A genetic program mediates cold-warming response and promotes stress-induced phenoptosis in C. elegans.
Wei JiangYuehua WeiYong LongArthur OwenBingying WangXuebing WuShuo LuoYongjun DangDengke K MaPublished in: eLife (2018)
How multicellular organisms respond to and are impacted by severe hypothermic stress is largely unknown. From C. elegans screens for mutants abnormally responding to cold-warming stimuli, we identify a molecular genetic pathway comprising ISY-1, a conserved uncharacterized protein, and ZIP-10, a bZIP-type transcription factor. ISY-1 gatekeeps the ZIP-10 transcriptional program by regulating the microRNA mir-60. Downstream of ISY-1 and mir-60, zip-10 levels rapidly and specifically increase upon transient cold-warming exposure. Prolonged zip-10 up-regulation induces several protease-encoding genes and promotes stress-induced organismic death, or phenoptosis, of C. elegans. zip-10 deficiency confers enhanced resistance to prolonged cold-warming stress, more prominently in adults than larvae. We conclude that the ZIP-10 genetic program mediates cold-warming response and may have evolved to promote wild-population kin selection under resource-limiting and thermal stress conditions.
Keyphrases
- stress induced
- transcription factor
- genome wide
- quality improvement
- cell proliferation
- long non coding rna
- long noncoding rna
- dna methylation
- copy number
- early onset
- gene expression
- dna binding
- high throughput
- genome wide identification
- subarachnoid hemorrhage
- binding protein
- multidrug resistant
- aedes aegypti
- single cell
- cerebral ischemia
- wild type