[bioundgrd] Biology Advanced Undergraduate Seminars, Spring 2006
Stu Dietz
dietzs at MIT.EDU
Thu Feb 2 16:45:49 EST 2006
Hello,
This is a reminder about the Spring Advanced Undergraduate Seminars
in Biology. Descriptions of the courses are included below.
There will be an informational session on the seminars on
Registration Day (Monday Feb. 6th) from 9am-4pm in the Bldg. 68 lobby
just outside the Biology Education Office, 68-120. Refreshments will
be provided.
--
December 12, 2005
TO: MIT students
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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