When the going gets hot, the heat shock response gets going. From the smallest insect to the largest mammal, once the mercury starts to rise, a suite of cellular protection systems sweep into action protecting cellular proteins from the catastrophic effects of heat damage. The protection mechanism is so vital that its components and progress are virtually indistinguishable from one species to the next; but not quite all. Fascinated by the environmental factors that trigger heat shock responses, Gretchen Hofmann and her team in Santa Barbara, California, have been investigating the heat shock response in some of the coolest organisms on the planet,notothenioid fish from the icy waters around Antarctica, and found that unlike most other creatures, Trematomus bernacchii, never has to switch its heat shock response on (). Instead, it keeps it running constantly.
Heading south in October for the Austral summer, Hofmann and two colleagues, Brad Buckley and Sean Place, travelled to the US's Antarctic facilities at McMurdo Station, ready to test T. bernacchii's thermal tolerance. Fortunately, the station was well equipped with all the gear Hofmann needed to drill holes in the thick sea ice, ready for a spot of traditional ice fishing. Back in the lab, the team extracted liver cells from the fish, to test their heat shock response. But working with tissue from the sub-zero, thermally stable environment was far from straightforward. Hofmann explains that it's simply not enough to work with buffers on ice. `We had to tweak a lot of lab protocols and think outside the box' remembers Hofmann, to keep the tissue happy.
After fine-tuning their procedures, the team were ready to warm the cells to 8°C and looked for the telltale signs of a heat shock response. But nothing happened; warming the cells didn't trigger a heat shock response!
Curious to know whether the fish were failing to switch on the response at 8°C, Hofmann decided to test the cells' responses to other stressful conditions. According to heat shock expert Richard Morimoto, if protein-turnover-blocking MG132 couldn't trigger a heat shock response,nothing would. But no matter how much MG132 the liver cells were exposed to,the heat shock response failed to appear.
Was the system simply missing, or had it lost its on/off switch? Hofmann and her team began looking for evidence of the switch's components in the fish's tissue: protein transcription factors called Heat Shock Factors and the mRNA that codes for them. Sure enough the team found both the protein and mRNA, and a key heat shock protein, Hsp70; the switch was there. In fact, T. bernacchii was continually producing heat shock proteins; the system was permanently switched on.
Puzzled why the fish were keeping the costly defence system running permanently, Hofmann remembers discussing the problem with Place, when it suddenly dawned on them why. Instead of using the system to protect proteins from heat denaturation, the heat shock response was protecting the fish from the permanent threat of cold protein damage.
`[Eureka] moments like that don't happen often in your career' recalls Hofmann, but now she's sure that the fish have adapted heat shock to a different type of thermal stress she's keen to discover other genes involved in the complex system. Which means booking back in to McMurdo Station for yet another Austral summer.
