Posts Tagged ‘Ashley Yeager’

Goldenrods that evolved in the presence of herbivores release volatile chemicals that trigger defenses in neighboring plants of their species, even those that are genetically unrelated.

by Ashley Yeager

When a beetle larva bites into the leaf of a goldenrod plant, a perennial herb known for its bright yellow flowers, it gets a mouthful of food to fuel its growth. But the plant’s perspective is rather different. The bite damages the goldenrod (genus: Solidago), causing it to launch molecular defenses against the insect and to emit a concoction of chemicals that change the physiology of goldenrod plants nearby. It’s as if the plants are communicating about the invader.

For researchers studying plants’ responses to herbivory, the reasons for this communication are something of a mystery. “We don’t have a good understanding of why these plants are emitting these cues,” Rick Karban, an entomologist who studies plant communication at the University of California, Davis, tells The Scientist. “We don’t even know if the cues that plants are emitting—that other plants can perceive and respond to—are somewhat intentional,” or just a byproduct of leaf damage.

The notion that plants communicate was controversial until the end of the 20th century. Biologists first argued that trees and plants could “talk” to one another in the 1980s, but data supporting the idea were dismissed by many researchers as statistically sketchy. Over the past few decades, however, the scientific community has revised its opinion. A series of papers have shown that when a plant such as goldenrod is damaged, it releases volatile organic compounds (VOCs) that prompt neighboring plants to mount their own chemical defenses against an impending herbivore attack. Karban says researchers are now focused on why the emitting plant puts out this signal, and whether it derives a benefit from telling those around it that it’s being eaten.

It’s possible that surrounding plants are merely eavesdropping on the signal emitter, which derives no benefit from the situation. Researchers have also proposed two alternative hypotheses that involve a benefit to the emitter. The first—the kin selection hypothesis—states that the plant emitting the signal indirectly benefits thanks to the increased survival of genetically related individuals in its vicinity, even if the plant itself is damaged by herbivory. The second—the mutual benefit hypothesis—posits that the plant emitting the signal directly benefits from communication because the preemptive chemical defenses launched by all its neighbors result in a hostile environment that encourages the herbivorous insect to move away from the area.

Finding evidence to distinguish between these scenarios hasn’t been easy, especially because plant communication is a small field. But a long-running project offers new clues. In 1996, a team at Cornell University started an elaborate experiment on one goldenrod species, S. altissima, regularly spraying rows and rows of the plant with the insecticide fenvalerate, while leaving other rows untreated. After 12 years, the researchers collected plants from each of the rows, brought them to the lab, snipped the stems, and grew clones. Then, the team set up collections of the clones in pots at a nearby farm, let goldenrod beetle larvae munch on some of the plants, and measured the emission of VOCs.

“This research was really mostly curiosity driven,” says Aino Kalske, a postdoctoral researcher in ecology and evolution biology at the University of Turku in Finland and a former graduate student at Cornell who helped with the experiment. She and her colleagues were particularly interested to see if the goldenrod’s chemical messages would evolve differently depending on whether the plants had been treated with insecticide and were protected from insect attacks or had been left untreated and experienced higher levels of herbivory. Differences in signaling between the treated and untreated plants’ descendants might be a small step toward determining which hypothesis about plant communication was correct.

The team found that VOCs emitted by goldenrod plants whose predecessors had been sprayed with the insecticide only induced genetically identical plants to mount preemptive chemical defenses to insect invasion—consistent with the kin selection hypothesis. But VOCs emitted by goldenrod whose predecessors hadn’t been sprayed with the insecticide induced the preemptive defense from all the other goldenrod plants around them, even plants that weren’t their kin—consistent with the mutual benefit hypothesis.

Additionally, the plants exposed to herbivory converged on a shared VOC signal over the course of the study—with all of the goldenrod plants eventually emitting the same chemical signals whether they were genetically identical to the emitter plant or not. Plants treated with insecticide showed no such signal convergence, the researchers reported in Current Biology last September. This sort of convergence on a single chemical signal is thought to benefit plants exposed to herbivory by providing a stronger deterrent against invading insects or a stronger attraction for the herbivores’ natural enemies. Kalske says the study provides the first concrete evidence that plants aren’t merely eavesdropping on one another, and that the emitter derives a benefit from releasing its chemical messages.

