Heidi A Tissenbaum PhD
|Institution||University of Massachusetts Medical School|
|Department||Molecular, Cell and Cancer Biology|
|Address||University of Massachusetts Medical School|
364 Plantation Street, LRB-621
Worcester MA 01605
|Institution||UMMS - School of Medicine|
|Department||Program in Molecular Medicine|
Heidi Tissenbaum received her B.S. in Biology from Concordia University in Montreal, Quebec, Canada and an M.S. degree in Physiology from the University of Ottawa, in Ontario, Canada. In 1997, she graduated with a Ph.D. in Genetics from Harvard Medical School. From 1997 to 2001, she was a post-doc at MIT where she was supported by the Helen Hay Whitney Foundation. In 2001, Dr. Tissenbaum joined the Program in Gene Function and Expression at the University of Massachusetts Medical School, and also received a Career Award in the Biomedical Sciences from the Burroughs Wellcome Fund. Dr. Tissenbaum has received funding from the American Federation of Aging Research, the Worcester Foundation for Biomedical Research, the Concern Foundation, and the National Institute of Aging. Dr. Tissenbaum is also a William Randolph Hearst Young Investigator.
Dissecting Molecular Mechanisms of the Aging Process
What determines how we age? What defines how long we will live? Is this a clock that is set from birth? How can we tinker with this clock? These are the questions we seek to address in the lab. The ultimate goal of our work is to increase the healthy. reproductive years of individuals; redefining and prolonging healthy middle age.
We use the nematode C. elegans as our system to study the aging process. Worms have a short, reproducible life span and provide an excellent system for these studies. Similar to mammals, worms have many signaling ptahways that modulate lifespan, metabolism, stress and development. Using this simple system, we can begin to dissect the complex networks that regulate these processes.
- In C. elegans, the insulin/IGF-1 signaling pathway plays a central role in regulating lifespan, fat storage, stress and development. What are all the genes involved? How is each specific phenotype modulated? Are they modulated together?
- How do multiple conserved signaling pathways couple to the insulin/IGF-1 pathway to regulate lifespan? Fat storage? Stress? Development?
- How does the forkhead transcription factor DAF-16 function as a central mediator in C. elegans?
Potential Rotation Projects
Project #1: Genetic screen to identify genes that act in the sir-2.1 pathway that regulates aging.
Project #2: Identify new genes that affect aging by gene dosage.
Project #3: Create mutations in the C. elegans homologs of genes known to regulate insulin signaling in humans and determine their affects on life span.
Overall questions of the lab:
- Are the general mechanisms of life span conserved? How?
- How can we control the genes that affect life span?
- Is aging the sums of many processes or are there specific signaling pathways for aging?
- How does life span regulation relate to insulin signaling?
Gene Function and Expression, Interdisciplinary Graduate Program
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