Growing up on the Venezuelan coast, Santiago Perez spent much of his childhood camping on the keyes and visiting the coral reefs of Morrocoy Park. But over the years, Perez realised that the reefs were failing. Abused by uncontrolled tourism, and vulnerable to coral bleaching by ocean warming, the reefs were crumbling before his eyes. Perez was fascinated, and determined to learn more about the fragile organisms. Moving to the USA to continue his education, Perez became intrigued by the molecular mechanisms of coral bleaching, as the corals shed their symbiotic algae. Perez and Virginia Weis soon began to suspect that the signalling molecule, nitric oxide, which can be a key player in programmed cell death, could play a role in coral bleaching. But instead of working on delicate corals, the pair turned to a relatively robust symbiotic partnership, the sea anemone Aiptasia pallida and its dinoflagellate lodger, to look for nitric oxide(p. 2804).
At this point Perez had a stroke of luck. Thanks to nitric oxide expert Joe Beckman, Perez came across a nitric oxide sensitive fluorescent dye used to detect the molecule in mammalian tissue. Could this dye reveal nitric oxide production in heat shocked sea anemones too? Perez collected the symbiotic animals and bathed them in dye before exposing them to warm seawater. After carefully transferring them to a confocal microscope Perez focused laser beams on the tiny symbiont's tentacles to stimulate fluorescence; the whole tentacle lit up. The heat shocked symbiotic sea anemone was producing nitric oxide.
But was the signalling molecule delivering the algae's eviction notice?Exposing the intact sea anemone to sodium nitroprusside, which stimulates nitric oxide production, Perez reproduced the mass algal ejection; nitric oxide was the messenger.
Curious to know which half of the partnership generated the eviction notice, Perez gently separating the algae and its animal host, heat shocked the isolated partners and checked for nitric oxide production; but found none. The duo needed to be united for heat shock to stimulate nitric oxide production.
Changing his approach, Perez looked at nitric oxide production stimulated by another means in the intact symbiotic partnership to find which half of the duo ejected the lodger. Testing the effects of lipopolysaccharide, a compound that stimulates nitric oxide production in mammalian immune systems, on intact sea anemones and aposymbiotic sea anemones (where the algae had been gently removed), Perez returned to the confocal microscope and looked for nitric oxide production. Amazingly, the aposymbiotic sea anemone produced nitric oxide. The host was the source of the algae's eviction notice. More surprisingly, Perez realised that the animal host probably uses the same cellular mechanisms as the mammalian immune system to generate nitric oxide and trigger cell death.
But why are the sea anemones evicting their humble lodger when the algae are such valuable roommates? Perez explains that at times of stress, the algae switch off photosynthesis, and instead switch to generating toxic reactive oxygen species. Which is probably why their hosts are quick to kick them out,but Perez points out that the eviction comes at a high price, `it's like an immune reaction gone too far' says Perez, and can ultimately kill the anemone that remains.