[Bioundgrd] Advanced Undergraduate seminars

[Janice Chang]

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 2003-2004 academic year:  a 
set of 13 new and very current seminar courses, 7.340-7.346, 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, genomics, biochemistry, 
proteomics, bioinformatics, molecular biology, cell biology, 
immunology, cancer biology, 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.

         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 for 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 2003 and Spring 2004 semesters, please 
join the instructors at a poster session on Registration Day 
(September 2, 2003) from 10 am to 2 pm in room W35-199, just across 
from Registration.

FALL, 2003

7.340  Animal Models of Human Disease
Fall, 2003. Thursdays, 1-3 pm.  Room 68-151.
Instructors:	Joe Kissil (jkissil at mit.edu, 3-0264; laboratory of Tyler Jacks)
Kevin Haigis (kmhaigis at mit.edu, 3-0264; laboratory of Tyler Jacks)

Animal models of human disease are essential tools in basic science 
and medicine.  Such models have proven indispensable to the 
understanding of molecular mechanisms underlying disease and in the 
development of therapeutics.  In the past, most animal models have 
relied on experimentally or pharmacologically altered wild-type 
animals as well as on naturally-occurring mutant strains.  More 
recently, the genetic basis of numerous human diseases has been 
elucidated, and emerging technologies involving mutagenesis, 
transgenic animals (in which specific altered genes have been 
introduced into animals), and gene knockouts (in which specific 
endogenous genes have been inactivated) have led to the creation of 
rationally designed animal models.  In this course we will consider 
different approaches to generating models for a variety of human 
diseases, including cancer and autoimmune and neurodegenerative 
diseases.  The strengths, limitations and medical implications of 
these models will be addressed.  The ethics of using animal models 
and the potential of biochemical or cellular rather than animal model 
systems will also be discussed.


7.341  Age and the Malleable Brain:  Biological and Clinical 
Perspectives on the Loss of Adaptability by the Maturing Brain   
Fall, 2003.  Tuesdays, 11 am - 1 pm.  Room 68-151.
Instructor:  Matt Colonnese (colonnese at wi.mit.edu; 8-5252; laboratory 
of Alan Jasanoff)

Can you teach an old brain new tricks?  For most of the last 100 
years, the answer has been no.  The brain was thought to be like 
plastic:  easy to mold at first, but once set no longer malleable. 
After a certain age, it was thought, new neurons are not born, neural 
processes do not grow, and new synapses are no longer made.  However, 
neurobiological research over the last 20 years has shown that much 
of this thinking is untrue.  What has changed?  In this class we will 
ask why we once thought that the brain does not change in adulthood, 
and why we now think it does.  We will explore the differential 
abilities of the young and mature brain to recover from injury.  For 
example, an infant can have half of his or her cerebral cortex 
removed and behave apparently normally, an impossibility for an 
adult.  What is the neurobiological basis of this difference?  How 
exactly does a young brain differ from a mature one, and can we use 
this knowledge to promote recovery from brain or other nervous system 
damage?  We will answer these questions by examining both studies of 
humans with brain damage and of animals subjected to experimental 
manipulations that have helped reveal the biological mechanisms 
involved.   


7.342  Evolution of the Immune System
Fall, 2003. Tuesdays, 1 - 3 pm.  Room 68-151.
Instructors:	Susann Beetz (sbeetz at mit.edu; 3-6705; laboratory of 
Lisa Steiner)
Nadia Danilova (ndanilov at mit.edu; 3-6705; laboratory of Lisa Steiner)

 From very early in evolution, organisms encountered the problem of 
protecting themselves from invading pathogens.  Such protection 
requires the ability to discriminate self from non-self.  In response 
to this problem, a complex and sophisticated immune system capable of 
detecting and destroying pathogens, as well as of similarly 
responding to cancer cells, has evolved.  Even prokaryotes have 
self-protective mechanisms, including restriction endonucleases, 
antimicrobial peptides, and RNA-interference.  In multicellular 
organisms, specialized immune cells have evolved, with the ability to 
recognize and engulf foreign cells.  Such defensive mechanisms are 
based upon germline-encoded receptors and are said to constitute a 
system of innate immunity.  In jawed vertebrates, innate immunity 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 diversification 
of immune receptors and distinct immunological memories 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 shaped the evolution of immune 
system.


