Long-term recovery from acute cold shock in Caenorhabditis elegans

Abstract

BackgroundAnimals are exposed to a wide range of environmental stresses that can cause potentially fatal cellular damage. The ability to survive the period of stress as well as to repair any damage incurred is essential for fitness. Exposure to 2 °C for 24 h or longer is rapidly fatal to the nematode Caenorhabditis elegans, but the process of recovery from a shorter, initially non-lethal, cold shock is poorly understood.ResultsWe report that cold shock of less than 12-hour duration does not initially kill C. elegans, but these worms experience a progression of devastating phenotypes over the next 96 h that correlate with their eventual fate: successful recovery from the cold shock and survival, or failure to recover and death. Cold-shocked worms experience a marked loss of pigmentation, decrease in the size of their intestine and gonads, and disruption to the vulva. Those worms who will successfully recover from the cold shock regain their pigmentation and much of the integrity of their intestine and gonads. Those who will die do so with a distinct phenotype from worms dying during or immediately following cold shock, suggesting independent mechanisms. Worms lacking the G-protein coupled receptor FSHR-1 are resistant to acute death from longer cold shocks, and are more successful in their recovery from shorter sub-lethal cold shocks.ConclusionsWe have defined two distinct phases of death associated with cold shock and described a progression of phenotypes that accompanies the course of recovery from that cold shock. The G-protein coupled receptor FSHR-1 antagonizes these novel processes of damage and recovery.Electronic supplementary materialThe online version of this article (doi:10.1186/s12860-015-0079-z) contains supplementary material, which is available to authorized users.

Stress and timing associated with Caenorhabditis elegans immobilization methods

“…This technique works by slowing metabolic processes to the point that the worm is no longer able to move. However, exposure time and temperature have a significant impact on the survival of the worm and internal integrity of the structures within it [ 18 , 19 ]. As a result, exposure time was reduced and temperature increased when compared to the previous studies to improve survival rates [ 18 , 20 ].…”

Evolutionarily conserved regulation of immunity by the splicing factor RNP-6/PUF60

“…Cellular stress resistance mechanisms help manage diverse environmental and physiologic challenges. Animals have evolved adaptive mechanisms to survive heat and cold stress ( Morley and Morimoto, 2004 ; Robinson and Powell, 2016 ). While heat stress mechanisms have been well studied, cold stress mechanisms are not well understood ( Ohta et al, 2014 ).…”

Surviving hypothermia by ferritin-mediated iron detoxification

“…Recently, another transcription factor, PQM-1, was shown to complement DAF-16 in promoting the lifespan in DAF-2 deficient animals 25 . In the intestinal cells, PQM-1 and DAF- 16 nuclear occupancy has been shown to be mutually exclusive, and they appear to regulate largely separate sets of target genes 25 . Additionally, these transcription factors can play opposing roles; for example, while the formation of an alternative "dauer" larval stage (deployed to survive adverse environmental conditions) depends on DAF-16 22 , PQM-1 facilitates the recovery from the dauer arrest 25 .…”