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Updated: Jul 18, 2026
Cell Type-specific Gene Expression Profiling in the Mouse Liver
Published on: September 17, 2019
Delayed liver regeneration in mice lacking liver serum response factor
M Ujue Latasa1, Dominique Couton, Claude Charvet
1Institut Cochin, Genetics and Development Department, 24 Rue du Fbg St. Jacques, 75014 Paris, France.
Abstract:
Various immediate early genes (IEGs) upregulated during the early process of liver regeneration are transcriptional targets of the serum response factor (SRF). We show here that the expression of SRF is rapidly induced in rodent liver after partial hepatectomy. Because the inactivation of the SRF gene in mice is embryonic lethal, the in vivo role of SRF in liver regeneration after partial hepatectomy was analyzed in mutant mice conditionally deleted for SRF in the liver. We demonstrate that SRF is not an essential factor for liver ontogenesis. However, adult mutant mice show impaired liver regeneration after partial hepatectomy, associated with a blunted upregulation of various SRF target IEGs. In conclusion, our work suggests that SRF is an early response transcription factor that may contribute to the initial phases of liver regeneration through its activation of IEGs.
Insights
Serum response factor (SRF) is crucial for early liver regeneration. Conditional SRF deletion in adult mice impaired liver regrowth and blunted immediate early gene upregulation, highlighting SRF's role in initiating regeneration.
Area of Science:
- Molecular Biology
- Regenerative Medicine
- Hepatology
Background:
- Immediate early genes (IEGs) are upregulated during liver regeneration.
- These IEGs are transcriptional targets of the serum response factor (SRF).
- SRF expression is rapidly induced in the liver post-partial hepatectomy.
Purpose of the Study:
- To investigate the in vivo role of SRF in liver regeneration after partial hepatectomy.
- To analyze the necessity of SRF for liver ontogenesis.
- To understand the impact of SRF deficiency on the upregulation of its target IEGs during regeneration.
Main Methods:
- Utilized mutant mice with liver-specific conditional deletion of the SRF gene.
- Performed partial hepatectomy on adult mutant and control mice.
- Assessed liver regeneration capacity and IEG expression levels.
Main Results:
- SRF is not essential for normal liver development (ontogenesis).
- Adult mice lacking SRF in the liver exhibited impaired liver regeneration.
- The impaired regeneration was associated with reduced upregulation of SRF target IEGs.
Conclusions:
- SRF is an early response transcription factor in liver regeneration.
- SRF contributes to the initial phases of liver regeneration.
- SRF's role is mediated through the activation of immediate early genes.
