What question did this study set out to answer?

To determine whether serum response factor is targeted by caspases during apoptosis and to assess the functional consequences of this cleavage on cell survival.

September 1, 2001Journal of Biological ChemistryOpen Access

Serum Response Factor Cleavage by Caspases 3 and 7 Linked to Apoptosis in Human BJAB Cells

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Authors

VDVictoria DrewettF-star (United Kingdom)ADAndrew DevittUniversity of Nottingham JSJanice SaxtonUniversidad Complutense de Madrid

Discussion

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Implication

In vitro study demonstrates that caspase cleavage of serum response factor promotes apoptosis in human B cells, indicating survival transcription must be dismantled for programmed cell death.

Key Points

To determine whether serum response factor is targeted by caspases during apoptosis and to assess the functional consequences of this cleavage on cell survival.
Assessed caspase-mediated cleavage of serum response factor (SRF) in proliferating murine fibroblasts and human BJAB B-lymphoma cells.
Mapped the specific cleavage sites to Asp(245) and Asp(254) and engineered a cleavage-resistant SRF mutant.
Evaluated c-fos transcriptional activity and measured apoptotic response following Fas receptor cross-linking in the presence of wild-type or noncleavable SRF.
Identified Asp(245) and Asp(254) as the two primary target sites cleaved by executioner caspases 3 and 7, generating fragments devoid of transcriptional activity.
Observed that SRF cleavage directly correlates with the downregulation and loss of proliferation-associated c-fos expression.
Demonstrated that expressing a cleavage-resistant SRF mutant significantly suppresses Fas-induced apoptosis in human BJAB cells.

Cite This Study

Drewett et al. (2001) studied this question.

synapsesocial.com/papers/6a9ee9b86c41c41abd716ae5 https://doi.org/10.1074/jbc.m103877200

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Implication

In vitro study demonstrates that caspase cleavage of serum response factor promotes apoptosis in human B cells, indicating survival transcription must be dismantled for programmed cell death.