7.343  RNA Interference, a Revolutionary Technology Based on an 
Ancient Gene-Silencing Pathway
Fall, 2003.  Thursdays, 3 - 5 pm.  Room 68-151.
Instructors:	Michael McManus (mmcmanus at mit.edu; 3-6458; laboratory 
of Phil Sharp)
Alla Grishok (agrishok at mit.edu; 3-0265 laboratory of Phil Sharp)

Now that the sequence of the entire human genome is known and the 
number of predicted genes is estimated, the next challenge is to 
assign biological function to each of the genes.  A new and very 
powerful way for exploring gene function is offered by RNA 
interference (RNAi).  In this method, the introduction of 
double-stranded RNA identical in sequence to that of the gene of 
interest inactivates the gene or, more precisely, "interferes" with 
its function.  Initially discovered in worms, this method was viewed 
as a "magic wand" for shutting down genes, with little understanding 
about how it worked.  With the efforts of many scientists the magic 
of RNAi began to unfold from being a curiosity in worms to being an 
ancient gene-silencing mechanism common to plants, fungi, and 
animals.  Researchers have discovered that specific genes are 
required for RNAi to occur and that these genes constitute an 
evolutionarily conserved pathway that uses endogenous cellular dsRNA 
to silence developmentally important genes in a precise manner. 
Although the field of RNAi has emerged only recently, it has already 
made a profound impact in biology.  This course will discuss the 
discovery of RNAi, its mechanisms, and applications in uncovering 
gene function and curing human disease.


7.344  Genomics and Bioinformatics of Gene Expression
Fall, 2003.  Wednesdays 1-3 pm.  Room 68-151.
Instructors:	Uwe Ohler  (ohler at mit.edu; 3-7039; laboratory of Chris Burge)
Gabriel Kreiman (kreiman at mit.edu; 3-0547; E25-201B; laboratory of 
                                 Tommy Poggio)

A large number of both normal and disease biological processes depend 
on specific spatial and temporal patterns of the expression of 
particular genes or groups of genes.  The recent availability of DNA 
sequence information (from humans and other organisms) as well as 
high-throughput methods for the analysis of gene expression data 
(e.g., from microarrays) allow us to use computational algorithms to 
study gene expression (transcription).  In this seminar we will focus 
on transcriptional initiation, regulation, and networks and on how 
expression levels are measured using high-throughput techniques.  We 
will discuss recent advances in the methods of genomics and 
bioinformatics available to a biologist interested in this area of 
research.  Many of these tools also have applications in other areas 
of biological research.


7.345  The Chemistry and Biology of Carbohydrates, Key Molecules of Life
Fall 2003. Wednesdays, 3-5 pm.  Room 68-151.
Instructor:  Kuberan Balagurunathan (kuby at mit.edu, 3-8803; laboratory 
of Robert Rosenberg)

Carbohydrates differ from other biological polymers, such as nucleic 
acids and proteins, in many ways.  Most importantly, they have 
different functional groups that provide almost unlimited variations 
in their structures.  Carbohydrates that are conjugated to proteins 
or lipids are termed glycoconjugates.  They decorate the outer 
surface of mammalian cells.  Their strategic location enables them to 
regulate many important biological processes, including 
fertilization, cell growth, cell-cell adhesion, cell-cell 
communication, development, immune defense, viral and parasitic 
infection, degradation of blood clots, inflammation etc. 
Furthermore, alterations in the synthesis or catabolism of 
cell-surface carbohydrates are associated with various pathological 
conditions, including malignant transformations and congenital and 
neurological disorders.  Deciphering the enigmatic structures of 
carbohydrates and understanding their biosynthetic/catabolic pathways 
are critical for the development of carbohydrate-based therapeutics. 
In this course, we will discuss the tools available to characterize 
carbohydrate structures, methods to synthesize carbohydrates, the 
biosynthesis and catabolism of carbohydrates, and the role of 
carbohydrates in human diseases and developmental disorders such as 
cancer, congenital defects, and Sanfilippo disease.


