Andreas Hochwagen
Cell division is a tricky process, one that’s
driven by some heavy back-end calculus. If anything
goes wrong in the equation, the resulting daughter cells
can be plagued by genetic mistakes that lead to birth
defects or cancer. Fortunately, our cells have installed
surveillance mechanisms that guard against this. Whitehead
Fellow Andreas Hochwagen is determined to discover exactly
how our cells guide this essential biological process.
Selected Achievements
• Discovered that a widely used immunosuppressant
drug interferes with cell division
• Named Lester Wolfe Fellow at MIT (2001-2004)
• Diploma Thesis Award, Austrian Chemical
Society (2001)
• Boehringer Ingelheim Fund Doctoral Fellowship
Award (2000)
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With the exception of egg and sperm cells, all cells
in our body contain two sets of chromosomes, one from
our father and one from our mother. Egg and sperm cells,
however, contain only one copy of each chromosome. Only
a small population of cells in our body, called germ
cells, can produce egg and sperm cells, through meiosis.
This process requires many additional steps, which in
turn increases the likelihood of error.
Luckily, our cells constantly monitor the integrity
of DNA. If mistakes are found, the cells repair these
mistakes prior to further division. These mechanisms
are called “checkpoints.”
Early in Hochwagen’s graduate work, he decided
that yeast would be the perfect testbed for understanding
how these checkpoints work. While yeast cells are not
in the business of creating sperm and eggs, they still
undergo meiosis when they reproduce.
Hochwagen discovered that a widely used immunosuppressant
drug called rapamycin may be interfering with a cell’s
ability to correct genetic mistakes during meiosis,
a finding that’s particularly alarming since patients
who take this drug often take it for life.
At Whitehead, Hochwagen continues to delve into the
deeper question of how cells repair genetic damage,
something for which yeast continues to provide us with
essential insights.
Hochwagen received his PhD in 2006 from MIT, in the
lab of former Whitehead Fellow and Howard Hughes Medical
Institute Investigator Angelika Amon. In 2000 he received
the Boehringer Ingelheim Fund Doctoral Fellowship Award,
and in 2001 the Diploma Thesis Award from the Austrian
Chemical Society.
Selected Publications
Hochwagen A., Amon A. (2006). Checking Your Breaks:
Surveillance Mechanisms of Meiotic Recombination. Curr
Biology 16 (6), R217-28.
Hochwagen A., Tham W.-H., Brar G.A., Amon A. (2005).
The FK506-binding protein Fpr3 counteracts protein phosphatase
1 to maintain meiotic recombination checkpoint activity.
Cell 122 (6): 861-73.
Hochwagen A., Wrobel G., Cartron M., Demougin P., Niederhauser-Wiederkehr
C., Boselli M., Primig M., Amon A. (2005). A novel response
to microtubule perturbation in meiosis. Mol Cell
Biol, 25 (11): 4767-81.
Haering C.H., Lowe J., Hochwagen A., Nasmyth K. (2002).
Molecular architecture of SMC proteins and the yeast
cohesin complex. Mol Cell, 9 (4): 773-88.
Panizza S., Tanaka T., Hochwagen A., Eisenhaber F.,
Nasmyth K. (2000). Pds5 Cooperates with Cohesin in Maintaining
Sister Chromatid Cohesion. Curr Biology,10
(24): 1557-64.
[lab]
[publications
(pubmed database)] |