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The Journal of Neuroscience, April 18, 2007, 27(16):4396-4402; doi:10.1523/JNEUROSCI.4054-06.2007

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Behavioral/Systems/Cognitive
Receptor-Like Tyrosine Phosphatase PTP10D Is Required for Long-Term Memory in Drosophila

Meng Qian,^1 * Guohui Pan,^1 * Lu Sun,¹ Chunhua Feng,³ Zuoping Xie,¹ Tim Tully,² and Yi Zhong^1,2

¹Department of Biological Science and Biotechnology, Tsinghua University, Beijing, China 100084, ²Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, 11724, and ³JoeKai Inc., Beijing, China 100084

Correspondence should be addressed to Yi Zhong, Cold Spring Harbor Laboratory, P.O. Box 100, Cold Spring Harbor, NY 11724. Email: zhongyi{at}cshl.edu

Tyrosine phosphorylation mediates multiple signal transduction pathways that play key roles in developmental processes and behavioral plasticity. The level of tyrosine phosphorylation is regulated by protein tyrosine kinases and protein tyrosine phosphatases (PTPs). Extensive studies have investigated the roles of tyrosine kinases in memory formation. However, there were few studies on PTPs. To date, learning has been shown to be defective only for mouse knock-outs of PTP, leukocyte common antigen-related, or PTP. A major limitation of these studies arises from their inability to distinguish an acute (biochemical) impairment of memory formation from a more chronic abnormality in neurodevelopment. From a behavioral screen for defective long-term memory, we found chi mutants to disrupt expression of the PTP10D protein tyrosine phosphatase gene. We show that chi mutants are normal for learning, early memory, and anesthesia-resistant memory, whereas long-term memory specifically is abolished. Significantly, induction of a heat shock-PTP10D⁺ transgene before training fully rescues the memory defect of chi mutants, thereby demonstrating an acute role for PTP10D in behavioral plasticity. We show that PTP10D is widely expressed in the embryonic CNS and in the adult brain. Transgenic expression of upstream activating sequence-PTP10D⁺ in mushroom bodies is sufficient to rescue the memory defect of chi mutants. Our data clearly demonstrate that signaling through PTP10D in mushroom bodies is critical for the formation of long-term memory.

Key words: PTP10D; long-term memory; mushroom bodies; chi; behavior; screen

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Received Sept. 16, 2006; revised Feb. 13, 2007; accepted Feb. 16, 2007.

Correspondence should be addressed to Yi Zhong, Cold Spring Harbor Laboratory, P.O. Box 100, Cold Spring Harbor, NY 11724. Email: zhongyi{at}cshl.edu

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