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J. Biol. Chem., Vol. 281, Issue 47, 35863-35872, November 24, 2006

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Differential Transcriptional Control of the Superoxide Dismutase-2 B Element in Neurons and Astrocytes^*

Xianrong Mao, Andréa M. Moerman-Herzog, Wei Wang, and Steven W. Barger^¶1

From the Departments of Geriatrics and Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 and the ^¶Geriatric Research Education and Clinical Center, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205

In addition to their conventional G-C/T target sequences, Sp1 family transcription factors (Sp-factors) can interact with a subset of the target sequences for NFB. Due to the low level of bona fide NFB activity in most resting cells, this interaction between Sp-factors and B-sites could play important roles in cell function. Here we used mutagenesis of a canonical B element from the immunoglobulin and HIV promoters to identify the GC-rich sequences at each end required for Sp-factor targeting. Through screening of multiple B elements, a sequence element located in the second intron of superoxide dismutase-2 (SOD2) was identified as a good candidate for both NFB and Sp-factor binding. In neurons, the prominent proteins interacting with this site were Sp3 and Sp4, whereas Sp1, Sp3, and NFB were associated with this site in astroglia. The neuronal Sp-factors repressed transcriptional activity through this B-site. In contrast, astroglial Sp-factors activated promoter activity through the same element. NFB contributed to control of the SOD2 B element only in astrocytes. These findings imply that cell-type specificity of transcription in the central nervous system, particularly with regard to B elements, may include two unique aspects of neurons: 1) a recalcitrant NFB and 2) the substitution of Sp4 for Sp1.

Received for publication, May 2, 2006 , and in revised form, September 22, 2006.

^* This work was supported by NINDS, National Institutes of Health Grant R01NS046439. 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.

¹ To whom correspondence should be addressed: Reynolds Institute on Aging, 629 Jack Stephens Dr., #807, Little Rock, AR 72205. Tel.: 501-526-5811; Fax: 501-526-5830; E-mail: bargerstevenw{at}uams.edu.

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