This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Qin, Z.
Right arrow Articles by Chang, Z.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Qin, Z.
Right arrow Articles by Chang, Z.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, July 2009, p. 3633-3643, Vol. 29, No. 13
0270-7306/09/$08.00+0     doi:10.1128/MCB.00362-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

ZNF536, a Novel Zinc Finger Protein Specifically Expressed in the Brain, Negatively Regulates Neuron Differentiation by Repressing Retinoic Acid-Induced Gene Transcription{triangledown}

Zhen Qin,1 Fangli Ren,1 Xialian Xu,1 Yongming Ren,1 Hongge Li,2 Yinyin Wang,1 Yonggong Zhai,3 and Zhijie Chang1*

School of Medicine, Department of Biological Sciences and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing, China,1 Northwest Plateau Institute of Biology, Chinese Academy of Sciences, Xining, and Graduate University of Chinese Academy of Sciences, Beijing, China,2 College of Life Science, Beijing Normal University, Beijing, China3

Received 20 March 2009/ Accepted 20 April 2009

Neuronal differentiation is tightly regulated by a variety of factors. In a search for neuron-specific genes, we identified a highly conserved novel zinc finger protein, ZNF536. We observed that ZNF536 is most abundant in the brain and, in particular, is expressed in the developing central nervous system and dorsal root ganglia and localized in the cerebral cortex, hippocampus, and hypothalamic area. During neuronal differentiation of P19 cells induced by retinoic acid (RA), ZNF536 expression is increased at an early stage, and it is maintained at a constant level in later stages. Overexpression of ZNF536 results in an inhibition of RA-induced neuronal differentiation, while depletion or mutation of the ZNF536 gene results in an enhancement of differentiation. We further demonstrated that ZNF536 inhibits expression of neuron-specific marker genes, possibly through the inhibition of RA response element-mediated transcriptional activity, as overexpression of RA receptor {alpha} can rescue the inhibitory role of ZNF536 in neuronal differentiation and neuron-specific gene expression. Our studies have identified a novel zinc finger protein that negatively regulates neuron differentiation.


* Corresponding author. Mailing address: School of Medicine, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing (100084), China. Phone: (86-10) 62785076. Fax: (86-10) 62773624. E-mail: zhijiec{at}tsinghua.edu.cn

{triangledown} Published ahead of print on 27 April 2009.


Molecular and Cellular Biology, July 2009, p. 3633-3643, Vol. 29, No. 13
0270-7306/09/$08.00+0     doi:10.1128/MCB.00362-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.