Large warm bodied animals hardly notice thermal fluctuations, but for tiny insects they can be life threatening. If temperatures drop below 7°C, Drosophila melanogaster slip into a coma due to malfunctions at the neuromuscular level. Hervé Colinet, Siu Fai Lee and Ary Hoffmann from the University of Melbourne, Australia, explain that stricken insects can recover from these drastic symptoms, thanks to a suite of proteins known as small heat shock proteins (sHsps). However, it wasn't clear how these proteins aided recovery. As genes first have to be transcribed into mRNA before the mRNA is translated into proteins, Colinet and his colleagues decided to knock down mRNA production (reduce transcription) of two sHsp genes, Hsp22 and Hsp23, to see how losing them affected D. melanogaster recovering from chill coma ().
Knocking down one gene or the other in groups of D. melanogaster, the team first checked that they had successfully inactived the gene. Having proved that the insects did not produce Hsp22 or Hsp23 mRNA, the team chilled the insects to 0°C for 12 h before allowing them to recover at 25°C. Tracking the flies' recovery in the short, medium and long term, the team examined how well the Hsp23 and Hsp22 deficient insects compared with insects that could transcribe both genes.
Insects lacking Hsp22 and insects lacking Hsp23 both took significantly longer to stand up during the recovery period than insects that transcribed the genes. And when the team measured the extent of the insects' injuries by testing their climbing ability 2, 4, 6 and 8 h after recovery, they found that initially, insects lacking Hsp22 took longer to recover than insects that transcribed the gene, but by 6 h the Hsp22 deficient flies were doing as well as flies that transcribed the gene. ‘This suggests that the kinetics of the chill coma recovery process was impaired, at least during the first 4 h period immediately after the cold stress,’ the team say.
Meanwhile, insects lacking Hsp23 seemed to be no worse off than insects that transcribed the gene during the first 2 h of recovery. However, their recovery was slower than that of the intact flies, with almost 50% of the Hsp23 deficient insects showing injuries 8 h after recovery, compared with 10% of the insects that produced Hsp23. ‘Our results imply that Hsp23 might be more strongly involved in cold recovery compared to Hsp22,’ say Colinet and his colleagues.
Outlining the potential protective roles of both genes in cold shock recovery, the team suggest that the neuroprotective effects of Hsp22 and Hsp23 may aid the flies' recovery from chill coma.
