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2007-2008</title></head><body>
<div><font color="#000000">Dear Biology Undergraduatse - please take
note of the following letter from Prof. Horvitz on the biology
Advanced Undergraduate seminar offerings for 2007-2008.</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></font></div>
<div><font color="#000000">TO: Biology
Majors<br>
FROM: H. Robert Horvitz, Professor of Biology<br>
<br>
I am writing to inform you
of an exciting course offering from the Department of Biology for the
2007-2008 academic year: a set of 11 very current seminar
courses, 7.341-7.346, 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, biochemistry, molecular biology, cell
biology, developmental biology, stem cells, immunology, neurobiology,
epigenetics, aging, ecology, biotechnology and human disease.<br>
<br>
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 in one
of these seminar courses. Please feel free to contact any of the
instructors to learn more about their courses.<br>
<br>
<x-tab> </x-tab>To learn
more about the Advanced Undergraduate Seminars to be offered during
both the Fall 2007 and Spring 2008 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><font color="#000000"><br></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"><u><b>Fall 2007-2008</b></u></font></div>
<div><font color="#000000"><u><b><br>
</b></u><b>7.341 DNA Damage Checkpoints: the Emergency Brake on
the Road to Cancer<br>
</b>Instructors: Marcel van Vugt (</font><font
color="#0000FF"><u>vanvugt@mit.edu</u></font><font color="#000000">,
2-2443; Laboratory of Michael Yaffe)<br>
<span
></span> Christian Reinhardt
(</font><font color="#0000FF"><u>reinharc@mit.edu</u></font><font
color="#000000">, 2-2443; Laboratory of Michael Yaffe)<br>
Fall 2007. Thursdays, 1 pm - 3 pm. Room
68-151.</font><br>
</div>
<div><font color="#000000">The DNA contained in human cells is under
constant attack by both foreign and endogenous agents that can damage
one of its three billion base pairs. To cope with this permanent
exposure to DNA-damaging agents, such as the sun's radiation or
by-products of our normal metabolism, powerful DNA damage checkpoints
have evolved that allow organisms to survive this constant assault on
their genomes. The tremendous importance of checkpoints is
underlined by the fact that defects in checkpoint genes are commonly
seen in cancer. Once DNA damage checkpoints detect DNA lesions,
cellular proliferation is stopped immediately and DNA repair is
initiated. If the extent of damage is beyond the capacity of the
cell's repair systems, checkpoint signaling ensures elimination of
such damaged cells by the induction of a cellular suicide program
known as programmed cell death or apoptosis. Cellular responses
to DNA damage constitute one of the most important fields in cancer
biology. Exciting work in this area has taught us important
lessons, such as: DNA damage can cause cancer; paradoxically,
the induction of DNA damage is the mechanism of action of the major
approaches to treating cancer (radiation and chemotherapy); and DNA
damage of normal tissues is responsible for most of the side effects
of cancer therapy, such as hair loss. We will analyze classical
and recent papers from the primary research literature to gain a
profound understanding of checkpoints that act as powerful emergency
brakes to prevent cancer. We will consider basic principles of
cell proliferation and molecular details of the DNA damage response.
