[bioundgrd] Biology Advanced Undergraduate Seminars 2007-2008
Janice Chang
jdchang at MIT.EDU
Mon Aug 20 11:47:16 EDT 2007
Dear Biology Undergraduatse - please take note of the following
letter from Prof. Horvitz on the biology Advanced Undergraduate
seminar offerings for 2007-2008.
*********************
TO: Biology Majors
FROM: H. Robert Horvitz, Professor of Biology
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.
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.
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.
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.
To learn more about the Advanced Undergraduate Seminars to be
offered during both the Fall 2007 and Spring 2008 semesters, please
check our website
(http://mit.edu/biology/www/undergrad/adv-ugsem.html) and/or contact
the instructors.
************
Fall 2007-2008
7.341 DNA Damage Checkpoints: the Emergency Brake on the Road to Cancer
Instructors: Marcel van Vugt (vanvugt at mit.edu, 2-2443; Laboratory of
Michael Yaffe)
Christian Reinhardt (reinharc at mit.edu, 2-2443;
Laboratory of Michael Yaffe)
Fall 2007. Thursdays, 1 pm - 3 pm. Room 68-151.
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.
7.342 Pathogen-Induced Chronic Diseases: Clinical Relevance and
Molecular Mechanisms
Instructors: Eva Frickel (frickel at wi.mit.edu; 4-1751; laboratory of
Hidde Ploegh)
Sara Gredmark (gredmark at wi.mit.edu; 4-1713;
laboratory of Hidde Ploegh)
Fall 2007. Tuesdays, 3-5 pm. Room 68-151.
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 Helicobacter pylori 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.
7.343 The Radical Consequences of Respiration: Reactive Oxygen
Species (ROS) in Aging and Disease
Instructor: Priya Rai (rai at wi.mit.edu, 8-5173; laboratory of Bob Weinberg)
Fall 2007. Thursdays, 11 am - 1 pm. Room 68-151.
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.
7.344 The Fountain of Life: From Dolly to Customized Embryonic Stem Cells
Instructor: Alexander Meissner (meissner at wi.mit.edu, 8-7111,
laboratory of Rudolf Jaenisch)
Fall 2007. Thursdays, 3 pm - 5 pm. Room 68-151.
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.
7.345 Sex, Chromosomes, and Disease
Instructors: Dena Cohen (greendna at mit.edu, 3-3567; laboratory of
Leonard Guarente)
Sheryl Krevsky Elkin (skelkin at mit.edu, 4-1963;
laboratory of Angelika Amon)
Fall 2007. Wednesdays 3-5 pm. Room 68-151.
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.
7.346 Synaptic Plasticity and Memory, from Molecules to Behavior
Instructor: Ariel Kamsler (kamsler at mit.edu, 3-8762; laboratory of
Susumu Tonegawa)
Fall 2007. Wednesdays, 11 am - 1 pm. Room 68-151.
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.
Spring 2007-2008
7.341 Under the Radar Screen: How Pathogens Evade Immune Surveillance
Instructors: Gijsbert Grotenbreg (grotenbreg at wi.mit.edu; 4-2081;
laboratory of Hidde Ploegh)
John Antos (antos at wi.mit.edu; 4-2081; laboratory of Hidde Ploegh)
Spring 2008. Wednesdays, 3 pm - 5 pm. Room 68-151.
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.
7.342 Developmental and Molecular Biology of Regeneration.
Instructor: Christian Petersen (petersen at wi.mit.edu; 324-2132;
laboratory of Peter Reddien)
Spring 2008. Thursdays, 3 pm - 5 pm. Room 68-151.
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.
7.343 Sophisticated Survival Skills of Simple Microorganisms:
Bacterial Stress Responses and their Relevance to Ecology,
Health and Industry
Instructor: Adrienne Dolberry (dolberry at mit.edu, 3-8686; laboratory
of Penny Chisholm)
Spring 2008. Thursdays, 11 am - 1 pm. Room 68-151.
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 Escherichia coli, Bacillus subtilis 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 Psychrobacter bacteria from the Artic, help us to identify life on
Mars? What types of cellular morphologies do pathogenic Escherichia
coli 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.
7.344 Directed Evolution: Engineering Biocatalysts
Instructor: Kerry Love (klove at wi.mit.edu, 4-2081; laboratory of Hidde Ploegh)
Spring 2008. Thursdays, 1-3 pm. Room 68-151.
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.
7.345 Antibiotics, Toxins, Protein Engineering and The Ribosome
Instructors: Caroline Koehrer (koehrer at mit.edu, 3-1870; laboratory
of Uttam RajBhandary)
Mandana Sassanfar (mandana at mit.edu, 452-4371; Education Office)
Spring 2008. Wednesdays, 1 - 3 pm. Room 68-151.
The lethal poison Ricin (best known as a weapon of bioterrorism),
Diphtheria 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.
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