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--></style><title>Biology Advanced Undergraduate
Seminars</title></head><body>
<div><font color="#000000">August 30, 2004</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">TO: MIT
students</font></div>
<div><font color="#000000">FROM: H. Robert Horvitz,
Professor of Biology</font><br>
</div>
<div><font color="#000000">
I am writing to inform you of an exciting course offering from the
Department of Biology for the 2004-2005 academic year: a set of
10 new and very current seminar courses, 7.340-7.349, Advanced
Undergraduate Seminars
http://web.mit.edu/biology/www/undergrad/adv-ugsem.html. The topics
are highly varied and encompass areas of genetics, genomics,
biochemistry, proteomics, bioinformatics, molecular biology, cell
biology, immunology, cancer biology, aging, 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.</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 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"><x-tab>
</x-tab>To learn more about the Advanced Undergraduate Seminars to be
offered during both the Fall 2004 and Spring 2005 semesters, please
join the instructors at a poster session on Registration Day (Tuesday,
September 7, 2004) from 10 am to 2 pm in or near Registration at
the Johnson Ice Rink.</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">***</font></div>
<div><font face="Times" size="+2"
color="#000000"><b><br></b></font></div>
<div><font face="Times" size="+2" color="#000000"><b>FALL 2004-05<br>
<br>
7.340 Ubiquitination, the Proteasome, and Human Disease<br>
</b>Instructor: Marta Rubio (<u>mrubiotx@mit.edu</u>, 3-9838;
laboratory of Chris Kaiser)<br>
Fall 2004. Wednesdays, 11 am - 1 pm. Room 68-151.<br>
<br>
The proper functioning of cells depends not only on their ability to
synthesize active proteins but also on their ability to turn proteins
off when they are not needed. Unneeded proteins are usually targeted
for degradation, so the cells can reutilize their amino acids in
making new proteins. Post-translational mechanisms have evolved to
generate signals that target proteins for degradation. Tagging the
proteins to be destroyed by the attachment of special molecules
enables special cellular machines, such as the proteasome, to
recognize tagged proteins as substrates. Ubiquitin is a small protein
that gets appended as such a "label" to target proteins. In
this course we will discuss the mechanisms of the ubiquitin-
conjugation system and its importance in the correct functioning of
eukaryotic cells. We will study how ubiquitination is key for the
global control of many cellular processes. We will learn how defects
in the ubiquitination process are involved in a variety of human
disorders, including neurodegenerative diseases (such as Alzheimer's,
Huntington's, and Parkinson's); affect the activation of the immune
response (antigen presentation and the inflammatory response); affect
the regulation of the cell cycle and apoptotic pathways (important in
cancer and muscular atrophy); and affect the ability to downregulate
signal transduction pathways involved in hormonal responses, leading
to tumorigenesis. We will also see how viruses such as HIV and HPV
deceive their cellular hosts by hijacking the cellular machinery
involved in regulating ubiquitination to promote their own
proliferation. We will discuss how our increasing knowledge of the
ubiquitin system may facilitate the design of new pharmacological
agents to battle disease. </font></div>
<div><font face="Times" size="+2" color="#000000"><br>
<br>
<b>7.341 RNA Splicing and Human Disease: Molecular and
Computational Approaches</b></font></div>
<div><font face="Times" size="+2" color="#000000">Instructors:
Zefeng Wang (<u>zefeng@mit.edu</u>, 3-6726; laboratory of Chris
Burge); Dirk Holste (<u>holste@mit.edu</u>, 3-7039; laboratory of
Chris Burge)</font></div>
<div><font face="Times" size="+2" color="#000000">Fall 2004.
Tuesdays, 11 am - 1 pm. Room 68-151.<br>
<br>
How can the number of human proteins outnumber that of genes
several-fold? How do a small variety of cells in the developing embryo
differentiate into hundreds of cell types in the adult? The
answer to these questions depend upon RNA splicing, a process by which
non-coding, intervening regions of genes are removed to produce a
transcript of that gene ready for translation into protein.
