Skip to main content

Induction of dystrophin Dp71 expression during neuronal differentiation: Opposite roles of Sp1 and AP2α in Dp71 promoter activity

16Citations
Citations of this article
30Readers
Mendeley users who have this article in their library.

This artice is free to access.

Abstract

In this study, we delineated the molecular mechanisms that modulate Dp71 expression during neuronal differentiation, using the N1E-115 cell line. We demonstrated that Dp71 expression is up-regulated in response to cAMP-mediated neuronal differentiation of these cells, and that this induction is controlled at promoter level. Functional deletion analysis of the Dp71 promoter revealed that a 5′-flanking 159-bp DNA fragment that contains Sp1 and AP2α binding sites is necessary and sufficient for basal expression of this TATA-less promoter, as well as for its induction during neuronal differentiation. Electrophoretic mobility shift and chromatin immunoprecipitation assays revealed that Sp1 and AP2α bind to their respective DNA elements within the Dp71 basal promoter. Overall, mutagenesis assays on the Sp1 and AP2α binding sites, over-expression of Sp1 and AP2α, as well as knock-down experiments on Sp1 and AP2α gene expression established that Dp71 basal expression is controlled by the combined action of Sp1 and AP2α, which act as activator and repressor, respectively. Furthermore, we demonstrated that induction of Dp71 expression in differentiated cells is the result of the maintenance of positive regulation exerted by Sp1, as well as of the loss of AP2α binding, which ultimately releases the promoter from repression. © 2009 International Society for Neurochemistry.

Cite

CITATION STYLE

APA

Morales-Lázaro, S. L., González-Ramírez, R., Gómez, P., Tapia-Ramírez, V., De León, M. B., & Cisneros, B. (2010). Induction of dystrophin Dp71 expression during neuronal differentiation: Opposite roles of Sp1 and AP2α in Dp71 promoter activity. Journal of Neurochemistry, 112(2), 474–485. https://doi.org/10.1111/j.1471-4159.2009.06467.x

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free