Related Experiment Video
Updated: Aug 5, 2026
09:36
Studying Oxidative Stress Caused by the Mitis Group Streptococci in Caenorhabditis elegans
Published on: March 23, 2019
LIN-23 Affects C. elegans Pathogen and Stress Resistance by Modulating SKN-1 Activity
Larissa A Tavizón1,2, Carolaing Gabaldón1, Melissa R Cruz1
1Department of Microbiology and Molecular Genetics, The University of Texas Health Science Center at Houston, Houston, TX 77030.
Biorxiv : the Preprint Server for Biology
|August 1, 2026
Summary
The F-box protein LIN-23 positively regulates the transcription factor SKN-1 during pathogen infection in C. elegans, promoting host survival. LIN-23 achieves this by targeting the negative regulator WDR-23 for degradation.
Area of Science:
- Molecular Biology
- Cellular Biology
- Genetics
Background:
- SKN-1 is a transcription factor crucial for stress response and survival in C. elegans, activated by p38 MAPK.
- LIN-23, an F-box protein in SCF E3 ubiquitin ligase complexes, regulates diverse cellular processes.
- LIN-23 has been previously shown to negatively regulate SKN-1 in other contexts.
Purpose of the Study:
- To investigate the role of LIN-23 in regulating SKN-1 activity during adult stress conditions, specifically pathogen exposure.
- To elucidate the mechanism by which LIN-23 influences SKN-1 activity.
Main Methods:
- Utilized C. elegans as a model organism.
- Investigated the effects of LIN-23 loss-of-function on SKN-1 activity and animal survival during infection.
- Examined p38 MAPK phosphorylation and SKN-1 nuclear localization.
- Assessed the dependency of LIN-23 function on WDR-23.
Main Results:
- LIN-23 acts as a positive regulator of SKN-1 activity during pathogen exposure, contrary to previous findings.
- Loss of LIN-23 reduced SKN-1 activity and decreased survival in infected adult animals.
- LIN-23 does not affect p38 MAPK phosphorylation or SKN-1 nuclear localization.
- LIN-23's function in regulating SKN-1 is dependent on WDR-23, a known negative regulator of SKN-1.
Conclusions:
- LIN-23 plays a novel, positive role in regulating SKN-1 activity and promoting survival under pathogen stress in adult C. elegans.
- A proposed model suggests LIN-23 promotes SKN-1 activity by mediating the degradation of nuclear WDR-23.
