. healthcare system posed by diabetes was
estimated to be $92 billion dollars of direct medical costs in 2002.
In this course, we will discuss insulin, its signal transduction
pathway and how muscle can be sensitive or resistant to the action of
insulin. We will study AMP-activated protein kinase, a master
sensor for cellular energy status. We will examine the actions
of the hormone leptin and its role in controlling body weight and
feeding behavior as revealed by studies of genetically engineered
mouse models. Besides leptin, other adipose tissue cytokines
such as adiponectin will be discussed. Finally, we will examine
the molecular consequences of beneficial activities such as exercise
and discuss pharmacological agents that are currently being used to
treat patients with Type II diabetes.<br>
<br>
<br>
<br>
<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.<br>
<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.<br>
<br>
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>
<br>
<b> <br>
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. <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>
</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>
</body>
</html>