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J. Biol. Chem., Vol. 279, Issue 43, 45130-45138, October 22, 2004

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A Tissue-specific, Naturally Occurring Human SNF2L Variant Inactivates Chromatin Remodeling^*

Orr Barak, Maribeth A. Lazzaro¶||, Neil S. Cooch, David J. Picketts¶**, and Ramin Shiekhattar, Supported by National Institutes of Health Grant GM61204 and the American Cancer Society

From the The Wistar Institute, Philadelphia, Pennsylvania 19104, the ^¶Ottawa Health Research Institute, Ottawa, Ontario K1H 8L6, Canada, and the ^**University of Ottawa, Centre for Neuromuscular Disease and Departments of Medicine, Biochemistry, Microbiology, and Immunology, Ottawa, Ontario K1H 8M5, Canada

Mammalian genomes encode two imitation switch family chromatin remodeling proteins, SNF2H and SNF2L. In the mouse, SNF2H is expressed ubiquitously, whereas SNF2L expression is limited to the brain and gonadal tissue. This pattern of SNF2L expression suggests a critical role for SNF2L in neuronal physiology. Indeed, SNF2L was shown to promote neurite outgrowth as well as regulate the human engrailed homeotic genes, important regulators of brain development. Here we identify a novel splice variant of human SNF2L we call SNF2L+13, which contains a nonconserved in-frame exon within the conserved catalytic core domain of SNF2L. SNF2L+13 retains the ability to incorporate into multiprotein complexes; however, it is devoid of enzymatic activity. Most interestingly, unlike mouse SNF2L, human SNF2L is expressed ubiquitously, and regulation is mediated by isoform variation. The human SNF2L+13 null variant is predominant in non-neuronal tissue, whereas the human wild type active SNF2L isoform is expressed in neurons. Thus, like the mouse, active human SNF2L is limited to neurons and a few other tissues.

Received for publication, June 3, 2004 , and in revised form, August 11, 2004.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Supported by National Institutes of Health Grant CA09171-28.

^|| Supported by the Ontario Mental Health Foundation. Present address: Health Canada, Therapeutic Products Directorate, Bureau of Cardiology, Allergy, and Neurological Sciences, Tunney's Pasteur, Ottawa, Ontario K1A 1B9, Canada.

Canadian Institutes of Health Research New Investigator and supported by Canadian Institutes of Health Research Grant MOP53224

To whom correspondence should be addressed: The Wistar Institute, 3601 Spruce St., Philadelphia, PA 19104. Tel.: 215-898-3896; Fax: 215-898-3986; E-mail: shiekhattar{at}wistar.upenn.edu.

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