[Bioundgrd] Biology Advanced Undergraduate Seminars

[Janice Chang]

Dear Biology undergraduates:

Please take note of the following information from Prof. Horvitz on 
the Biology Advanced Undergraduate Seminars.

Best wishes,
Janice

*******

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 2005-2006 academic year:  a set of 14 
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, biochemistry, molecular 
biology, structural biology, cell biology, developmental biology, 
virology, 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 2005 and Spring 2006 semesters, please check our 
website (http://mit.edu/biology/www/undergrad/adv-ugsem.html), join 
the instructors for the seminars at a poster session on Registration 
Day, Tuesday, September 6 from 1-3pm in the Biology Building (68) 
lobby, and/or contact the instructors directly.


***


FALL 2005-2006

7.340  Nano-life: An Introduction to Virus Structure and Assembly
Instructors:  Melissa Kosinski-Collins (kosinski at mit.edu, 2-1876; 
HHMI Education Group), Peter Weigele (pweigele at mit.edu, 3-3545; 
laboratory of Jon King)
Fall 2005.  Wednesdays, 11 am - 1 pm.  Room 68-151.

Watson and Crick noted that the size of a viral genome was 
insufficient to encode a protein large enough to encapsidate it and 
postulated that a virus shell is composed of multiples of identical 
relatively small subunits. Today, high-resolution structures of virus 
capsids reveal the products of such genetic economy to be highly 
symmetrical structures, much like a geodesic dome composed of protein 
subunits. Structures determined by X-ray crystallography and 
reconstructions from cryo-electron micrographs combined with data 
from traditional molecular approaches are beginning to reveal how 
these nano-structures are assembled. In this course, we will discuss 
basic principles of virus structure and symmetry, capsid assembly, 
strategies for enclosing nucleic acid, proteins involved in entry 
into and exit from cells, and the life cycles of well understood 
pathogens such as HIV, influenza, polio, and herpes. We will also 
review cutting-edge methods of structural biology and will 
participate in a visit to the Department of Biology's transmission 
electron microscope (TEM).

7.341  Not Just a Bag of Enzymes: DNA Dynamics in the Tiny Bacterial Cell
Instructors:  Melanie Berkmen (mberkmen at mit.edu, 3-6702; laboratory 
of Alan Grossman), Lyle Simmons (simmon57 at mit.edu, 3-3745; laboratory 
of Graham Walker)
Fall 2005.  Tuesdays, 11 am - 1 pm.  Room 68-151.

Bacteria were among the first organisms to inhabit the earth, and 
they will probably be the last. While some bacteria are the causative 
agents of diseases such as anthrax and cholera, other bacteria play 
helpful roles, e.g., in plant development and antibiotic production. 
Studies of bacteria have been important in the understanding of 
central biological principles. For example, all cells possess 
mechanisms that ensure that each daughter cell inherits a full 
complement of genes after cell division. In humans, improper 
chromosome segregation may lead to cancer or other diseases. In 
bacteria, failed chromosome segregation results in death. Many 
bacteria must also segregate relatively small DNA molecules called 
plasmids, which can encode antibiotic-resistance and virulence genes. 
In this course, we will investigate the molecular mechanisms by which 
bacteria ensure the faithful segregation of their chromosomal and 
plasmid DNAs. For example, to ensure proper DNA segregation, some 
bacteria use an apparatus similar to that used for mitosis in 
eukaryotic cells. If a chromosome inadvertently gets trapped between 
daughter cells, a DNA pump is assembled at the site to help move the 
DNA to its correct destination. Fluorescence microscopy has played a 
pivotal role in studying the protein and DNA choreography involved in 
plasmid and chromosome maintenance. We will visit an MIT research 
laboratory focused on bacterial chromosome dynamics, and students 
will experience first-hand several fluorescent microscopic techniques 
used in this type of research. In addition, the class will tour the 
Novartis Institutes for Biomedical Research in Cambridge and meet the 
Novartis project leader in microbiology and infectious diseases.

7.342	Evolution of the X, Y and Other Sex Chromosomes
Instructor:  Jennifer Hughes (jhughes at wi.mit.edu,  8-8420; 
laboratory of David Page)
Fall 2005.  Tuesdays, 1-3 pm.  Room 68-151.

