[bioundgrd] Biology Advanced Undergraduate Seminars

Janice Chang jdchang at MIT.EDU
Tue Aug 29 09:43:47 EDT 2006


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 2006-2007 academic year:  a 
set of ten new and very current seminar courses, 7.340-7.344, 
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, chemical biology, cell biology, stem cells, 
immunology, 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 in 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 2006 and Spring 2007 semesters, please 
check our website 
(http://mit.edu/biology/www/undergrad/adv-ugsem.html) and/or contact 
the instructors.



Fall 2006-2007

7.340  Avoiding Genomic Instability: DNA Replication, the Cell Cycle, 
and Cancer
Instructors: John Randell (jrandell at mit.edu, 8-7352, laboratory of Steve Bell)
Robyn Tanny (ret at mit.edu, 3-1979, HHMI Education Group postdoctoral associate)
Fall 2006.  Wednesdays, 11 am - 1 pm.  Room 68-151.

Every time a cell divides, it must faithfully duplicate its genetic 
material once and only once.  At the same time, the cell must ensure 
that this process does not introduce errors that could lead to either 
cell death or tumorigenesis.  In fact, mutations in genes that 
control DNA replication can be found in a wide variety of tumors. In 
this class we will learn about how the process of DNA replication is 
regulated throughout the cell cycle and what happens when DNA 
replication goes awry.  How does the cell know when and where to 
begin replicating its DNA?  How does a cell prevent its DNA from 
being replicated more than once?  How does damaged DNA cause the cell 
to arrest DNA replication until that damage has been repaired?  And 
how is the duplication of the genome coordinated with other essential 
processes? We will examine both classical and current papers from the 
scientific literature to provide answers to these questions and to 
gain insights into how biologists have approached such problems.  We 
will also learn how the misregulation of DNA replication contributes 
to tumor formation and how some anti-cancer drugs target 
proliferating cells by disrupting DNA replication.  Finally, we will 
see how viruses overcome the cellular controls on DNA replication to 
promote their own multiplication and cause disease.

7.341  Brightening Up Life:  Harnessing The Power of Fluorescence 
Imaging to Observe Biology in Action
Instructors:  Anthony Leung (akleung at mit.edu 3-0265; laboratory of 
Phillip Sharp)
	        Mark Howarth (mhowarth at mit.edu, 8-0218; laboratory of 
Alice Ting)
Fall 2006.  Tuesdays, 11 am - 1 pm.  Room 68-151.

One summer in the 1960s a young Japanese researcher, with the help of 
a few high school students, chopped up 10,000 jellyfish.  As a 
by-product of this harvest, they isolated a green fluorescent protein 
(GFP).  Since then, GFP has triggered a revolution in our 
understanding of gene expression and signaling in live cells.  In 
this seminar, we will examine how this small protein generates 
fluorescence, i.e. absorbs light of one wavelength and emits light of 
a longer wavelength.  We will discuss how the color palette has been 
extended from green to blue, red and many other colors, based on 
protein engineering of GFP and the study of vividly colorful coral 
reefs.  We will then investigate how these fluorescent proteins can 
be used to track the motion of DNA, RNA and protein in living cells, 
as well as to see waves of signaling molecules propagate across a 
cell.  GFP is also a powerful tool for fluorescent imaging of whole 
organisms, from worms to mice, and we will see how it has been used 
in tracking the spread of cancer cells, controlling malaria and in 
understanding how neuronal connections form.  In this seminar, we 
will explore this wonderful protein as well as other important 
methods of and reagents for fluorescent imaging.



7.342  Reading the Blueprint of Life:  Transcription, Stem Cells and 
Differentiation
Instructors:  Matt Guenther (guenther at wi.mit.edu; 258-7822; 
laboratory of Rick Young)
	        Roshan Kumar (roshan at wi.mit.edu; 258-7822; laboratory 
of Rick Young)
Fall 2006.  Thursdays, 3-5 pm.  Room 68-151.

Stem cells have the unique ability to give rise to all human tissues 
and hold great potential for tissue regeneration and treating human 
disease.  Realizing this potential will require an understanding of 
the fundamental mechanisms that allow stem cells to generate 
descendants that have a variety of fates and that lock in the 
specialized states and distinctive RNA and protein expression 
patterns of differentiated cells. Transcriptional regulation is 
believed to account for a large part of the specialized gene 
expression programs of cells.  In this course, we will address how 
transcriptional regulators both prohibit and drive differentiation 
during the course of development.  How does a stem cell know when to 
remain a stem cell and when to become a specific cell type?  Are 
there global differences in the way the genome is read in multipotent 
and terminally differentiated cells?  We will explore how stem cell 
pluripotency is preserved, how master regulators of cell-fate 
decisions execute developmental programs, and how chromatin 
regulators control undifferentiated versus differentiated states. 
Additionally, we will discuss how aberrant regulation of 
transcriptional regulators produces disorders such as developmental 
defects and cancer.


