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Updated: Feb 5, 2026
Application of RNAi and Heat-shock-induced Transcription Factor Expression to Reprogram Germ Cells to Neurons in C. elegans
Published on: January 1, 2018
The mTOR Target S6 Kinase Arrests Development in Caenorhabditis elegans When the Heat-Shock Transcription Factor Is
Peter Chisnell1,2, T Richard Parenteau1, Elizabeth Tank3
1Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158.
Abstract:
The widely conserved heat-shock response, regulated by heat-shock transcription factors, is not only essential for cellular stress resistance and adult longevity, but also for proper development. However, the genetic mechanisms by which heat-shock transcription factors regulate development are not well understood. In Caenorhabditis elegans, we conducted an unbiased genetic screen to identify mutations that could ameliorate the developmental-arrest phenotype of a heat-shock factor mutant. Here, we show that loss of the conserved translational activator rsks-1/S6 kinase, a downstream effector of mechanistic Target of Rapamycin (mTOR) kinase, can rescue the developmental-arrest phenotype of hsf-1 partial loss-of-function mutants. Unexpectedly, we show that the rescue is not likely caused by reduced translation, nor by activation of any of a variety of stress-protective genes and pathways. Our findings identify an as-yet unexplained regulatory relationship between the heat-shock transcription factor and the mTOR pathway during C. elegans development.
Insights
Loss of the translational activator RSKS-1/S6 kinase rescues developmental defects in heat-shock factor mutants. This study reveals an unknown link between heat-shock transcription factors and the mTOR pathway in development.
Area of Science:
- Cellular biology
- Developmental biology
- Genetics
Background:
- The heat-shock response is crucial for cellular stress resistance, longevity, and development.
- Heat-shock transcription factors (HSFs) regulate this response, but their developmental roles are not fully understood.
Purpose of the Study:
- To identify genetic factors influencing HSF-regulated development.
- To elucidate the mechanisms by which HSFs control development.
Main Methods:
- Conducted an unbiased genetic screen in *Caenorhabditis elegans* to find suppressors of a heat-shock factor (HSF) mutant's developmental arrest.
- Utilized genetic analysis to investigate the role of RSKS-1/S6 kinase in HSF pathway signaling.
Main Results:
- Loss of the translational activator RSKS-1/S6 kinase, a downstream target of the mechanistic Target of Rapamycin (mTOR) pathway, rescues the developmental arrest phenotype of *hsf-1* partial loss-of-function mutants.
- The rescue mechanism does not appear to involve reduced translation or the activation of known stress-protective genes/pathways.
Conclusions:
- Identified a novel regulatory relationship between HSFs and the mTOR pathway in *C. elegans* development.
- This finding suggests an unexpected connection between translational control and developmental regulation mediated by HSFs.
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