You may have heard the rumor that the human Y chromosome is heading 
towards extinction or that the X chromosome is a repository for most 
of our "brainy" and "sexy" genes.  While evidence is mounting to 
dispel such rumors, there is clearly a fascination in the popular 
press and the general public with the sex chromosomes.  They are 
unique components of our genomes, because of their sex-specific 
distribution: females have two X chromosomes, while males have an X 
and a Y.  The Y chromosome has taken on the primary role in male sex 
determination and, as a consequence, has become specialized over 
hundreds of millions of years of evolution to become a concentrated 
center for sperm-production factors.   The sex chromosome system that 
we share with all mammals has been well characterized but is only one 
example of a tremendous variety of systems that are found in nature. 
In this class, we will explore the diversity of sex-determining 
mechanisms, with a focus on chromosomal systems and their evolution, 
ranging from the familiar (XX female  - XY male in mammals and ZZ 
male - ZW female in birds) to the bizarre (10 Xs female  - 5 XYs male 
in the duck-billed platypus).  Despite this diversity, the evolution 
of sex chromosomes appears to follow a strikingly similar path across 
lineages as diverse as humans, birds, and insects: the member of the 
sex chromosome pair that is present in only one sex degenerates over 
time, losing the majority of its genes and shrinking in size.  We 
will learn about the evolutionary theories that attempt to explain 
this degeneration, study experimental systems that allow these 
theories to be tested, and discuss the influences of such factors as 
lifespan, generation time, and even mating behavior.

7.343  A Love-Hate Relationship: Cholesterol in Health and Disease
Instructor:  Ayce Yesilaltay  (ayce at mit.edu; 3-8802; laboratory of 
Monty Krieger)
Fall 2005.  Thursdays, 3-5 pm.  Room 68-151.

After World War II, a new mysterious epidemic was killing men over 55 
like never before.  To find out what was happening, researchers 
focused on a small town in Massachusetts and started the largest and 
longest epidemiological study of its kind.  Our lives have not been 
the same since.  The results from the Framingham Heart Study linked a 
person's blood cholesterol levels to the risk of having heart 
disease, the number one killer in western industrialized societies 
today.  How could a small molecule like cholesterol, a major 
constituent of our cell membranes, be to blame?  In this class, we 
will examine cholesterol's role in the cell and in the body as a 
whole, from its function as a structural component of the membrane to 
its function in signaling.  We will learn that every cell is faced 
with a choice either to make cholesterol or to take it up from 
circulating blood.  How does a cell know how much cholesterol is 
inside it?  We will talk about the transcriptional and 
post-transcriptional mechanisms of cholesterol sensing and of 
feedback regulation in cells.  We will discuss cholesterol in the 
brain and in the circulation, "good cholesterol" and "bad 
cholesterol" and how they are taken up and used in cells.  We will 
consider what happens when cholesterol regulation goes awry in 
cholesterol-related human disorders and in animal models of such 
disorders.  We will learn how the drugs that deal with some of these 
disorders were discovered, their targets and current strategies for 
discovering better drugs in the future.

7.344  Lost in Translation: From Egg to Embryo and Beyond
Instructor:  Leah Vardy (vardy at wi.mit.edu, 8-5246; laboratory of 
Terry Orr-Weaver)
Fall 2005.  Thursdays 11 am -1 pm.  Room 68-151.

Have you ever wondered how an egg becomes a fly, a frog, a mouse or a 
human? Why heads are heads and tails are tails? While we look so 
different from the humble toad, given that we both use many of the 
same processes to develop. What lies at the heart of development 
includes not just our genes, but also how these genes are expressed, 
i.e., how mRNA is regulated.  In this course we will explore some of 
the ways in which mRNA is regulated and see the developmental 
consequences when translation of mRNA into protein is disrupted. We 
will consider flies, frogs and mice to see how they turn on and off 
different mRNAs to meet their developmental needs. Topics will 
include mRNA localization, which is fundamental in distinguishing the 
head from the tail of a fruit fly. We will look at the importance of 
protein translation in the maturation of frog and mouse eggs and in 
the production of sperm and eggs in a hermaphrodite worm. We will 
discuss the variety of ways an embryo can fine-tune its mRNA 
expression to ensure production of a protein in the exact space and 
at the exact time required.  Examples will include different ways to 
activate and suppress translation, including polyadenylation, the 
action of specific RNA-binding proteins and the recently discovered 
important role played by microRNAs. Finally, we will see that 
misregulation of translation plays a central role in a number of 
human diseases.   

