Caterpillars Get Infection-Fighting Genes From Parasitic Wasps


The next butterfly you see flitting about might just be a genetically modified organism, given genes from a virus that protects it from other viruses. This isn’t the work of scientists trying to save pollinators, but parasitic wasps intent on rendering their hosts defenseless. 

These genetic engineers are braconids, members of a large wasp family that begin their lives inside the bodies of other insects like beetles, flies, aphids, and caterpillars. Many of them get help subduing their hosts from viruses. A female wasp injects her eggs, along with some viral particles, into an insect’s body. The virus—called a bracovirus—messes with the host’s immune system and keeps it from mounting a defense against the eggs. With no resistance from the host’s body, the eggs develop unchecked. When the wasp larvae hatch, they eat their way out of their host. 

A caterpillar’s body is the birthplace for a new generation of wasps, but it’s usually a dead end for bracoviruses. Their new hosts rarely survive their encounters with the wasps, and the viruses can’t replicate themselves like other viruses do. They are, in a way, domesticated, and part of the wasps. They’re produced inside the ovaries of the female wasps and can’t make copies of themselves because some of the genes they need to do that are in the wasps’ own genomes. 

Every once in a while, though, a caterpillar gets lucky. It might get attacked by a wasp that it’s not a compatible host for, or it may interrupt a wasp while she’s laying her eggs. The caterpillar “lives to tell the tale,” as biologist Jean-Michel Drezen puts it, and survives the encounter, but it still has bracoviruses inside it. 

In these cases, Drezen and other scientists have found that something strange can happen (as if wasps churning out domesticated viruses in order to use caterpillars are nurseries for their kids wasn’t weird enough). Genes from the bracoviruses sometimes find their way into the caterpillars’ genomes and get passed down to their offspring. Sometimes this continues for ages—one butterfly Drezen found the viral genes in isn't a host for braconid wasps, but its ancestors were, and the viral genes have persisted in the lineage’s DNA for around five million years. 

The viral genes appear to be repurposed once they’re integrated into the caterpillars’ DNA. While they were once part of a biological attack meant to subdue the caterpillars’ immune systems, they now help the insects resist infection from another group of viruses—the baculoviruses, which attack a variety of butterflies and moths via contaminated leaves. One of the bracovirus genes prevents these other viruses from reproducing, while another one can block the initial infection. Even something as awful as getting attacked by a parasitic wasp, it seems, can sometimes have a silver lining.

Andreas Trepte via Wikimedia Commons // CC BY-SA 2.5
Climate Change Has Forced Mussels to Toughen Up
Andreas Trepte via Wikimedia Commons // CC BY-SA 2.5
Andreas Trepte via Wikimedia Commons // CC BY-SA 2.5

Researchers writing in the journal Science Advances say blue mussels are rapidly evolving stronger shells to protect themselves against rising acid levels in sea water.

Bivalves like mussels, clams, and oysters aren’t good swimmers, and they don’t have teeth. Their hard shells are often the only things standing between themselves and a sea of dangers.

But even those shells have been threatened lately, as pollution and climate change push the ocean's carbon dioxide to dangerous levels. Too much carbon dioxide interferes with a bivalve’s ability to calcify (or harden) its shell, leaving it completely vulnerable.

A team of German scientists wondered what, if anything, the bivalves were doing to cope. They studied two populations of blue mussels (Mytilus edulis): one in the Baltic Sea, and another in the brackish waters of the North Sea.

The researchers collected water samples and monitored the mussel colonies for three years. They analyzed the chemical content of the water and the mussels’ life cycles—tracking their growth, survival, and death.

The red line across this mussel larva shows the limits of its shell growth. Image credit: Thomsen et al. Sci. Adv. 2017

Analysis of all that data showed that the two groups were living very different lives. The Baltic was rapidly acidifying—but rather than rolling over and dying, Baltic mussels were armoring up. Over several generations, their shells grew harder.

Their cousins living in the relatively stable waters of the North Sea enjoyed a cushier existence. Their shells stayed pretty much the same. That may be the case for now, the researchers say, but it definitely leaves them vulnerable to higher carbon dioxide levels in the future.

Inspiring as the Baltic mussels’ defiance might be, the researchers note that it’s not a short-term solution. Tougher shells didn’t increase the mussels’ survival rate in acidified waters—at least, not yet.

"Future experiments need to be performed over multiple generations," the authors write, "to obtain a detailed understanding of the rate of adaptation and the underlying mechanisms to predict whether adaptation will enable marine organisms to overcome the constraints of ocean acidification."

University of Adelaide
Scientists Find Potential Diabetes Drug in Platypus Venom
University of Adelaide
University of Adelaide

The future of diabetes medicine may be duck-billed and web-footed. Australian researchers have found a compound in platypus venom (yes, venom) that balances blood sugar. The team published their results in the journal Scientific Reports.

So, about that venom. The platypus (Ornithorhynchus anatinus) may look placid and, frankly, kind of goofy, but come mating season, the weaponry comes out. Male platypuses competing for female attention wrestle their opponents to the ground and kick-stab them with the venom-tipped, talon-like spurs on their back legs. It’s not a pretty sight. But it is an interesting one, especially to researchers.

Animal venoms are incredible compounds with remarkable properties—and many of them make excellent medicine. Many people with diabetes are already familiar with one of them; the drug exenatide was originally found in the spit of the venomous gila monster. Exenatide works by mimicking the behavior of an insulin-producing natural compound called Glucagon-like peptide 1 (GLP-1). The fact that the lizard has both venom and insulin-making genes is not a coincidence; many animal venoms, including the gila monster’s, induce low blood sugar in their prey in order to immobilize them.

It’s a good strategy with one flaw: GLP-1 and compounds like it break down and stop working very quickly, and people who have trouble making insulin really need their drug to keep working.

With this issue in mind, Australian researchers turned their attention to our duck-billed friends. They knew that platypuses, like people, made GLP-1 in their guts, and that platypuses, like gila monsters, make venom. The real question was how these two compounds interacted within a platypus’s body.

The researchers used chemical and genetic analysis to identify the chemical compounds in the guts and spurs of platypuses and in the guts of their cousins, the echidnas.

They found something entirely new: a tougher, more resilient GLP-1, one that breaks down differently—and more slowly—than the compounds in gila monster spit. The authors say this uber-compound is the result of a "tug of war" between GLP-1’s two uses in the gut and in venom.

"This is an amazing example of how millions of years of evolution can shape molecules and optimise their function," co-lead author Frank Gutzner of the University of Adelaide said in a statement.

"These findings have the potential to inform diabetes treatment, one of our greatest health challenges, although exactly how we can convert this finding into a treatment will need to be the subject of future research."


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