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Updated: Jul 12, 2026
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Quantitative Analysis of Alternative Pre-mRNA Splicing in Mouse Brain Sections Using RNA In Situ Hybridization Assay
Published on: August 26, 2018
Expression pattern and splicing function of mouse ZNF265
Jing Li1, Xian-hua Chen, Ping-jie Xiao
1State Key Laboratory of Medical Neurobiology and Laboratory of Genomic Physiology, Brain Research Center, Fudan University, Shanghai 200032, PR China.
Neurochemical Research
|September 7, 2007
Summary
Zinc finger protein 265 (ZNF265) isoforms regulate pre-mRNA splicing. ZNF265-1, a major isoform, influences neuronal function and spinal muscular atrophy (SMA) pathogenesis by affecting specific exon usage.
Area of Science:
- Molecular Biology
- Genetics
- Neuroscience
Background:
- Zinc finger protein 265 (ZNF265) is a newly identified arginine/serine-rich (SR) protein.
- ZNF265 exists in two transcript isoforms, ZNF265-1 and ZNF265-2, which autoregulate each other.
- Previous research indicated ZNF265's role in regulating Tra2 beta isoform splicing.
Purpose of the Study:
- To investigate the expression patterns and functional roles of ZNF265 transcript isoforms in mouse tissues.
- To determine the subcellular localization of ZNF265 isoforms.
- To elucidate the impact of ZNF265 isoforms on pre-mRNA splicing of specific genes.
Main Methods:
- Analysis of ZNF265 isoform expression across various mouse tissues.
- Expression and purification of recombinant ZNF265 proteins for localization studies.
- Pre-mRNA splicing assays using GluR-B and SMN2 minigenes to assess ZNF265-mediated splicing regulation.
Main Results:
- Both ZNF265-1 and ZNF265-2 isoforms are expressed in multiple mouse tissues, with ZNF265-1 being predominant.
- ZNF265-1 protein levels are notably lower in the cerebral cortex compared to other tissues.
- Recombinant ZNF265 proteins localize to the nucleus, consistent with splicing regulatory functions.
- ZNF265-1 was shown to inhibit Flop exon usage in GluR-B splicing and exon 7 usage in SMN2 splicing.
Conclusions:
- The two ZNF265 transcript isoforms are widely expressed in mouse tissues, with ZNF265-1 being the major form.
- ZNF265-1 exhibits nuclear localization and functions as a pre-mRNA splicing regulator.
- ZNF265-1's regulation of GluR-B and SMN2 splicing suggests its potential involvement in neuronal function and spinal muscular atrophy (SMA) pathogenesis.
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