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Published on: October 27, 2017
Expression changes in Fasl-deficient calvaria-derived osteoblasts: an RNA-seq analysis
Adela Kratochvilova1, Martina Zapletalova2, Reinhard Gruber3
1Institute of Animal Physiology and Genetics, Czech Academy of Sciences, Brno, Czech Republic. adela.kratochvilova@iapg.cas.cz.
Abstract:
Fasl-deficient (gld) mice display an altered bone phenotype, but the underlying molecular mechanisms remain incompletely understood. Here we evaluated the role of FASL in the gene expression profile of osteogenic cells. To this aim, RNA sequencing was performed on calvaria-derived primary cells from wild-type and Fasl-deficient mice that underwent osteogenic differentiation. The outcome dataset (GSE250608) contains gene expression profiles and enrichment analyses. Based on a log2 fold change >1 and adjusted p-value < 0.01, the lack of Fasl revealed 480 up- and 301 down-regulated genes. These signature changes were annotated to extracellular matrix-related pathways and chemokine signalling. This resource provides a publicly available transcriptomic dataset that can be used to better understand the complex role of FASL in bone biology.
Insights
The absence of FasL significantly alters gene expression in bone cells, impacting extracellular matrix and chemokine pathways. This study provides crucial transcriptomic data for understanding FasL
Area of Science:
- Molecular Biology
- Genomics
- Bone Biology
Background:
- FasL deficiency in mice (gld) is linked to bone abnormalities.
- The molecular basis for FasL's role in bone biology is not fully understood.
Purpose of the Study:
- To investigate the role of FasL in the gene expression profile of osteogenic cells.
- To identify molecular mechanisms underlying bone phenotype alterations in FasL-deficient mice.
Main Methods:
- RNA sequencing of primary calvaria-derived cells from wild-type and Fasl-deficient (gld) mice.
- Analysis of gene expression profiles during osteogenic differentiation.
- Enrichment analysis of differentially expressed genes.
Main Results:
- The absence of FasL resulted in 480 upregulated and 301 downregulated genes.
- Key affected pathways include extracellular matrix organization and chemokine signaling.
- A publicly available transcriptomic dataset (GSE250608) was generated.
Conclusions:
- FasL plays a significant role in regulating gene expression within osteogenic cells.
- Transcriptomic changes associated with FasL deficiency provide insights into bone biology.
- This dataset serves as a valuable resource for future research on FasL and bone health.