SPRING, 2004

7.340  Immune Evasion: How Sneaky Pathogens Avoid Host Surveillance
Spring, 2004.  Thursdays, 1 - 3 pm.  Room 68-151.
Instructor:  Dina Gould Halme (dghalme at mit.edu; 2-2557; HHMI 
Education Group postdoctoral associate)

Every infection consists of a battle between the invading pathogen 
and the resisting host.  To be successful, a pathogen must escape the 
many defenses of the host's immune system until it can replicate and 
spread to another host.  Therefore, a pathogen must prevent at least 
one of three stages of immune function: detection, activation, or 
effector function.  Human Cytomegalovirus (HCMV) has at least three 
genes that act to prevent the detection of virally-infected cells, 
helping it to infect 90% of people living in urban settings.  Human 
Immunodeficiency Virus (HIV), which causes AIDS,  produces a protein 
that prevents the activation of immune cells.  Many gastric, 
colorectal and pancreatic cancers bear surface receptors that prevent 
the tumors from being lysed by the immune system.  In this course, we 
will discuss these examples and many other mechanisms used by 
pathogens to prevail over their hosts' immune systems and cause 
disease.  We will consider what these host-pathogen interactions 
reveal not only about the causes of persistent disease but also about 
the normal function of the immune system and basic cell biological 
processes, such as protein maturation and degradation.


7.341  The Molecular Basis of Aging
Spring, 2004.  Tuesdays 3-5 pm.  Room 68-151.
Instructors:	Gil Blander (gblander at mit.edu; 3-6717; laboratory of 
Lenny Guarente)
Marcia Haigis (mchaigis at mit.edu; 3-3567; laboratory of Lenny Guarente)

Aging is a basic feature of the biology of humans and other 
organisms.  Research has shown that 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 also 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 laboratories at MIT and in 
industrial settings.


7.342  Obesity, a Big Fat Problem: from the Transcriptional Control 
of Adipogenesis and Energy Balance to a Worldwide Epidemic
Spring, 2004.  Tuesdays 1-3 pm.  Room 68-151.
Instructor:  Frederic Picard (picard at mit.edu; 3-6717; 68-289; 
laboratory of Lenny Guarente)

Maintaining a healthy body weight has been recognized worldwide as a 
primary goal by national health agencies.  Recent increases in the 
frequency of obesity have been alarming. In the last two decades, our 
understanding of the transcriptional pathways regulating the 
differentiation of fat cells, or adipogenesis, has grown remarkably. 
This course will review the molecular biology and function of fat 
cells (adipocytes), how new adipocytes are made, the regulatory 
pathways of energy balance and current and potential therapeutic 
targets to treat obesity.


7.343  Tagged for Destruction: How Ubiquitin Controls Our Lives
Spring, 2004.  Wednesdays, 3 - 5 pm. Room 68-151.
Instructor:  Marta Rubio (mrubiotx at mit.edu; 3-9838; 68-541; 
laboratory of Chris Kaiser)

The proper functioning of cells depends not only on the activation 
but also on the inactivation of cellular proteins.  Many proteins are 
targeted for degradation in a highly regulated fashion. 
Post-translational mechanisms have evolved to generate signals that 
target proteins for degradation.  Tagging proteins to be destroyed by 
the attachment of special molecules enables specific cellular 
machinery, the "proteasome," to recognize those proteins as 
substrates.  Ubiquitin is a small protein used as such a label to 
target proteins for degradation.  The aim of this course is to 
discuss the mechanisms of the ubiquitin-conjugation system and its 
importance in the functioning of eukaryotic cells.  We will study how 
ubiquitination is key for the global control of many cellular 
pathways.  We will learn about how dysfunctions in ubiquitination can 
lead to the development of a variety of human diseases, including 
neurodegenerative disease (such as Alzheimer's, Huntington's and 
Parkinson's), disorders associated with acute cellular injury 
(ischemia), immune disorders (e.g., in antigen presentation), 
disorders caused by abnormalities in the regulation of the cell 
cycle, signal transduction, or programmed cell death (cancer, 
muscular atrophy).  We will also see how viruses like HIV, human 
papilloma virus, and other infectious agents deceive their cellular 
hosts by hijacking cellular machinery that acts in regulatory steps 
involving ubiquitination.  Finally, we will consider how our 
increasing knowledge of the ubiquitin system offers the possibility 
of designing new pharmacological agents to battle disease.