We will discuss the methods and model organisms typically used in this
field as well as how an understanding of checkpoint mechanisms
translates into the development of treatments for human
cancer.</font></div>
<div><font color="#000000"><br>
<br>
<br>
<b>7.342 Pathogen-Induced Chronic Diseases: Clinical Relevance
and Molecular Mechanisms<br>
</b>Instructors: Eva Frickel (frickel@wi.mit.edu; 4-1751;
laboratory of Hidde Ploegh)<br>
<span
></span> Sara Gredmark
(gredmark@wi.mit.edu; 4-1713; laboratory of Hidde Ploegh)<br>
Fall 2007. Tuesdays, 3-5 pm. Room 68-151.<br>
<br>
Today we can treat certain cancers and other chronic diseases with
vaccines, antibiotics and antiviral drugs. Not so many years
ago, such treatments were topics for science fiction. New
discoveries have helped us understand common chronic diseases, such as
cancer, atherosclerosis and diabetes. Many chronic diseases are
caused by pathogens or by the chronic inflammatory response of our own
bodies to pathogens. One striking clinical success story is the
development of a vaccine against the virus that causes cervical
cancer, human papilloma virus (HPV). About 20 years ago the causal
relationship between HPV and cervical cancer was discovered. Through
increasing molecular knowledge about HPV a recombinant vaccine was
developed and has recently been introduced for broad use. It has been
predicted that this vaccine will drastically reduce the incidence of
cervical cancer. In this course we will explore the new emerging field
of pathogen-induced chronic diseases. Work in this field has
redefined the causes of some major disorders, such as ulcers. By
reading the primary research literature we will learn about the
molecular mechanisms through which pathogens cause disease. The
diseases that we cover will be introduced with a short patient case
study. We will discuss the bacterium<i> Helicobacter pylori</i> and
gastric disease, HPV and cervical cancer, hepatitis C virus and liver
disease, Epstein-Barr virus and lymphoma, Cytomegalovirus and
atherosclerosis, as well as diabetes and multiple sclerosis. We will
study technical advances in the fight against microbes and explore
future directions for new treatment strategies of chronic infections
and inflammation.<br>
<br>
<b>7.343 The Radical Consequences of Respiration: Reactive
Oxygen Species (ROS) in Aging and Disease<br>
</b>Instructor: Priya Rai (</font><font
color="#0000FF"><u>rai@wi.mit.edu</u></font><font color="#000000">,
8-5173; laboratory of Bob Weinberg)<br>
Fall 2007. Thursdays, 11 am - 1 pm. Room 68-151.<br>
<br>
The emergence of oxygen was responsible for the origin of much of life
as we know it, coinciding with the evolution of eukaryotic and
multicellular organisms. However, environmental oxygen was
highly toxic to almost an entire subset of species, namely the
anaerobes, making oxygen arguably the most fatal pollutant in the
existence of the Earth. To deal with the damaging effects of
oxygen radicals generated during mitochondrial respiration, aerobic
organisms have had to develop protective mechanisms, such as
antioxidant enzymes, redox regulatory proteins and repair pathways.
At controlled levels, reactive oxygen species (ROS) perform important
biological functions, for example acting as signal transducers in
mitogenic pathways and in mediating the immune inflammatory response.
However, excessive levels of oxygen radicals have been implicated in a
wide array of human diseases, ranging from premature aging to cancer.
In this course, we will discuss the physiological consequences of
oxidative stress and altered ROS levels, with emphasis on
understanding the complex dual role of ROS as both cellular signaling
molecules and cellular damaging agents. To understand how we are
protected from the intrinsic reactivity of oxygen, we will start with
a survey of basic oxygen radical biochemistry followed by a discussion
of the mechanisms of cellular as well as dietary antioxidants.
