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A filtering strategy identifies FOXQ1 as a potential effector of lamin A dysfunction
Jose Candelario1, Leng-Ying Chen, Paul Marjoram
1Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, CA 90033, USA.
Aging
|September 6, 2012
Summary
Elevated prelamin A or progerin causes progeroid phenotypes through shared molecular pathways. Researchers identified the transcription factor FOXQ1 as a key player in this cell dysfunction.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- Progeria is linked to the mutant lamin A protein, progerin.
- Elevated wild-type prelamin A also causes progeroid phenotypes, suggesting shared molecular mechanisms with progerin.
Purpose of the Study:
- To investigate the molecular effectors responsible for progeroid phenotypes caused by elevated prelamin A or progerin.
- To identify genes involved in the onset of reduced cell growth and nuclear morphology defects.
Main Methods:
- Comparative transcriptome analysis of fibroblasts expressing progerin or elevated wild-type prelamin A.
- Phenotypic rescue by farnesyltransferase inhibitor (FTI) or ZMPSTE24 overexpression was used as a filtering strategy.
- Overexpression of candidate genes in normal fibroblasts to assess phenotype induction.
Main Results:
- Transcriptome analysis revealed FOXQ1 gene induction in both progerin- and elevated wild-type prelamin A-expressing cells.
- FOXQ1 expression decreased upon conditions that ameliorated the progeroid phenotypes.
- Overexpression of FOXQ1 in normal fibroblasts induced reduced cell growth and nuclear abnormalities.
Conclusions:
- FOXQ1 is identified as a gene linked to the onset of progeroid phenotypes.
- Findings suggest a role for FOXQ1 in cell dysfunction associated with altered prelamin A metabolism.