7.344  Biological Computing-at the Crossroads of Engineering and Science
Spring 2004. Wednesdays, 11 am-1 pm.  Room 68-151.
Instructor:  Julia Khodor (jkhodor at mit.edu; 324-0055; HHMI Education 
Group postdoctoral associate)

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 welcome.  Care will be taken to fill in any 
knowledge gaps for both scientists and engineers.




7.345  Microarray Analysis: From Functional Genomics to the Clinic
Spring, 2004. Thursdays, 3 - 5 pm.  Room 68-151.
Instructor:  Bérengère Bouzou (bbouzou at mit.edu; 2-3851; laboratory of 
Robert Rosenberg)

Gene expression analysis has reached a new dimension with the 
development of microarray chip technologies.  Microarrays exploit the 
preferential binding of complementary single-stranded nucleic acid 
sequences.  A microarray is typically a glass slide, on to which DNA 
molecules are attached at fixed locations (spots).  There may be tens 
of thousands of spots on an array, each containing a huge number of 
identical fragments of DNA molecules, of lengths from 20 to hundreds 
of nucleotides.  A typical dimension of such an array is about 1 inch 
or less, the spot diameter is of the order of 0.1 mm, and for some 
microarrays even smaller.  These potentially powerful methods can 
allow the screening of millions of genes with a single small array 
chip and perhaps one day will allow the screening of the whole genome 
with one chip.  This technology promises a revolution in clinical 
diagnosis, as apparently similar diseases with different prognoses 
and requiring different treatments can be distinguished by their 
molecular fingerprints.  Microarray analysis requires first the 
extraction of quantitative information from the images resulting from 
the readout of fluorescent or radioactive hybridizations and then the 
collection of these data into a database that supports both 
mathematical analysis and a connection to available information about 
the structure and function of the individual genes.  The goal of this 
course is to explore how gene expression can be analyzed using 
microarrays based upon the primary research literature.  We will 
examine the variability of patterns in gene expression among 
different mouse and human organs, tissue and cell types (e.g., brain, 
endothelium, cardiac muscle cells).  We will discuss how the 
screening of gene expression in human cancers before and after 
treatment with anticancer drugs has helped define distinct types of 
breast cancers and lymphomas.  We will consider the techniques 
employed to generate the biological samples used in microarray 
analysis, the types of available microarrays, and the bioinformatics 
and statistical tools commonly used to extract biological 
significance from microarray data.


7.346  The Role of DNA Repair in the Prevention of Human Disease
Spring 2004. Wednesdays ,1-3 pm.  Room 68-151.
Instructor:  Penny Beuning (beuning at mit.edu, 3-3745, laboratory of Graham
Walker)

The accurate maintenance and transmission of genetic information is 
of supreme importance to all organisms.  Although some mutations may 
give rise to useful properties and drive evolution, many mutations 
are harmful to the organism.  Mutations can arise from assaults on 
the genome either from the external environment or from inside the 
cell.  Mutations can also occur as a consequence of errors in DNA 
replication or DNA repair.  In prokaryotes loss of replicative 
fidelity can lead to mutations in and the death of a single cell.  In 
humans defects in DNA repair can lead to disease.  Such human 
diseases include premature aging syndromes, e.g., Werner's and 
Bloom's syndromes, and Xeroderma pigmentosum (XP), the main phenotype 
of which is severe UV light sensitivity leading to skin cancer.  In 
this course we will discuss mechanisms that have evolved to maintain 
accurate replication and transmission of genetic information, and the 
consequences of the loss of this accuracy.  We will focus on the 
roles of DNA repair enzymes, considering both structural and 
mechanistic viewpoints.  We will also discuss how the loss of 
specific DNA repair functions can lead to human disease.
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