After considering the normal physiological roles of oxidants, we will
examine the effects of elevated ROS action and a failure of cellular
redox capacity on the rate of organismal and cellular aging as well as
on the onset and progression of several major diseases that are often
age-related. Topics will include ROS-induced effects on stem
cell regeneration, insulin resistance as well as diabetes, heart
disease, neurodegenerative disorders and cancer. The role of
antioxidants in potential therapeutic strategies for modulating ROS
levels will also be discussed.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.344 The Fountain of Life: From Dolly to Customized
Embryonic Stem Cells<br>
</b>Instructor: Alexander Meissner (</font><font
color="#0000FF"><u>meissner@wi.mit.edu</u></font><font
color="#000000">, 8-7111, laboratory of Rudolf Jaenisch)<br>
Fall 2007. Thursdays, 3 pm - 5 pm. Room 68-151.<br>
<br>
During development, the genetic content of each cell remains, with a
few exceptions, identical to that of the zygote. Most
differentiated cells therefore retain all of the genetic information
necessary to generate an entire organism. It was through pioneering
technology of somatic cell nuclear transfer (SCNT) that this concept
was experimentally proven. Only 10 years ago the sheep Dolly was
the first mammal to be cloned from an adult organism, demonstrating
that the differentiated state of a mammalian cell can be fully
reversible to a pluripotent embryonic state. A key conclusion
from these experiments was that the difference between pluripotent
cells such as embryonic stem (ES) cells and unipotent differentiated
cells is solely a consequence of reversible changes. These
changes, which have proved to involve reversible alterations to both
DNA and to proteins that bind DNA, are known as epigenetic, to
distinguish them from genetic alterations to DNA sequence. In
this course we will explore such epigenetic changes and study
different approaches that can return a differentiated cell to an
embryonic state in a process referred to as epigenetic
reprogramming.<br>
<br>
<b>7.345 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>
Fall 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 sperm and eggs 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.<br>
<br>
<b>7.346 Synaptic Plasticity and Memory, from Molecules to
Behavior<br>
</b>Instructor: Ariel Kamsler (</font><font
color="#0000FF"><u>kamsler@mit.edu</u></font><font color="#000000">,
3-8762; laboratory of Susumu Tonegawa)<br>
Fall 2007. Wednesdays, 11 am - 1 pm. Room 68-151.<br>
<br>
How do we find our favorite store in the mall? And how do we
remember where we parked our car? By using simple animal models
and sophisticated electrophysiological, biochemical and molecular
biological methods, neuroscientists over the past 40 years have found
fascinating answers to these questions. In this course we will
discover how innovative technologies combined with profound hypotheses
have given rise to our current understanding of neuroscience. We
will study both new and classical primary research papers with a focus
on the plasticity between synapses in a brain structure called the
hippocampus, which is believed to underlie the ability to create and
retrieve certain classes of memories. We will discuss the basic
electrical properties of neurons and how they fire. We will see
how firing properties can change with experience, and we will study
the biochemical basis of these changes. We will learn how
molecular biology can be used to specifically change the biochemical
properties of brain circuits, and we will see how these circuits form
a representation of space giving rise to complex behaviors in living
animals. A special emphasis will be given to understanding why
specific experiments were done and how to design experiments that will
answer the questions you have about the brain.</font></div>
<div><font color="#000000"><br>
<u><b>Spring 2007-2008<br>
<br>
</b></u><b>7.341 Under the Radar Screen: How Pathogens Evade
Immune Surveillance<br>
</b>Instructors:<x-tab> </x-tab>Gijsbert
Grotenbreg (</font><font
color="#0000FF"><u>grotenbreg@wi.mit.edu</u></font><font
color="#000000">; 4-2081; laboratory of Hidde Ploegh)<br>
John Antos (</font><font
color="#0000FF"><u>antos@wi.mit.edu</u></font><font color="#000000">;
4-2081; laboratory of Hidde Ploegh)<br>
Spring 2008. Wednesdays, 3 pm - 5 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 (Toll-like receptors, the
ubiquitin/proteasome pathway, MHC I/II antigen presentation). Through
our discussion and dissection of the primary research
literature, we will analyze numerous 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>7.342 Developmental and Molecular Biology of
Regeneration.<br>
</b>Instructor: Christian Petersen (</font><font
color="#0000FF"><u>petersen@wi.mit.edu</u></font><font
color="#000000">; 324-2132; laboratory of Peter Reddien)<br>
Spring 2008. Thursdays, 3 pm - 5 pm. Room 68-151.<br>
<br>
Regeneration is widespread throughout the animal kingdom.
Remarkably, planarian flatworms and hydra can regenerate an entirely
new body. Salamanders can regenerate entirely new limbs, and
fish can regenerate fins, spinal cords, and even heart tissue.
Mammals can regenerate digit tips, liver, and hair. Mammals also
maintain blood, skin and gut throughout adulthood. How does a
regenerating animal "know" what is missing? How are stem cells or
differentiated cells used to create new tissues during regeneration?
