Position title: Professor
Medical Genetics and Neurology
cAMP/PKA/dCREB2 signaling in sleep, memory formation, neurodegenerative diseases, developmental disabilities
- 3434 Genetics/Biotech
- Ph.D., University of Wisconsin-Madison (1986), Postdoctoral Research: MIT, 1988-93 Cold Spring Harbor Laboratory, 1993-95
- Genetics and Neurology
- Research Interests
- We study how the cAMP/PKA/dCREB2 signaling pathway is involved in neuronal function (sleep and memory formation) and dysfunction (neurodegenerative diseases and developmental disabilities).
- Research Fields
- Disease Biology, Cell Biology, Gene Expression, Neuro & Behavioral Genetics, Drosophila
Our goal is to understand nervous system function during complex behavior at the molecular level. There are three broad areas of interest:
Animals can be trained in behavioral tasks, and the resulting memory can be divided into various phases based on pharmacological, genetic and behavioral criteria. We are interested in a cellular and molecular description of what signaling events distinguish the different phases of memory. Of special interest are the molecular events that distinguish memory after repetitive massed training from memory after repetitive spaced training.
In all animals, the longest lasting phase of memory, long-term memory, requires acute gene expression around the time of training. This requirement for transcription and translation raises the issue of synaptic specificity: how does the neuron only strengthen the recently active synapse, when transcription and translation are activated? The solution to this cell biological dilemma will require the coordinated use of genetics, cell biology, molecular biology, imaging, biochemistry and behavior. This problem has also led us to an interest in the molecular basis of psychiatric dysfunctions that have attention-based components to the disease.
How can memories persist for periods of time much longer than the half-lives of most proteins and protein structures? If “use it or lose it” applies to the persistence of memory, as it seemingly does to synaptic plasticity, how and when do neurons “re-play” experiences? A third goal is to understand the basis for memory persistence that might involve other complex neuronal processes like sleep and circadian rhythms.
Our basic approach involves transgenic manipulation of genes followed by behavioral, cellular and molecular analyses.
Search PubMed for more publications by Jerry Yin
Horiuchi, J., Jiang, W., Zhou, H., Wu, P., and Yin, J. C. P. 2004. Phosphorylation of conserved casein kinase sites regulates cAMP-response element-binding protein DNA binding in Drosophila. J. Biol. Chem. 279:12117-12125.
Drier, E. A., Cowan, M., Tello, M. K., Wu, P., Blace, N., Sacktor, T. C. and Yin, J. C. P. 2002. Memory formation and enhancement by atypical PKM activity in Drosophila melano-gaster. Nat. Neurosci 5:316-324.
Stebbins, M. J., Urlinger, S., Byrne, G., Bello, B., Hillen, W. and Yin, J. C. P. 2001. Tetra-cycline-inducible systems for Drosophila PNAS 98:10775-10780.
Belvin, M. P., Zhou, H. and Yin, J. C. P. 1999. The Drosophila dCREB2 gene encodes a component of the circadian clock. Neuron 22:777-787.
Yin, J. C. P., Del Vecchio, M., Zhou, H. and Tully, T. 1995. CREB as a memory modulator: induced expression of a dCREB2 activator isoform enhances long-term memory in Drosophila. Cell 81:107-115.