7.345  Diabetes and Obesity: Energy Balance and Disease
Instructor:  Kelly Wong (kwong at wi.mit.edu, 8-0377; laboratory of Harvey Lodish)
Fall 2005.  Thursdays, 1-3 pm.  Room 68-151.

Do you know how your eating behavior is controlled at the molecular 
and cellular levels?  How do the cells in your body determine how 
much energy they need?  What mechanisms does your body activate to 
burn fat?  Importantly, what happens when these processes go wrong, 
leading to diabetes and obesity?  Diabetes and obesity constitute one 
of the fastest growing epidemics in the United States.  According to 
the U.S. Center for Disease Control, over the last 10 years there has 
been an alarming increase in the number of patients diagnosed with 
diabetes and/or obesity across the United States.  The burden on the 
healthcare system imposed by diabetes was estimated to be $92 billion 
dollars of direct medical costs in 2002.  In this course, we will 
discuss insulin, its signal transduction and the sensitivity and 
resistance of muscle to the actions of insulin.  We will study the 
AMP-activated protein kinase, a master sensor of cellular energy 
status. We will also examine the actions of the hormone leptin and 
its role in controlling body weight and feeding behavior, as revealed 
by studies of genetically engineered mouse models.  Besides leptin, 
other adipose tissue cytokines such as adiponectin will be discussed. 
Finally, we will examine the molecular consequences of beneficial 
activities, such as exercise, and discuss pharmacological agents that 
are currently being used to treat patients with Type II diabetes.

7.346   RNA Editing from A to I
Instructors:  Ben Wong (bwong at mit.edu, 3-4704; laboratory of Alex 
Rich), Alekos Athanasiadis (alekos at mit.edu, 
alekosathanasiadis at hotmail.com, 3-4704; laboratory of Alex Rich)
Fall 2005.  Wednesdays, 1-3 pm.  Room 68-151.

Being human takes only about 30,000 genes, being a fruitfly takes 
about 14000 genes and being a yeast takes about 5-6,000 genes. Many 
of these genes are highly similar among these and other species. How 
is such wide range of organismal complexity achieved from a largely 
similar set of basic genes? This question has become central in 
molecular biology since the revealing of genome sequences a few years 
ago. One answer to this question appears to lie in mechanisms that 
allow single genes to encode a large number of variant products 
(usually proteins). In contrast to the classic hypothesis that one 
gene encodes one protein, post or co-transcriptional modifications of 
messenger RNA often allow single genes to generate hundreds or even 
thousands of proteins tailored to specific needs of the cells in 
different tissues or at developmental stages. RNA editing by dsRNA 
adenosine deaminases (ADARs), which convert adenosine to inosine, is 
one mechanism that generates RNA diversity present in organisms as 
diverse as primates and insects. In organisms as evolutionary diverse 
as nematode roundworms and humans, RNA editing has a particular role 
in the the central nervous system, altering the properties of 
neurotransmitter receptors and ion channels. Abnormalities in these 
activities have linked RNA editing to some of the most challenging 
and mysterious diseases, such as schizophrenia, depression and 
epilepsy. In addition, while useful for cells in fine-tuning protein 
and RNA functions, RNA editing also can combat viruses by altering 
their genomes and messages in a way that destroys information needed 
for their replication and function.  During this course we will study 
ADARs, the enzymes responsible for A-to-I RNA editing, focusing on 
ADAR biochemistry and structure. The study of the known substrates of 
ADARs, mostly brain ion channels, will show us how editing modulates 
function. We will also discuss computational methods for identifying 
new ADAR substrates and the role that ADARs may play in molecular 
evolution.


SPRING 2005-2006

7.340  Molecular Mechanism of Aging
Instructors:  Danica Chen (danicac at mit.edu, 2-4140; laboratory of 
Lenny Guarente), Agnieszka Czopik (czopik at mit.edu, 3-3567; laboratory 
of Lenny Guarente)
Spring 2006. Thursdays, 1-3 pm.  Room 68-151.

Aging is a degenerative process that results in decreased viability 
and increased susceptibility to diseases. This course will focus on 
molecules and molecular pathways that regulate the aging process, 
such as the insulin-signaling pathway and members of the Sir2 gene 
family. We will discuss the molecular mechanism of calorie 
restriction, the only known dietary regimen that extends the 
lifespans of a variety of organisms. Other topics will include the 
human premature aging disorders Werner's Syndrome and 
Hutchinson-Gilford Progeria, the role of oxidative damage and the 
mitochondria in aging, and the effects of metabolism on aging. We 
will explore the reciprocal effects of aging and immunity at the 
cellular and molecular levels and the ways these effects may be 
relevant to human biology. The class will be concluded with tours of 
a research laboratory at MIT and a biotech company both focused on 
aging.