“The main value of the paper is the extremely long-lasting experiment needed to assess an evolutionary change in an organism,” Emilio Guerrieri, a researcher at the National Research Council of Italy’s Institute for Sustainable Plant Protection who was not involved in the study, writes in an email to The Scientist. The experiment, he says, “represents a sound demonstration that herbivores shape the VOC emission of a plant.”

Researchers still don’t know much about how the plants actually receive and respond to the VOC cues, Kalske notes, or whether the presence of other types of herbivores, such as mammals, influences similar signal changes. These are questions that the team would still like to answer, she says, not least because of the potential agricultural applications. “Understanding the intricacies of the plant world and plant-plant communication in more detail can potentially help us in plant protection in the agricultural context, if we can learn how to use these volatiles to turn on defenses in crop plants effectively.”



A gene drive has successfully caused the collapse of a malaria-carrying mosquito population in the lab, researches report today (September 24) in Nature Biotechnology. This is the first time a gene drive—a genetic element that ensures its own inheritance—has caused a population of mosquitoes to self-destruct, a result that holds promise for combating malaria.

“This breakthrough shows that gene drive can work, providing hope in the fight against a disease that has plagued mankind for centuries,” study coauthor Andrea Crisanti, a molecular parasitologist at Imperial College London, says in a university statement.

In the study, the team targeted a region of a gene called doublesex that is responsible for female development. Female Anopheles gambiae mosquitoes with two copies of the altered doublesex gene did not lay eggs. After eight generations, the drive had spread through the entire population, such that no eggs were laid.

“It’s a really stunning development,” Omar Akbari, an entomologist at the University of California, Irvine who was not involved to the study, tells Wired, noting that mosquitoes are under “huge evolutionary pressure” to resist gene drives that cause the population to collapse. However, Akbari tells Science News that this gene drive might not work well in the wild because resistance will probably pop up.

Crisanti, however, is more confident. “We are not saying this is 100 percent resistance-proof,” he tells The New York Times. “But it looks very promising.” Still, he adds in the university statement, “[i]t will still be at least 5-10 years before we consider testing any mosquitoes with gene drive in the wild.” First, his team will need to test the gene drive in larger containers, where the mosquitoes can act more naturally, Crisanti tells Wired—swarming to find a mate, for instance. Such details were difficult to mimic in the 20 cubic centimeter cages used in this study.

Despite the need for further testing, some researchers hailed the current study as a major success. “With this achievement,” Kevin Esfelt, who studies the evolution of gene drives at MIT, tells The New York Times, “the major barriers to saving [human] lives are arguably no longer mostly technical, but social and diplomatic.”–gene-drive-wipes-out-lab-mosquitoes-64849

By Ashley Yeager

Researchers have transferred a memory from one snail to another via RNA, they report today (May 14) in eNeuro. If confirmed in other species, the finding may lead to a shift in scientists’ thinking about how memories are made—rather than cemented in nerve-cell connections, they may be spurred on by RNA-induced epigenetic changes.

“The study suggests that RNA populations are the missing link in the search for memory,” Bridget Queenan, a neuroscientist at the University of California, Santa Barbara, who was not involved in the study, writes in an email to The Scientist. “If circulating neural RNAs can transfer behavioral states and tendencies, orchestrating both the transient feeling and the more permanent memory, it suggests that human memory—just like mood—will only be explained by exploring the interplay between bodies and brains.”

For decades, researchers have tried to pinpoint how, when, and where memories form. In the 1940s, Canadian psychologist Donald Hebb proposed memories are made in the connections between neurons, called synapses, and stored as those connections grow stronger and more abundant. Experiments in the 1960s, however, suggested RNA could play a role in making memories, though the work was largely written off as irreproducible.

