Switch-like genes populate cell communication pathways and are enriched for extracellular proteins
1Center for Integrated Bioinformatics, School of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, USA. ame28@drexel.edu
BMC Genomics
|January 8, 2008
Summary
This study identified bimodal (switch-like) genes in mouse gene expression data, finding 17% of genes exhibit this pattern. These bimodal genes are linked to cell signaling, extracellular matrix interactions, and various diseases, including diabetes.
Area of Science:
- Genomics
- Molecular Biology
- Bioinformatics
Background:
- Gene expression can follow housekeeping, graded, or bimodal (switch-like) profiles.
- Bimodal expression is observed in healthy cell signaling and diseases like cancer.
- Identifying bimodal genes is challenging due to noise in human microarray data.
Purpose of the Study:
- To detect and annotate switch-like genes in mouse gene expression data.
- To analyze the roles of bimodal genes in cell signaling and disease progression.
- To develop a comprehensive list of bimodal genes in the mouse genome.
Main Methods:
- Utilized two-component mixture analysis on mouse gene expression data (Affymetrix MG-U74Av2 array).
- Fit two-component normal mixtures to identify genes with bimodal expression patterns.
- Annotated identified bimodal genes and analyzed associated pathways and diseases.
Main Results:
- Identified 17% (1519/9091) of genes on the array as bimodal or switch-like.
- Enriched KEGG pathways included ECM-receptor interaction, cell communication, and focal adhesion.
- Bimodal genes were associated with diseases like diabetes, Alzheimer's, and hypertension, with hundreds showing altered expression in diabetic tissues.
Conclusions:
- Successfully identified and annotated bimodal genes in the mouse genome using microarray data.
- Bimodal genes are enriched in the cell membrane and extracellular environment.
- Bimodal genes represent potential biomarkers for numerous diseases due to tight transcriptional regulation.
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