[Bioundgrd] Sp04 Advanced Undergraduate Seminars in Biology

[H. Robert Horvitz]

TO:     Biology Majors

FROM:   H. Robert Horvitz, Professor of Biology


         I am writing to inform you of the exciting Advanced 
Undergraduate Seminars courses being offered by the Department of 
Biology for the Spring 2004 term.  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.


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.


-- 
Stuart Dietz
Biology Education Office, Rm. 68-120
Massachusetts Institute of Technology
77 Massachusetts Ave.
Cambridge, MA  02139

Phone (617) 252-1783
Fax (617) 258-9329
  
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