Scientists discover how some flowers mimic the smell of death

As the saying goes, you catch more flies with honey than vinegar, but (discounting that vinegar is actually a great way to trap fruit flies), there’s an even better method: smell like rotting meat. As a subset of flowering plants figured out long ago, many flies and some beetles are drawn to the putrid and foul over the pretty and floral. Exploited correctly, these insects‘ instincts can make them great pollinators.

But how does a flower conjure up the odor of decaying flesh? For a long time, scientists haven’t been quite sure. One persistent theory was that plants produce these compounds passively, through oxidation of more common precursor chemicals, or that these plants partner with bacteria to produce their stenches. Yet new research indicates that, actually, many plants have everything they need to actively stink it up solo. Flowers across at least three stinky families share a similarly evolved genetic pathway to carrion mimicry, according to a study published May 8 in the journal Science.

With a few small modifications, a single gene that’s present in most plants and animals can turn flowers into stink factories. The altered gene works by generating a specific enzyme. That enzyme subsequently transforms a common protein byproduct into dimethyl disulfide (DMDS), a strong-smelling chemical that’s created when bacteria break down rotting flesh. 

Depending on the context, DMDS’s odor also suggests notes of fermented, pickled radish, dried meat, or human feces, says Yudai Okuyama, lead study author and an evolutionary biologist who studies plants at the National Museum of Nature and Science in Tokyo. “It’s a very bad smell,” he notes. But Okuyama and his colleagues managed to follow that stink to a beautiful set of discoveries. 

The scientists began their research by surveying plants in the genus Asarum, commonly known as wild gingers. Across 30 species, they found that many of them produce DMDS at high levels–higher than what could be reasonably generated passively. Then, they used RNA sequencing to determine which genes correlated best with high DMDS expression. They narrowed the search down to a handful of candidates, which the researchers then inserted into E. coli bacteria. They fed the E. coli  the precursor chemical to DMDS, and homed in on the gene that actually contributes to DMDS generation. Additional work showed that this gene is present in nearly-identical form in the skunk cabbage genus (Symplocarpus) and another species of plants common in Japan, Eurya japonica. All three plant groups are in distantly related families. (Corpse flowers, however, seem to rely on a slightly different strategy).

“I think it’s an excellent piece of work,” says Lorenzo Caputi, a chemical ecologist who studies the compounds plants make at the Max Planck Institute in Germany. Caputi wasn’t involved in the new research, but co-wrote an accompanying commentary article about the study, also published in Science. “I like this paper because it actually puts what happens between plants and insects into evolutionary context,” he says. 

Usually, plant-pollinator interactions are mutualisms. Plants advertise their nectar and pollen with a sweet, enticing odor. Insects visit, harvest what they need as food, and then spread that pollen around. In the case of carrion mimicry, however, plants are generally tricking their insect visitors. Foul-smelling plants don’t offer a reward to flies or beetles, but they do reap the benefit of mobile insects spreading their pollen around where a plant couldn’t on its own. 

The research findings show just how much selective pressure plants face to attract new pollinators. Competition over insects is fierce enough that the same stinky mutation has emerged multiple times–showing up in three disparate families. Perhaps these plants emerged in an environment where flies were more abundant than butterflies and bees. Or, perhaps the nectar market was already saturated. Regardless, it “means that evolution really pushed very hard for these plants to start making this compound,” Caputi explains. 

The gene in question, a form of selenium-binding protein, abbreviated SBP, has a long history among animals, plants, and bacteria. It’s an “ancient” bit of DNA code that’s clearly been important enough to stick around as species shifted and diverged, says Okuyama–though all of the other critical functions the gene performs aren’t yet clear.

In humans, a couple of studies indicate our version of SBP acts as an antioxidant, breaking down harmful waste products into benign, easily excreted chemicals. Yet, when a mutation goes awry and SBP malfunctions in people, it becomes a case of clinically bad breath and body odor, as unprocessed smell compounds seep into the mouth and through the skin. It goes to show that one species’ maladaptive malodorous B.O. can be another species’ genetic win. 

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