7.341. Virus-Host Interactions: A Molecular Arms Race Important for 
Cell Biology and Disease
Instructor:  Richard Jenner (rjenner at wi.mit.edu, 8-7181; laboratory 
of Rick Young)
Spring 2006. Tuesdays 3-5 pm. Room 68-151.

Viruses are tiny genetic entities that lie in between living and 
non-living things. Consisting of DNA or RNA protected in a protein 
shell, viruses are inert until they come alive inside a host cell. 
Viruses travel lightly with very few proteins and genes, instead 
hijacking cellular proteins to replicate themselves. The cell 
responds with an armament of antiviral proteins, attacking many 
aspects of viral replication. Viruses in turn express specialized 
proteins that act to block this host antiviral response. During this 
course, we will examine multiple examples of this molecular arms race 
between virus and host. We will learn about viruses that remain 
undetected within cells and the thousands of viral elements that we 
all carry within our genomes. We will also discuss how the battle 
between viruses and human cells causes diseases such as AIDS and 
cancer and what the study of virology teaches us about normal 
cellular functions.

7.342  The RNA Revolution
Instructors:  Rickard Sandberg (sandberg at mit.edu, 3-7039; laboratory 
of Chris Burge), Michael Stadler (stadler at mit.edu, 3-7039; laboratory 
of Chris Burge)
Spring 2006.  Thursdays, 3-5 pm.  Room 68-151.

Recent findings have revolutionized our view of the roles of RNA in 
biology. For example, short non-coding RNAs (microRNAs and short 
interfering RNAs) play key roles in development and cancer by 
regulating gene expression. The biology of short non-coding RNAs and 
their importance in these processes will be topics for this course. 
In addition, the mechanism of alternative splicing explains in part 
how humans can express 500,000 different proteins with only 25,000 
genes. Alternative splicing, the process by which exons are joined in 
different combinations to generate multiple variants of a gene, is 
estimated to affect about 75% of all human genes. We will discuss how 
alternative splicing diversifies the human protein repertoire, 
influences sex determination and courtship behavior in fruit flies 
and when disrupted can cause diseases such as spinal muscular 
atrophy. Attention will also be given to catalytic RNAs that act in 
the ribosome during protein synthesis. In each session we will 
critically evaluate both the experimental and the computational 
techniques used in the primary literature to foster an understanding 
of their strengths and limitations. This course will give you an 
overview of the exciting newly emerging roles for RNA.

7.343  Takin' Out the Trash: Quality Control in Cellular Processes
Instructors: Peter Chien (pchien at mit.edu; laboratory of Tania Baker), 
Eric Spear (espear at mit.edu; laboratory of Chris Kaiser)
Spring 2006.  Wednesdays, 3-5 pm. Room 68-151. 

Messenger RNAs are synthesized from a DNA blueprint, the proteins 
resulting from these messages are produced using the complex 
machinery of the ribosome, and finally these proteins must attain 
their proper mature folded state. Although this process is 
extraordinarily accurate, care must be taken by the cell to cope with 
the inevitable mistakes that occur along this long and complicated 
pipeline.  To this end, the cell has evolved a broad range of 
mechanisms to ensure the quality of the final protein product.  For 
example, improperly folded proteins are often recognized as aberrant 
and subsequently degraded, relieving the cell of the potentially 
detrimental effects of a non-functional and abnormal protein.  In 
this class, we will discuss some of the many mechanisms used for 
cellular quality control. We will consider the stresses that can 
generate such aberrant protein products and how the cell continuously 
fights these challenges.  The recognition of misfolded proteins and 
how these proteins are targeted to the degradative machinery will 
also be discussed.  We will consider both prokaryotic and eukaryotic 
quality control, drawing attention to the similarities between these 
two systems as well as highlighting differences between them.  The 
importance of these quality control mechanisms will be emphasized 
throughout the course by discussing a number of relevant human 
diseases, including cystic fibrosis, Huntington's Disease, and 
certain types of cancer.