About two-thirds of human genes undergo alternative splicing, in which
the coding regions of a gene are combined to different mRNAs, and the
disruption of splicing can cause human disease. In this course,
we will discuss (1) the basic principles and mechanisms of splicing,
(2) classical and more recent high-throughput methods (such as DNA
microarray, RNA binding and single-molecule detection assays) that can
identify<i> cis</i>-acting elements and<i> trans</i>-acting factors
that regulate splicing either in general or of specific RNAs; (3)
recent methods in genomics, transcriptomics and bioinformatics that
address splicing pathways in a systematic manner; (4) mutations that
affect splicing and cause human diseases, including breast cancer,
cystic fibrosis, myotonic dystrophy, spinal muscular atrophy, and
ataxia telangiectasia; and (5) recent advances in potential
therapeutic treatments that can restore normal splicing.<br>
<br>
<br>
<b>7.342 Cancer biology: From Basic Research to the
Clinic</b></font></div>
<div><font face="Times" size="+2" color="#000000">Instructors:
Kevin Haigis (<u>kmhaigis@mit.edu</u>, 3-6789; laboratory of Tyler
Jacks); Carla Kim (<u>cfkim@mit.edu</u>, 3-0264; laboratory of Tyler
Jacks)</font></div>
<div><font face="Times" size="+2" color="#000000">Fall 2004.
Tuesdays, 1-3 pm. Room 68-151.<br>
<br>
In 1971, President Nixon declared the "War on Cancer."
After three decades the war is still raging. How much progress
have we made toward winning this war, and what are we doing to improve
the fight? Understanding the molecular and cellular events
involved in tumor formation, progression, and metastasis is crucial to
the development of innovative therapy for cancer patients.
Insights into these processes have been gleaned though basic research
using biochemical, molecular, and genetic analyses of yeast,<i> C.
elegans</i>, mice, and mammalian cells grown in culture. We will
explore the laboratory tools and techniques used to perform cancer
research, major discoveries in cancer biology, and the medical
implications of these breakthroughs. A focus of the class will
be critical analysis of the primary literature to foster understanding
of the strengths and limitations of various approaches to cancer
research. Special attention will be given to the clinical implications
of cancer research performed using model organisms and the prospects
for winning the battle against this devastating disease.<br>
<br>
<br>
<b>7.343 When Good Proteins Go Bad: Incorrectly Folded Proteins
Cause Mad Cow, Creutzfedt-Jakob, Alzheimer's, and Huntington's
Diseases.</b></font></div>
<div><font face="Times" size="+2" color="#000000">Instructor:
Melissa Kosinski-Collins (<u>kosinski@mit.edu</u>; HHMI Education
Group postdoctoral associate)<br>
Fall 2004. Thursdays, 3-5 pm. Room 68-151.<br>
<br>
Maintenance of the complex three-dimensional structure adopted by a
protein in the cell is vital for its function. Oftentimes, as a
consequence of environmental stress, genetic mutation, and/or
infection, the folded structure of a protein gets altered and multiple
proteins stick and fall out of solution in a process known as
aggregation. Such protein aggregation can cause disease, and in
many such diseases incorrectly folded proteins self-associate to form
fiber-like aggregates that cause brain cell death and dementia.
In this course we will examine the molecular and biochemical basis of
the prion diseases, which include bovine spongiform encephalopathy
(mad cow disease), Creutzfedt-Jakob Disease and kuru. We will
also discuss other classes of protein misfolding diseases, such as
Alzheimer's Disease and Huntington's Disease. We will examine
the proteins involved in all of these disorders and how the proteins'
three-dimensional structures change during the course of these
afflictions. We will discuss why prions from certain species
cannot infect animals from other species based on protein sequence and
structure. We will consider methods that can detect unfolded
proteins and will discuss therapies under development for the
treatment of the protein aggregation diseases.</font></div>
<div><font face="Times" size="+2" color="#000000"><br>
<br>
<b>7.344 RNA Interference: A New Tool for Genetic Analyses and
Therapy</b></font></div>
<div><font face="Times" size="+2" color="#000000">Instructors:
Andrea Ventura (aventura@mit.edu, 3-0264; laboratory of Tyler Jacks);
Stephan Kissler (skissler@mit.edu, 8-8308; laboratory of Luk van
Parijs)</font></div>
<div><font face="Times" size="+2" color="#000000">Fall 2004.
