Journal article
Targeted deletion of the antisilencer/enhancer element from intron 1 of the myelin proteolipid protein gene in mouse reveals that the element is dispensable for Plp1 expression in brain during development and remyelination
Journal of neurochemistry, Vol.124(4), pp.454-465
02/01/2013
DOI: 10.1111/jnc.12092
PMCID: PMC3557533
PMID: 23157328
Abstract
Myelin proteolipid protein gene (Plp1) expression is temporally regulated in brain, which peaks during the active myelination period of CNS development. Previous studies with Plp1-lacZ transgenic mice demonstrated that (mouse) Plp1 intron 1 DNA is required for high levels of expression in oligodendrocytes. Deletion-transfection analysis revealed the intron contains a single positive regulatory element operative in the N20.1 oligodendroglial cell line, which was named ASE (antisilencer/enhancer) based on its functional properties in these cells. To investigate the role of the ASE in vivo, the element was deleted from the native gene in mouse using a Cre/lox strategy. Although removal of the ASE from Plp1-lacZ constructs profoundly decreased expression in transfected oligodendroglial cell lines (N20.1 and Oli-neu), the element was dispensable to achieve normal levels of Plp1 gene expression in mouse during development (except perhaps at postnatal day 15) and throughout the remyelination period following cuprizone-induced (acute) demyelination. Thus, it is possible that the ASE is non-functional in vivo, or that loss of the ASE from the native gene in mouse can be compensated for by the presence of other regulatory elements within the Plp1 gene.
Details
- Title: Subtitle
- Targeted deletion of the antisilencer/enhancer element from intron 1 of the myelin proteolipid protein gene in mouse reveals that the element is dispensable for Plp1 expression in brain during development and remyelination
- Creators
- Glauber B. PereiraFanxue MengNeriman T. KockaraBaoli Yang - University of IowaPatricia A. Wight
- Resource Type
- Journal article
- Publication Details
- Journal of neurochemistry, Vol.124(4), pp.454-465
- DOI
- 10.1111/jnc.12092
- PMID
- 23157328
- PMCID
- PMC3557533
- NLM abbreviation
- J Neurochem
- ISSN
- 0022-3042
- eISSN
- 1471-4159
- Publisher
- Wiley Subscription Services, Inc
- Grant note
- DOI: 10.13039/100000890, name: National Multiple Sclerosis Society, award: RG 2705; name: NIH, award: R01NS037821, P30NS047546, UL1TR000039; name: UAMS College of Medicine Research Council
- Language
- English
- Date published
- 02/01/2013
- Description audience
- Academic
- Academic Unit
- BioVentures Center; Obstetrics and Gynecology
- Record Identifier
- 9983557405002771
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