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Cell-cycle dependent alternative splicing of the tenascin primary transcript
L Borsi1, E Balza, P Castellani
1Laboratory of Cell Biology, Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
Cell Adhesion and Communication
|January 1, 1994
Summary
Mitogenic stimulation alters tenascin (TN) mRNA levels in fibroblasts, indicating a primary response. This impacts TN isoform synthesis and accumulation, suggesting a role in cell proliferation.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Tenascin (TN) isoforms, generated by alternative splicing, play roles in cell adhesion and migration.
- The larger TN isoform is associated with cell migration and focal adhesion loss.
- Higher molecular mass TN isoforms are markers of stromal cell proliferation in breast tissues.
Purpose of the Study:
- To investigate the pattern of TN alternative splicing in proliferating and non-proliferating cultured fibroblasts.
- To understand how mitogenic stimulation affects TN expression and isoform balance.
Main Methods:
- Cultured fibroblasts were stimulated with mitogens (serum or cytokines).
- Steady-state levels of TN mRNAs were analyzed.
- Synthesis and accumulation of TN isoforms were assessed.
Main Results:
- Mitogenic stimulation rapidly and significantly altered the steady-state levels of the two major TN mRNAs.
- These changes occurred independently of de novo protein synthesis, classifying them as a primary response.
- Mitogenic stimulation also induced changes in the synthesis and accumulation of different TN isoforms.
Conclusions:
- Fibroblast proliferation is associated with specific alterations in TN alternative splicing and isoform expression.
- TN isoforms are dynamically regulated in response to mitogenic signals.
- These findings highlight the role of TN alternative splicing in cellular responses to growth factors.