[bioundgrd] advanced undergrad seminars -- spring 2006

[Rachel McPherson]

		December 12, 2005

TO:     Biology Majors
FROM:   H. Robert Horvitz, Professor of Biology

         I am writing to inform you of the exciting Advanced 
Undergraduate Seminar courses being offering by the Department of 
Biology for the Spring 2006 term.  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, cell biology 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 this Spring 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 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.




7.342  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. 


7.346  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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