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Sci. Signal., 11 August 2009
Vol. 2, Issue 83, p. ra42
[DOI: 10.1126/scisignal.2000224]

RESEARCH ARTICLES

Neuronal and Intestinal Protein Kinase D Isoforms Mediate Na+ (Salt Taste)–Induced Learning

Ya Fu1, Min Ren1*, Hui Feng1{dagger}, Lu Chen1, Zeynep F. Altun2, and Charles S. Rubin1{ddagger}

1 Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
2 Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

* Present address: Ben-May Department for Cancer Research, University of Chicago, Chicago, IL 60637, USA.

{dagger} Present address: Humanzyme Inc., 2201 West Campbell Park Drive STE24, Chicago, IL 60612, USA.

Abstract: Ubiquitously expressed protein kinase D (PKD) isoforms are poised to disseminate signals carried by diacylglycerol (DAG). However, the in vivo regulation and functions of PKDs are poorly understood. We show that the Caenorhabditis elegans gene, dkf-2, encodes not just DKF-2A, but also a second previously unknown isoform, DKF-2B. Whereas DKF-2A is present mainly in intestine, we show that DKF-2B is found in neurons. Characterization of dkf-2 null mutants and transgenic animals expressing DKF-2B, DKF-2A, or both isoforms revealed that PKDs couple DAG signals to regulation of sodium ion (Na+)–induced learning. EGL-8 (a phospholipase Cβ4 homolog) and TPA-1 (a protein kinase C{delta} homolog) are upstream regulators of DKF-2 isoforms in vivo. Thus, pathways containing EGL-8–TPA-1–DKF-2 enable learning and behavioral plasticity by receiving, transmitting, and cooperatively integrating environmental signals targeted to both neurons and intestine.

{ddagger} To whom correspondence should be addressed. E-mail: rubin{at}aecom.yu.edu

Citation: Y. Fu, M. Ren, H. Feng, L. Chen, Z. F. Altun, C. S. Rubin, Neuronal and Intestinal Protein Kinase D Isoforms Mediate Na+ (Salt Taste)–Induced Learning. Sci. Signal. 2, ra42 (2009).

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