7.344  Toxins, Antibiotics, 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 2006. Tuesdays, 1-3 pm. Room 68-151.

What do the lethal poison Ricin, Diphtheria toxin, and the widely 
used antibiotic tetracycline have in common? They all inhibit protein 
synthesis by targeting the cell's translation machinery. Why is Ricin 
such a powerful toxin? How does it work? If Diphtheria toxin and 
tetracycline also inhibit translation, why do they have such 
different consequences? How does resistance to antibiotics like 
tetracycline arise? In this course, we will explore the mechanisms of 
action of toxins and antibiotics that specifically target components 
of the translational apparatus leading to the disruption of protein 
synthesis. We will discuss the roles of these antibiotics and toxins 
in everyday medicine, the emergence and spread of drug resistance, 
and how we might overcome this increasing problem by identifying new 
drug targets and designing new drugs. We will also discuss how the 
detailed understanding of the structure of the ribosome and the 
translation machinery has led to new technologies in protein 
engineering and promising applications for human therapy.

7.345  Jellyfish, FRET and Quantum Dots:  Illuminating Biology with 
Fluorescent Probes
Instructors:  Andrew Dutton (adutton at mit.edu, 2-2826; laboratory of 
Barbara Imperiali), Bianca Sculimbrene (sculimbr at mit.edu, 2-2826; 
laboratory of Barbara Imperiali)
Spring 2006.  Wednesday 1-3 pm.  Room 68-151.

Significant advances in biology have occurred through the use of 
fluorescence techniques. The sensitivity and selectivity of 
fluorescent probes has advanced our understanding of human diseases 
and of many other areas of biology by allowing the study of proteins 
within living cells.   This course will focus on fluorescence 
spectroscopy as a powerful probe to study biological systems. We will 
first discuss fluorescence and methods to fluorescently label 
biomolecules. Examples of the in vitro chemical labeling of proteins 
and the hijacking of naturally-occurring fluorescent proteins, such 
as GFP (a green fluorescent protein from jellyfish), will be 
considered. Recent examples will be used to demonstrate the power of 
fluorescence methods at the frontier of biological research. We will 
learn how Fluorescence Resonance Energy Transfer (FRET), quantum dots 
and single-molecule experiments have impacted fields such as cancer 
biology and infectious disease. This course will endow students with 
the ability to understand and critically evaluate the primary 
literature, which is fundamental to advanced careers in science and 
medicine. Fluorescence technologies lie at the interface of chemistry 
and biology, and we hope that any student interested in either of 
these areas will find the information taught in this course extremely 
useful.

7.346  How Abnormal Protein Folding Causes Alzheimer's, Parkinson's, 
Mad Cow and Other Neurodegenerative Diseases
Instructor:  Atta Ahmad (giftee6 at mit.edu, 3-3707; laboratory of Vernon Ingram)
Spring 2006.  Thursdays, 11 am - 1 pm.  Room 68-151.

The cause of both Alzheimer's Disease (AD) and Parkinson's Disease 
(PD) is abnormal deposition of proteins in brain cells. In addition, 
there are 20 other neurological diseases caused by similar protein 
deposition. Millions of people suffer from these diseases. The latest 
research shows that these diseases arise as a consequence of a 
specific series of molecular events.  First, a protein assumes a 
non-native sticky "misfolded state." Two or more such sticky proteins 
associate together to generate a multi protein "oligomeric state." 
These oligomers can associate with each other or can recruit newly 
formed sticky proteins, thereby growing into bigger thread-like 
structures called "amyloid fibrils." These fibrils can deposit either 
inside or outside brain cells, disrupting normal biological functions 
and resulting in neuronal cell death. Depending on the region of the 
brain affected, this cell death leads to visible symptoms, such as 
memory loss, loss of cognitive ability, abnormal muscular movements, 
involuntary shaking and, in many cases, death. In this course, we 
will discuss the processes that trigger protein aggregation (such as, 
mutations and environmental effects) with an emphasis on Alzheimer's 
Disease, Parkinson's Disease and Mad Cow Disease. The methods used to 
study the processes of aggregation (e.g., fluorescence spectroscopy, 
circular dichroism, infrared spectroscopy, transmission electron 
microscopy, confocal microscopy) will be discussed. We will consider 
the consequences of the aberrant proteins on cellular processes. We 
will also discuss potential targets for intervening with these 
processes and approaches that could lead to possible treatments for 
these disorders.

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