Trauma-induced regulation of VHP-1 modulates the cellular response to mechanical stress

Nathan Egge, Sonja L. B. Arneaud, Rene Solano Fonseca, Kielen R. Zuurbier, Jacob McClendon and Peter M. Douglas ()
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Nathan Egge: UT Southwestern Medical Center
Sonja L. B. Arneaud: UT Southwestern Medical Center
Rene Solano Fonseca: UT Southwestern Medical Center
Kielen R. Zuurbier: UT Southwestern Medical Center
Jacob McClendon: UT Southwestern Medical Center
Peter M. Douglas: UT Southwestern Medical Center

Nature Communications, 2021, vol. 12, issue 1, 1-18

Abstract: Abstract Mechanical stimuli initiate adaptive signal transduction pathways, yet exceeding the cellular capacity to withstand physical stress results in death. The molecular mechanisms underlying trauma-induced degeneration remain unclear. In the nematode C. elegans, we have developed a method to study cellular degeneration in response to mechanical stress caused by blunt force trauma. Herein, we report that physical injury activates the c-Jun kinase, KGB-1, which modulates response elements through the AP-1 transcriptional complex. Among these, we have identified a dual-specificity MAPK phosphatase, VHP-1, as a stress-inducible modulator of neurodegeneration. VHP-1 regulates the transcriptional response to mechanical stress and is itself attenuated by KGB-1-mediated inactivation of a deubiquitinase, MATH-33, and proteasomal degradation. Together, we describe an uncharacterized stress response pathway in C. elegans and identify transcriptional and post-translational components comprising a feedback loop on Jun kinase and phosphatase activity.

Date: 2021
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DOI: 10.1038/s41467-021-21611-8

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