- NIH Outstanding Investigator R35 Award 2016
- Glenn Award for Research in the Biological Mechanisms of Aging 2015
- Member of the American Academy of Arts and Sciences, since 2014
- Member of the National Academy of Medicine, since 2012
- Member of the National Academy of Sciences, since 2012
- Member of the American Association for the Advancement of Science, since 2012
- Ellison Medical Foundation Senior Scholar Award in Aging Research 2009
- NIH EUREKA 2009
- David and Lucile Packard Fellowship for Science and Engineering 1997
- Basil O'Connor Award, March of Dimes 1996
- John Merck Scholars Award in the Biology of Developmental Disabilities in Children 1995
- Postdoc, Caltech, Neurogenetics, 1988-1994
- Ph.D., University of Wisconsin-Madison, Neuroscience, 1987
- A.B., Princeton University, Biology, 1981
Genetic Modulation of Neurodegenerative and Neurological Disease
The laboratory focuses on using Drosophila melanogaster to a tool to define genes important for human brain disease. For example, a class of human neurodegenerative diseases involves expansion of polyglutamine repeat domain within the disease proteins. This polyglutamine expansion results in a dominant, toxic property of the disease protein, leading to neural degeneration. Huntington's disease is of this class. We recreated this class of human neurodegenerative disease in Drosophila by expressing one of these human disease proteins with the mutant expanded polyglutamine domain. Whereas expression of the protein with a normal polyglutamine repeat had no effect, expression of the protein with an expanded polyglutamine repeat resulted in late onset, progressive degeneration in the nervous system—remarkably mimicking the human disease. Our laboratory has continued to launch from Drosophila in order to define genes involved in mechanisms and progression of degenerative disease, identify modifier mutations that can prevent or delay brain degeneration, and extending these studies to additional diseases of dementia and motor neuron diseases. We are also expanding into neural injury and aging risk factors, to assess how these environmental components feed into disease. These studies provide the launching ground to extend our findings to other systems such as mouse and human tissue, to provide biological insight into pathways and provide the foundation for new treatments. We are always open to new ideas and applications, whereby application of a powerful and simple genetic system can launch vast new biological and molecular understanding of how the brain functions and is maintained.
BIOL 221: Molecular Biology & Genetics
BIOL 466: Molecular Genetics of Neurological Diseases
Nativio R, Donahue G, Berson A, Lan Y, Amlie-Wolf A, Tuzer F, Toledo JB, Gosai SJ, Gregory BD, Torres C, Trojanowski JQ, Wang LS, Johnson FB, Bonini NM, Berger SL. (2018) Dysregulation of the epigenetic landscape of normal aging in Alzheimer’s disease. Nat Neurosci doi: 10.1038/a41593-018-0101-9. PMID 29507413
Fang Y, Soares L, Teng X, Geary M and Bonini NM (2012) A novel Drosophila model of nerve injury reveals an essential role of endogenous Nmnat in maintaining axon integrity. Curr Biol 22: 590-595. PMC3347919.
Liu N, Landreh M, Cao K, Abe M, Hendriks GJ, Kennerdell JR, Zhu Y, Wang LS, Bonini NM (2012) The microRNA miR-34 modulates ageing and neurodegeneration in Drosophila. Nature 482: 519-23. Doi 10.1038/nature 10810. PMC3326599.
Fang Y, Soares L, Teng X, Geary M and Bonini NM (2012) A novel Drosophila model of nerve injury reveals an essential role of endogenous Nmnat in maintaining axon integrity. Curr Biol 22: 590-595. PMC3347919.
Lessing, D. and Bonini, N.M. (2009) Maintaining the brain: Insight into human neurodegeneration from Drosophila mutants. Nature Rev Genet 10: 359-370.
Li LB, Yu Z, Teng X and Bonini NM (2008) RNA toxicity is a component of ataxin-3 degeneration in Drosophila. Nature, 453:1107-11. Epub 2008 Apr 30
Jung J and Bonini NM (2007) CREB-binding Protein Modulates Repeat Instability in a Drosophila Model for PolyQ Disease. Science 315: 1857-1859..
Auluck P.K., and Bonini N.M. 2002. Pharmacological prevention of Parkinson disease in Drosophila. Nat Med 8:1185-6.
Auluck P.K., Chan H.Y., Trojanowski J.Q., Lee V.M., and Bonini N.M. 2002. Chaperone suppression of alpha-synuclein toxicity in a Drosophila model for Parkinson's disease. Science 295:865-8.
Bonini N.M. 2002. Chaperoning brain degeneration. Proc Natl Acad Sci U S A 99 Suppl 4:16407-11.
Warrick J., Chan H.Y.E., Chai Y., Paulson H. and N.M. Bonini1999. Suppression of polyglutamine disease in Drosophila by the molecular chaperone hsp70. Nature Genetics 23:425-428.
Warrick J.M., Paulson H., Gray-Board G.L., Bui Q.T., Fischbeck K., Pittman R.N., and N.M. Bonini 1998. Expanded polyglutamine protein forms nuclear inclusions and causes neural degeneration in Drosophila. Cell 93: 939-949.
- Society for Neuroscience
- American Society for Cell Biology
- Genetics Society of America
- American Society for Biochemistry & Molecular Biology
- American Association for the Advancement of Science