Study coauthor David Glanzman of the University of California, Los Angeles, has been working on the cell biology of learning and memory for nearly 40 years, and says for the majority of that time he believed memory was stored at synapses. Several years ago, though, he and his colleagues began replicating memory-erasing research done in rodents in California sea hares (Aplysia californica), a type of marine snail also called a sea slug. The team found that the snail synapses built to “store” a memory weren’t necessarily the synapses that were removed from the neural circuits in the memory-erasing experiments.

“It was completely arbitrary which synaptic connections got erased,” Glanzman says. “That suggested maybe the memory wasn’t stored at the synapse but somewhere else.”

Glanzman turned his attention to RNA because of those earlier hints it was related to memory, and also because of recent experiments suggesting long-term memory was stored in the cell bodies of neurons, not synapses. He picked Aplysia because it has been a longtime model organism for memory studies. Like all mollusks, these snails have groups of neurons called ganglia, rather than brains. Their nervous systems comprise about 20,000 neurons, and the cells are some of the biggest and easily identifiable among nerve cells in all animals. In the snail’s gut, for example, are specific sensory and motor neurons that control the withdrawal of a fleshy, spout-like organ on the snail’s back called a siphon and the contraction of a caterpillar-looking gill, which the animal uses to breathe.

When touched lightly on the siphon, the neurons fire, retract the tissue, and contract the gill within the body cavity for a few seconds to protect it against attack. Sticking electrodes in the snail’s tail and shocking it makes this defensive response last longer, tens of seconds, and sometimes up to almost a minute. By repeatedly shocking the snail’s tail, the animal learns to stay in that defensive position when touched on the siphon, even weeks after the shocks end.

In his team’s latest experiments, Glanzman and his colleagues zapped snails’ tails, then pulled the abdominal neurons from the shocked snails, extracted their RNA, dissolved the RNA into deionized water, and injected the solution into the necks of snails that had never been shocked. (For a control, the team also took RNA from non-shocked snails and injected into naive snails.) When tapped on the siphon 24 hours later, snails that got RNA from shocked snails withdrew their siphon and gill for significantly longer (almost 40 seconds) than did snails that got RNA from non-shocked animals (less than 10 seconds).

DNA methylation appeared to be essential for the transfer of the memory among snails. When Glanzman and his colleagues blocked DNA methylation in snails getting RNA from shocked ones, the injected snails withdrew their siphons for only a few seconds when tapped on the siphon.

Glanzman wanted to know if the RNA from shocked snails actually affected the neuronal connections of the snails receiving the injections any differently than RNA from nonshocked snails. So, in a third test, he and his team removed sensory neurons from nonshocked snails, cultured the cells in a dish, and then exposed the cells to RNA from shocked snails. Zapping the culture with a bit of current excited the sensory neurons much more than neurons treated with RNA from nonshocked snails. RNA from shocked snails also enhanced a subset of synapses between sensory and motor neurons in vitro, suggesting it was indeed the RNA that transported the memory, Glanzman explains.

The idea “seems quite radical as we don’t have a specific mechanism for how it works in a non-synaptic manner,” Bong-Kiun Kaang, a neuroscientist at Seoul National University who was not involved in the study, writes in an email to The Scientist. Kaang notes there are “many critical questions that need to be addressed to further validate the author’s argument,” such as what kinds of noncoding RNAs are specifically involved, how are the RNAs transferred among neurons, and how much do RNAs at the synapse play a role? The experiments should also be replicated in organisms other than snails, he says.

Glanzman says that in his next experiments he will attempt to identify the RNAs involved, and he has an idea for the mechanism, too. The memory is not stored in the RNA itself, he speculates—instead, noncoding RNA produces epigenetic changes in the nucleus of neurons, thereby storing the memory.

“This idea is probably going to strike most of my colleagues as extremely improbable,” Glanzman says. “But if we’re right, we’re just at the beginning of understanding how memory works.”

A. Bédécarrats et al., “RNA from trained Aplysia can induce an epigenetic engram for long-term sensitization in untrained Aplysia,” eNeuro,, 2018.