We will take a comparative approach to explore this fascinating
problem by critically examining classic and modern scientific
literature about the developmental and molecular biology of
regeneration. We will learn about conserved developmental
pathways that are necessary for regeneration, and we will discuss the
relevance of these findings for human medicine.<br>
<br>
<br>
<b> <br>
7.343 Sophisticated Survival Skills of Simple Microorganisms:
Bacterial Stress Responses<x-tab> </x-tab>and their
Relevance to Ecology, Health and Industry<br>
</b>Instructor: Adrienne Dolberry (</font><font
color="#0000FF"><u>dolberry@mit.edu</u></font><font color="#000000">,
3-8686; laboratory of Penny Chisholm)<br>
Spring 2008. Thursdays, 11 am - 1 pm. Room 68-151.<br>
<br>
The ability of bacterial cells to acclimate to unfavorable growth
conditions has allowed such "simple" microorganisms to thrive in
environments uninhabitable by more complicated forms of life. By
studying bacteria such as<i> Escherichia coli</i>,<i> Bacillus
subtilis</i> and others under conditions of extreme heat, artic
temperatures, high light and acidic surroundings, researchers have
identified and characterized genes involved in the acclimation of such
microorganisms to and survival under stressful environments. How
might organisms that are experts in cold acclimation, such as species
of<i> Psychrobacter</i> bacteria from the Artic, help us to identify
life on Mars? What types of cellular morphologies do
pathogenic<i> Escherichia coli</i> assume when they contaminate your
apple cider? How do starvation and light stresses control
primary energy production in lakes and ponds? In this course, we
will discuss the microbial physiology and genetics of stress responses
in aquatic ecosystems, astrobiology, bacterial pathogenesis and the
food industry. We will learn about classical and novel methods
utilized by researchers to uncover bacterial mechanisms induced under
both general and environment-specific stresses. Finally, we will
compare and contrast models for bacterial stress responses to gain an
understanding of distinct mechanisms of survival and of why there are
differences among bacterial genera.</font></div>
<div><font color="#000000"><br>
<br>
<b>7.344 Directed Evolution: Engineering Biocatalysts<br>
</b>Instructor: Kerry Love (</font><font
color="#0000FF"><u>klove@wi.mit.edu</u></font><font color="#000000">,
4-2081; laboratory of Hidde Ploegh)<br>
Spring 2008. Thursdays, 1-3 pm. Room 68-151.<br>
<br>
Enzymes, nature's catalysts, are remarkable biomolecules capable of
extraordinary specificity and selectivity. These characteristics
have made enzymes particularly attractive as an alternative to
conventional catalysts in numerous industrial processes.
Oftentimes, however, the properties of an enzyme do not meet the
criteria of the application of interest. While biological
evolution of an enzyme's properties can take several million years,
directed evolution in the laboratory is a powerful and rapid
alternative for tailoring enzymes for a particular purpose.
Directed evolution has been used to produce enzymes with many unique
properties, including altered substrate specificity, thermal
stability, organic solvent resistance and enantioselectivity -
selectivity of one stereoisomer over another. One example is the
improvement of the catalytic efficiency of glutaryl acylase, an
important enzyme in the manufacturing of semi-synthetic penicillin and
cephalosporin. The technique of directed evolution comprises two
essential steps: mutagenesis of the gene encoding the enzyme to
produce a library of variants, and selection of a particular variant
based on its desirable catalytic properties. In this course, we
will examine what kinds of enzymes are worth evolving and the
strategies used for library generation and enzyme selection. We
will focus on those enzymes that are used in the synthesis of drugs
and in biotechnological applications.<br>
<br>
<b> <br>
7.345 Antibiotics, Toxins, Protein Engineering and The
Ribosome<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 2008. Wednesdays, 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. The ribosome, the function of which is to synthesize all
proteins within a cell, has emerged as a prime drug target. Over the
past decade, we have gained new and fundamental insight into the
molecular workings of the ribosome, an amazing macromolecular machine.
In this course, we will explore the structure and function of the
ribosome. We will discuss the various mechanisms of action of toxins
and antibiotics, their roles in everyday medicine, and the emergence
and spread of drug resistance. We will also talk about 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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