Heat shock factor -- which exists in a single form in invertebrates but multiple forms in vertebrates -- is an essential part of the ability of living cells to survive stressful conditions such as heat, cold, radiation, and, it turns out, desiccation. In desert insects, the researchers found, the gene is able in certain conditions to upregulate itself, and this upregulation leads to a number of downstream processes, including the synthesis of heat shock proteins that are able to protect proteins in the cell from misfolding.
To perform the research, published in the Proceedings of the National Academy of Sciences, the researchers compared data on RNA expression in the sleeping chironomid with a closely related species, Polypedilum nubifer, which is not capable of surviving desiccation. They found that in the sleeping chironomid, hundreds of genes, including genes known to be involved in forming a "molecular shield" against damage due to dehydration, were already expressed during the early stages of desiccation. They discovered that a certain DNA motif, TCTAGAA, which is the binding site for HSF, was strongly enriched around the transcription start site of the genes activated by desiccation in the sleeping chironomid, but not the other species. Intriguingly, they found that in the desiccation-tolerant species, but not the other, genes responsible for the synthesis of trehalose -- a sugar that can stabilize cells in a dry state -- contained the TCTAGAA motif.
To shed further light on the role of trehalose, they treated a cultured cell line from the sleeping chironomid with the sugar, and found that many of the genes activated by desiccation were also activated, and further, that the trehalose treatment led to the activation of the HSF gene. This effect of trehalose was prevented by knocking down the HSF gene, showing the HSF was clearly involved in the response.
To perform the research, published in the Proceedings of the National Academy of Sciences, the researchers compared data on RNA expression in the sleeping chironomid with a closely related species, Polypedilum nubifer, which is not capable of surviving desiccation. They found that in the sleeping chironomid, hundreds of genes, including genes known to be involved in forming a "molecular shield" against damage due to dehydration, were already expressed during the early stages of desiccation. They discovered that a certain DNA motif, TCTAGAA, which is the binding site for HSF, was strongly enriched around the transcription start site of the genes activated by desiccation in the sleeping chironomid, but not the other species. Intriguingly, they found that in the desiccation-tolerant species, but not the other, genes responsible for the synthesis of trehalose -- a sugar that can stabilize cells in a dry state -- contained the TCTAGAA motif.
To shed further light on the role of trehalose, they treated a cultured cell line from the sleeping chironomid with the sugar, and found that many of the genes activated by desiccation were also activated, and further, that the trehalose treatment led to the activation of the HSF gene. This effect of trehalose was prevented by knocking down the HSF gene, showing the HSF was clearly involved in the response.
See:
Pavel V. Mazin, Elena Shagimardanova, Olga Kozlova, Alexander Cherkasov, Roman Sutormin, Vita V. Stepanova, Alexey Stupnikov, Maria Logacheva, Aleksey Penin, Yoichiro Sogame, Richard Cornette, Shoko Tokumoto, Yugo Miyata, Takahiro Kikawada, Mikhail S. Gelfand, Oleg Gusev. Cooption of heat shock regulatory system for anhydrobiosis in the sleeping chironomidPolypedilum vanderplanki. Proceedings of the National Academy of Sciences, 2018; 115 (10): E2477 DOI: 10.1073/pnas.1719493115
Posted by Dr. Tim Sandle
Posted by Dr. Tim Sandle