7.343  Photosynthesis:  Life from Light
Instructors:	Yongting Wang (ytwang at mit.edu, 2-1876; laboratory of Jon King)
   		Peter Weigele (pweigele at mit.edu, 3-3545; laboratory 
of Jon King)
Fall 2006.  Wednesdays, 3-5 pm.  Room 68-151.

The biological conversion of solar energy to chemical energy forms 
the basis of life as we know it.  Knowledge of this fundamental 
process is critical to our understanding of the biogeochemical cycles 
that mitigate global warming.  In this course, you will journey 
through the web of physical, chemical, and biological reactions that 
collectively constitute photosynthesis.  We will begin with light 
harvesting and follow photons to the sites of primary photochemistry: 
the photoreaction centers.  A molecular-scale view will show in 
atomic detail how these protein complexes capture and energize 
electrons.  Then we will follow the multiple pathways electrons take 
as they carry out their work.  Consequent reactions, such as the 
synthesis of ATP and the reduction of CO2 during the synthesis of 
carbohydrates, will also be discussed in structural detail.  Lastly, 
we will delve into the evolution of these systems and also discuss 
other photosynthetic strategies, such as light-driven proton pumps 
and anoxygenic photosynthesis.  The course will include a visit to an 
electron microscope to allow students to directly observe proteins 
involved in photosynthesis.



7.344  Diabetes and Obesity: Energy Balance and Disease
Instructor:  Kelly Wong (kwong at wi.mit.edu, 8-0377; Laboratory of Harvey Lodish)
Fall 2006.  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 are the mechanisms your body activates 
to burn fat?  Importantly, what happens when these processes go 
wrong?  Diabetes and obesity constitute one of the fastest growing 
epidemics in the United States.  According to the Center for Disease 
Control, over the last 10 years there has been an alarming increase 
in the number of patients diagnosed with diabetes and a startling 
increase in obesity across the United States.  The burden on the U.S. 
healthcare system posed 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 pathway and how muscle can 
be sensitive or resistant to the action of insulin.  We will study 
AMP-activated protein kinase, a master sensor for cellular energy 
status.  We will 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.



Spring 2006-2007

7.340  Under the Radar Screen: How Bugs Trick Our Immune Defenses
Instructors: Marie-Eve Paquet (paquet at wi.mit.edu; 4-1734; laboratory 
of Hidde Ploegh)
Gijsbert Grotenbreg (grotenbreg at wi.mit.edu; 4-2081; laboratory of Hidde Ploegh)
Spring 2007. Thursdays, 1-3 pm.  Room 68-151.

Why are infectious diseases such as HIV, mycobacterium tuberculosis, 
malaria or influenza thriving today and killing millions of people 
each year? These diseases are threats because our immune system 
sometimes fails. Although we are equipped to effectively counter most 
attacks from the microbial world, some pathogens have developed ways 
to evade both our innate and adaptive immune barriers to ensure their 
own survival. The strategies used by these viruses, bacteria or 
parasites are numerous, but all target specific branches and pathways 
of our immune defenses. In this course, we will explore the specific 
ways by which microbes defeat our immune system and the molecular 
mechanisms that are under attack (phagocytosis, the 
ubiquitin/proteasome pathway, MHC I/II antigen presentation). Through 
our discussion and  dissection of the primary research literature, we 
will explore aspects of host-pathogen interactions. We will 
particularly emphasize the experimental techniques used in the field 
and how to read and understand research data. Technological advances 
in the fight against microbes will also be discussed, with specific 
examples. These sessions will highlight the interplay among different 
disciplines of biology and the fact that much can be learned about 
the fundamental properties of our immune system through the study of 
immune evasion.


7.341  Sex, Chromosomes, and Disease
Instructors:	Dena Cohen (greendna at mit.edu, 3-3567; laboratory of 
Leonard Guarente)
		Sheryl Krevsky Elkin (skelkin at mit.edu, 4-1963; 
laboratory of Angelika Amon)
Spring 2007.  Wednesdays, 3-5 pm.  Room 68-151.