Wednesdays, 3-5 pm. Room 68-151.<br>
<br>
To understand and treat any disease with a genetic basis or
predisposition, scientists and clinicians need effective ways of
manipulating genes and the levels of gene products. In addition, much
of our basic understanding of biological systems stems from the
experimental modulation of gene function. Conventional methods for the
genetic modification of many organisms are technically demanding and
time consuming. Just over 5 years ago, a new mechanism of
gene-silencing, termed RNA interference (RNAi), was discovered. In
addition to being a fascinating biological process, RNAi provides a
revolutionary technology that has already changed the way biomedical
research is done and may prove useful for genetic interventions in a
clinical context. In this course, we will first discuss how RNAi was
discovered, how it works, and what its physiological relevance might
be. We will then see how RNAi can be harnessed to modulate gene
expression and to identify genes involved in a particular biological
process. Finally, we will discuss attempts to use RNAi for the
treatment of models of human disease in experimental animals.<br>
<br>
<br>
<b>SPRING 2004-05<br>
<br>
7.345 Evolution of the Immune System<br>
</b>Instructor: Nadia Danilova (<u>ndanilov@mit.edu</u>,
x3-6705; laboratory of Lisa Steiner)<br>
Spring 2005. Thursdays, 1 - 3 pm. Room 68-151.<br>
<br>
>From early in evolution, organisms had to protect themselves from
pathogens. Mechanisms for discriminating self from non-self
evolved to accomplish this task, which launched a long history of
host-pathogen co-evolution. The evolution of mechanisms for
immune defence has resulted in a variety of strategies.
Prokaryotes use restriction endonucleases, antimicrobial
peptides, and RNA interference for self-protection. In
multicellular organisms, specialized immune cells have evolved,
capable of the phagocytosis of foreign cells as well as of self cells
changed by infection or cancer. Defensive mechanisms based upon
germline-encoded receptors constitute a system of innate immunity.
In jawed vertebrates, this system is supplemented with a second
system, known as adaptive immunity, which involves a specialized
network of immune cells and organs. Adaptive immunity, in contrast to
innate immunity, is based on the diversification of immune receptors
and immunological memory in each individual. In this course, we
will analyze evolutionary pathways that have led to the development of
innate and adaptive immunity, trace both the conserved and unique
features of the immune response from bacteria to higher vertebrates,
and identify factors, such as adaptive changes in pathogens, that have
shaped the evolution of immune system.<br>
<br>
<br>
<b>7.346 How Life's Symphony Is Conducted: Molecular and
Bioinformatic Approaches to Transcriptional Regulation<br>
</b>Instructor: Ben Gordon (dbgordon@wi.mit.edu, 2-3826;
laboratory of Ernest Fraenkel)</font></div>
<div><font face="Times" size="+2" color="#000000">Spring 2005.
Tuesdays 3-5 pm. Room 68-151.</font></div>
<div><font face="Times" size="+2" color="#000000"> <br>
It is remarkable that cells as different as those make up your blood
and those allow you to see have identical genomic DNA sequences.
Such cellular diversity is achieved largely through the precise
control of the transcription of thousands of genes.
Transcriptional regulatory control also allows cells to respond to
changes in their environment. If the regulatory mechanisms go
awry, disease can be the result. How does the cell orchestrate
transcriptional control, and how does it "know" which genes
to turn on and off? In this course, we will learn how
transcriptional regulatory mechanisms function and how these
mechanisms have been discovered, with particular emphasis on studies
revealing how regulatory information is encoded in the genome itself.
