[Bioundgrd] Biology Advanced Undergraduate Seminars

[Janice Chang]

August 30, 2004

TO:     MIT students
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 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.

         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 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.

***

FALL 2004-05

7.340  Ubiquitination, the Proteasome, and Human Disease
Instructor:  Marta Rubio (mrubiotx at mit.edu, 3-9838; laboratory of Chris Kaiser)
Fall 2004.  Wednesdays, 11 am - 1 pm.  Room 68-151.

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. 


7.341  RNA Splicing and Human Disease: Molecular and Computational Approaches
Instructors:  Zefeng Wang (zefeng at mit.edu, 3-6726; laboratory of 
Chris Burge); Dirk Holste (holste at mit.edu, 3-7039; laboratory of 
Chris Burge)
Fall 2004.  Tuesdays, 11 am - 1 pm.  Room 68-151.

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 cis-acting elements and trans-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.


7.342  Cancer biology:  From Basic Research to the Clinic
Instructors:  Kevin Haigis (kmhaigis at mit.edu, 3-6789; laboratory of 
Tyler Jacks); Carla Kim (cfkim at mit.edu, 3-0264; laboratory of Tyler 
Jacks)
Fall 2004.  Tuesdays, 1-3 pm.  Room 68-151.

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, C. elegans, 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.


7.343  When Good Proteins Go Bad: Incorrectly Folded Proteins Cause 
Mad Cow, Creutzfedt-Jakob, Alzheimer's, and Huntington's Diseases.
Instructor:  Melissa Kosinski-Collins (kosinski at mit.edu; HHMI 
Education Group postdoctoral associate)
Fall 2004.  Thursdays, 3-5 pm.  Room 68-151.

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.


7.344  RNA Interference: A New Tool for Genetic Analyses and Therapy
Instructors:  Andrea Ventura (aventura at mit.edu, 3-0264; laboratory of 
Tyler Jacks); Stephan Kissler (skissler at mit.edu, 8-8308; laboratory 
of Luk van Parijs)
Fall 2004.  Wednesdays, 3-5 pm.  Room 68-151.

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.


SPRING 2004-05

7.345  Evolution of the Immune System
Instructor:  Nadia Danilova (ndanilov at mit.edu, x3-6705; laboratory of 
Lisa Steiner)
Spring 2005.  Thursdays, 1 - 3 pm.  Room 68-151.

 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.


7.346  How Life's Symphony Is Conducted: Molecular and Bioinformatic 
Approaches to Transcriptional Regulation
Instructor:  Ben Gordon (dbgordon at wi.mit.edu, 2-3826; laboratory of 
Ernest Fraenkel)
Spring 2005.  Tuesdays 3-5 pm.  Room 68-151.

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.


7.347  The Ribosome: A Most Incredible Molecular Machine
Instructors:  Caroline Koehrer (koehrer at mit.edu, 3-1870; laboratory 
of Uttam RajBhandary); Mandana Sassanfar (mandana at mit.edu, 452-4371; 
laboratory of Chris Kaiser)
Spring 2005.  Wednesdays, 3-5 pm.  Room 68-151.

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.


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

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.


7.349  Biological Computing: At the Crossroads of Engineering and Science
Instructor:  Julia Khodor (jkhodor at mit.edu; 324-0055; HHMI Education 
Group postdoctoral associate)
Spring 2005. Wednesdays, 1-3 pm.  Room 68-151.

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.
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