Organisms as diverse as the papaya and the platypus use sexual 
reproduction to generate genetic diversity.  How does an organism 
with two copies of each chromosome create a gamete with only one set 
of chromosomes?  What are the genetic determinants of gender, and how 
did these elements evolve?  In this course we will examine meiosis, 
the specialized cell division through which diploid organisms 
generate haploid gametes such as sperm and eggs.  During meiosis, 
cells undergo DNA replication, followed by two nuclear divisions, and 
the chromosomes must be properly segregated, one copy to each 
daughter cell.  Improper chromosome segregation during meiosis is the 
leading cause of miscarriage and can also result in a variety of 
disorders, such as Down's Syndrome (three copies of chromosome 21) 
and Klinefelter syndrome (men have an extra copy of the X chromosome, 
i.e. are XXY instead of XY).  We will talk about what makes the X and 
Y chromosomes different and how those chromosomes can cause 
individuals to be male (XY) or female (XX).  We will also think about 
how sex chromosomes have evolved and discuss special mechanisms, such 
as X-chromosome inactivation, that have evolved to help organisms 
cope with the fact that females have twice as many copies of the X 
chromosome as do males.


7.342  G-Protein Coupled Receptors: Vision and Disease
Instructor:   Parvathi Kota (pkota at mit.edu, 3-1866; laboratory of 
Gobind Khorana)
Spring 2007.  Thursdays, 3-5 pm.  Room 68-151.

How do we communicate with the outside world?  How are our senses of 
vision, smell, taste and pain controlled at the cellular and 
molecular levels?  What causes medical conditions like allergies, 
hypertension, depression, obesity and various central nervous system 
disorders?   G-protein coupled receptors (GPCRs) provide a major part 
of the answer to all of these questions.  GPCRs constitute the 
largest family of cell-surface receptors and in humans are encoded by 
more than 1,000 genes.  GPCRs convert extracellular messages into 
intracellular responses and are involved in essentially all 
physiological processes.  GPCR dysfunction results in numerous human 
disorders, and over 50% of all prescription drugs on the market today 
directly or indirectly target GPCRs.  In this course, we will discuss 
GPCR-mediated signal transduction pathways, GPCR oligomerization and 
the diseases caused by GPCR dysfunction.  We will study the structure 
and function of rhodopsin, a dim-light photoreceptor and a 
well-studied GPCR that converts light into electric impulses sent to 
the brain and leads to vision.  We will also discuss how mutations in 
rhodopsin cause retinal degeneration and congenital night blindness.




7.343  Neuron-glial Cell Interactions in Biology and Disease
Instructor: Bikem Akten (bikem at mit.edu, 2-2726, 46-3251, Supervisor: 
Dr. Troy Littleton) Spring 2007.  Thursdays, 11 am - 1 pm.  Room 
68-151.

Glia (Greek for "glue"), the non-neuronal elements of the nervous 
system, were first identified in 1846 by the anatomist Rudolph 
Virchow.  Since then, glial cells have been regarded as passive 
nervous system components that provide insulation and tropic support 
for neurons.  This view has been challenged in the last few years, 
and we now know that glial cells actively control synapse formation, 
synapse function and synaptic plasticity.  In the mammalian nervous 
system, glial cells outnumber neurons by a factor of ten, reflecting 
the importance of these cells.  Thus, it seems essential that we 
understand the functions of these cells and rethink our view of the 
nervous system as we learn more about the dynamic connections among 
neuronal and glial cells.  The main goal of this seminar will be to 
study the nervous system from the perspective of neuron-glia 
interactions.  In each class, we will focus on one type of glial cell 
and discuss its origin, classification and function within the 
nervous system.   Current findings concerning diseases associated 
with each type of glial cell will be discussed.  Topics will include 
the behavior of glial cells in diseases such as Multiple Sclerosis 
(MS), glioblastoma multiforme (GBM), HIV-associated dementia (HAD), 
Alzheimer's Disease (AD), ischemia, hypoxia and epilepsy.  We will 
also discuss the role of glial cells as neural stem cells in the 
adult brain and their importance in the effective rebuilding of 
damaged brains after injury or disease-associated neurodegeneration. 
The class will include a field trip to a medical school to observe 
clinical research concerning glial disorders. 


7.344   Antibiotics, Toxins, and Protein Engineering
Instructors:	Caroline Koehrer (koehrer at mit.edu, 3-1870; laboratory 
of Uttam RajBhandary)
Mandana Sassanfar (mandana at mit.edu, 452-4371; Education Office)
Spring 2007.  Tuesdays, 1-3 pm.  Room 68-151.

The lethal poison Ricin (best known as a weapon of bioterrorism), 
Diphtheria toxin (the causative agent of a highly contagious 
bacterial disease), and the widely used antibiotic tetracycline have 
one thing in common: they specifically target the cell's 
translational apparatus and disrupt protein synthesis.  In this 
course, we will explore the mechanisms of action of toxins and 
antibiotics, their roles in everyday medicine, and the emergence and 
spread of drug resistance.  We will also discuss the identification 
of new drug targets and how we can manipulate the protein synthesis 
machinery to provide powerful tools for protein engineering and 
potential new treatments for patients with devastating diseases, such 
as cystic fibrosis and muscular dystrophy
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