Angelika Amon

Angelika Amon, Ph.D. (b. 1967) is an Austrian American molecular and cell biologist and professor at the Massachusetts Institute of Technology (MIT) in Cambridge, Massachusetts, United States. Amon's research centers on how chromosomes are regulated, duplicated, and partitioned in the cell cycle.^[1]

Background

Amon had an early interest in plant and animal biology as a child, keeping a notebook full of newspaper clippings, and was motivated to study biology after learning about Mendelian genetics in middle school.^[2] She received her B.S. from the University of Vienna and continued her doctoral work there under Professor Kim Nasmyth at the Research Institute of Molecular Pathology, receiving a Ph.D. in 1993. She completed a two-year post-doctoral fellowship at the Whitehead Institute in Cambridge, Massachusetts and was subsequently named a Whitehead Fellow for three years.^[2] She joined the MIT Center for Cancer Research and MIT's Department of Biology in 1999 and was promoted to full professor in 2007.^[3][4]

Amon won a Presidential Early Career Award for Scientists and Engineers in 1998,^[5] was named an associate investigator at the Howard Hughes Medical Institute in 2000,^[6] and was the 2003 recipient of the National Science Foundation's Alan T. Waterman Award.^[7][8] Amon also shared the 2007 Paul Marks Prize for Cancer Research and won the 2008 National Academy of Sciences Award in Molecular Biology.^[9][10][11]

Amon is married and has two daughters.^[2]

Research

Amon's research has investigated how cells control and organize the segregation of their chromosomes during cell division. More specifically, her research examines the regulation of exit from mitosis, the regulation of the meiotic cell cycle, and effects of aneuploidy on normal physiology and tumorigenesis.^[1]

As a student under Nasmyth, Amon demonstrated that CDC28 protein kinase is not required for the metaphase to anaphase transition and CLB2 proteolysis continues until reactivation of CDC28 toward the end of G1.^[12][13]

The Amon lab primarily investigates yeast (Saccharomyces cerevisiae) as a model for understanding the controls that govern cell-cycle progression.^[7] As a Whitehead Fellow, her team discovered that CDC20 plays a crucial role in cell division.^[14] Her Whitehead team identified an interaction between phosphatase and CDC14 which initiates the exit of cells from mitosis to the G1 phase.^[15] Amon's team demonstrated that CDC20 is the target protein in the spindle checkpoint during mitosis.^[16]

Amon's more recent work has investigated the regulation of chromosome segregation and how chromosomes are accurately transmitted to gametes in meiosis by examining gene regulatory networks. She identified two regulatory networks (FEAR and MEN) that promote the release of CDC14 which have the potential to identify the mechanisms that control the final stages of the mitotic cell cycle.^{[17][18][19][20]}

Her research group recently created haploid yeast cells containing extra copies of chromosomes and discovered that these aneuploid strains elicit phenotypes independent of the identity of the additional chromosome such as defects in cell cycle progression, increased energy demands, and interference with protein biosynthesis.^[21] Amon has also examined trisomy in the mouse as a model of mammalian cell growth and physiology and demonstrated that mammalian aneuploidy results in a stress response analogous to yeast aneuploidy.^[22] Amon's aneuploidy research has potential applications to cancer research.^[23]

References

External links

• MIT Department of Biology homepage
• Amon Lab homepage
• Koch Institute homepage
• Howard Hughes Medical Institute homepage
• Angelika Amon seminar: Consequences of Aneuploidy