In addition to shedding light on how the cell is able to exert such
careful, dynamic control over its genes, our discussions will consider
structural, bioinformatic, and genetic methods that are being used to
elucidate these mechanisms.</font></div>
<div><font face="Times" size="+2" color="#000000"><br>
<br>
<b>7.347 The Ribosome: A Most Incredible Molecular Machine<br>
</b>Instructors: Caroline Koehrer (<u>koehrer@mit.edu</u>,
3-1870; laboratory of Uttam RajBhandary); Mandana Sassanfar
(<u>mandana@mit.edu</u>, 452-4371; laboratory of Chris Kaiser)<br>
Spring 2005. Wednesdays, 3-5 pm. Room 68-151.</font><br>
</div>
<div><font face="Times" size="+2" color="#000000">Can you imagine how
ribosomes, which are made of proteins and RNAs and in electron
micographs appear as thousands of tiny black dots in the cytoplasm,
can synthesize correctly and in parallel thousands of distinct
proteins at a rate of 15 amino acids per second? Do you wonder how the
correct tRNAs unload their amino acids in the correct order in the
ribosome time after time to make proteins that are neither too long
nor too short but rather exactly as spelled as in the mRNA? How many
proteins interact with the ribosomes and how? Do you know that most
important antibiotics target the ribosome? Now with the structure of
the ribosome available, the field of ribosome biology is more exciting
than ever. Structures of the entire 70S ribosome, obtained by x-ray
crystallography and cryo-electron microscopy, have revolutionized our
understanding of protein synthesis. These structures provide a
tremendous amount of information about the global architecture of and
details of protein-RNA interactions within the two ribosomal subunits,
as well as details of the interaction of the ribosome with ligands
such as initiation factors, mRNAs, and tRNAs. In this course, we will
discuss the structure and function of the ribosome and of many of its
RNA and protein partners in translation. In addition to facilitating
fundamental insights into the mechanisms of protein synthesis, the
structure and function of the ribosome has important implications for
applied biomedical research. We will discuss the mechanisms of action
of antibiotics and toxins that target the ribosome, human diseases
that result from defective protein translation, newly evolving
approaches to drug design and new technologies in protein engineering
to design proteins with novel properties and specific functions.<br>
<br>
<br>
<b>7.348 The Molecular Basis of Aging<br>
</b>Instructors: Gil Blander (<u>gblander@mit.edu</u>, 3-6717,
3-3567; laboratory of Lenny Guarente); Marcia Haigis
(<u>mchaigis@mit.edu</u>, 3-6717, 3-3567; laboratory of Lenny
Guarente)<br>
Spring 2004. Thursdays, 3-5 pm. Room 68-151.<br>
<br>
Aging is a basic feature of the biology of humans and other
organisms. In certain experimental organisms aging can be
postponed or accelerated. This course will explore key pathways
that regulate aging. Recent experiments in which the lifespans of
simple organisms have been extended will be discussed. We will
consider the molecular mechanisms responsible for the human premature
aging disorders Werner's Syndrome and Hutchinson-Gilford Progeria.
We will discuss the effect of caloric restriction, insulin-signaling,
and the Sir2 gene on lifespan extension. In addition, we will
explore the role of oxidative damage and the mitochondria in aging.
To allow students to see aging research first-hand, we will visit
research laboratories focused on aging at MIT and at a biotechnology
company.<br>
<br>
<br>
<b>7.349 Biological Computing: At the Crossroads of Engineering
and Science</b></font></div>
<div><font face="Times" size="+2" color="#000000">Instructor:
Julia Khodor (<u>jkhodor@mit.edu</u>; 324-0055; HHMI Education Group
postdoctoral associate)</font></div>
<div><font face="Times" size="+2" color="#000000">Spring 2005.
Wednesdays, 1-3 pm. Room 68-151.</font><br>
</div>
<div><font face="Times" size="+2" color="#000000">Imagine you are a
salesman needing to visit 100 cities connected by a set of roads. Can
you do it while stopping in each city only once? Even a supercomputer
working at 1 trillion operations per second would take longer than the
age of the universe to find a solution by considering each possibility
in turn. In 1994, Leonard Adleman published a paper in which he
described using the tools of molecular biology - including nucleic
acids, enzymes, and affinity purification with a biotin-avidin
magnetic bead system -- to solve a smaller 7-city example of this
problem. His paper generated enormous scientific and public interest,
and kick-started the field of Biological Computing. Mathematicians,
computer scientists, chemists, biologists, and engineers came together
to create a new field in which contributions from each are critical
for the success of the whole. Currently Biological Computing
encompasses many areas of active research. For example,
three-dimensional self-assembly of molecules can be used to create
stereometrical shapes or to effect computation. Molecule-based string
rewrite systems aim to emulate various mathematical models of
computation using DNA as rewritable tape. Work in the area of
exquisite detection focuses on lowering the number of solution
molecules that can be detected, while whole-cell computing focuses on
hijacking normal cellular processes for computation. We will discuss
how the engineering point of view differs from the scientific
perspective, and how each colors one's thinking and approach to
research. We will analyze the Adleman paper, as well as papers that
came before and after it, and critically examine them with an eye to
identifying engineering and scientific aspects of each paper and the
interplay between the two. Non-Biology majors are welcome. Care will
be taken to fill in any knowledge gaps for both scientists and
engineers.</font></div>
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