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When dolphins swim, they flap their tails up and down, which pushes water backward. That jostled water contains dozens of eddies of different sizes. To see if this turbulent water propels dolphins forward, researchers ran numerical simulations of the fluid dynamics on a supercomputer to see how the water swirls under different flapping conditions. They found that the dolphin’s tail produces a few large vortices that boost it along. The rest of the eddies are byproducts of the larger swirls and don’t help the creatures zip by. “We find that our results are unchanged across a wide range of swimming speeds ,” said lead author Yutaro Motoori in a statement.

In the future, the team hopes their findings could be applied to engineering, where researchers are always trying to make faster and more energy-efficient swimming robots.

Quantum uncertainty implies that empty space roils with pairs of particles flitting in and out of existence. In 1974, Stephen Hawking realized that if a pair of such “virtual” particles were to straddle a black hole’s event horizon—within which not even light can escape—one particle could be ripped from the vacuum and fall in while the other shoots into space, creating Hawking radiation.

Hawking radiation could destabilize an electrically charged black hole, argue theorists Francesco Di Filippo and Samuel Gralla, independently. A charged black hole would have two event horizons nested like Russian dolls. The outer horizon is the familiar point of no return. The inner horizon is weirder, marking where gravity becomes repulsive.

Hawking radiation would make the outer horizon inch inward. Bizarrely, inside the black hole, Hawking radiation has negative energy, which would accumulate on the inner horizon and make it balloon outward. Eventually, the inner and outer horizons would coincide, effectively canceling each other and disappearing before a singularity forms. Notably, Di Filippo and Gralla say the argument could apply to real, spinning black holes, which also have two event horizons.

Scientists are pretty sure that mitochondria came to exist when an archaeon somehow engulfed a bacterium, and the bacterium settled in. But how all the other organelles—the endoplasmic reticulum, lysosomes, the Golgi apparatus, and so on—came to exist is hotly debated. One hypothesis is that they resulted from little blebs shed by the mitochondria-to-be. That idea may have just gotten a boost from a seemingly odd source: research on the parasite Toxoplasma gondii.

Toxoplasma is perhaps most well-known as a mind-altering parasite. It makes its way into its final feline host by tinkering with the minds of its intermediate rodent hosts, dulling their fear. Lots of research has investigated how else this parasite manipulates its hosts, right the way down to cellular mechanisms. As an intracellular parasite, Toxoplasma has to thwart a cell’s defenses to survive. And it was in the course of studying how it pulls off this trick that researchers started paying extra close attention to its interactions with mitochondria.

One of the ways the cell can fight back against T. gondii is by hoarding nutrients in its mitochondria. But a lot of the time, the parasite gets the upper hand. It essentially glues mitochondria onto itself, forcing the organelles to spin off blebs of outer mitochondrial membrane. Several years ago, researchers showed that these structures positive for outer mitochondrial membrane, or SPOTs as the team dubbed them, help the parasite survive and grow. Now, the same group has figured out part of that process: SPOTs engulf lysosomes.

If mitochondria are powerhouses, then lysosomes are waste disposal centers; when there’s something to destroy inside a cell, these organelles are acidified, creating an environment that shreds biomolecules. The researchers found that after lysosomes are engulfed by SPOTs, they remain acidified—and this step is key to the parasite’s reproduction. If acidification is prevented with a specific inhibitor, the T. gondii struggle hard.

What’s really intriguing, though, is these SPOT-eaten lysosomes seem to become something else entirely. They’re not identifiable as lysosomes anymore. Thus, the team wrote, “mitochondrial membranes can be repurposed to create new cellular compartments.” Or, as study leader Lena Pernas explained at a symposium earlier this year: “Mitochondria are able to give rise to new organelles during infection.”

So, if they give rise to new organelles during infection, could they perhaps once have given rise to the organelles we know today?

The work isn’t actually the first time scientists have shown mitochondrial membranes can spawn organelles. Almost a decade ago, cell biologist Heidi McBride and colleagues discovered that cells engineered to lack peroxisomes—organelles that act a bit like sewage treatment plants, detoxifying harmful substances—made new ones by fusing mitochondrial vesicles with vesicles from the endoplasmic reticulum. McBride told Knowable that this strongly supports the notion that “the presence of mitochondria launched the biogenesis of new organelles.”

Many brushed off McBride’s findings as exceedingly rare or an artifact of engineered cells, but the new evidence from Pernas and colleagues—on top of other studies that have found unexpected roles for mitochondrial vesicles—is forcing another look. At the symposium, Pernas even made the “heretical” suggestion that this is part of what mitochondria do: They act as a “reservoir” for constructing new organelles in response to stress. And in light of the growing body of evidence that mitochondria are key to surviving all sorts of stressful conditions, the idea doesn’t sound quite so radical.

And really, that would just make what T. gondii does all the more impressive. “What is so cool and surprising is the ability of a pathogen to completely, not only manipulate the mitochondria, but use the mitochondria to generate an entire new organelle in the cell, with such precision,” cell biologist and immunologist Shaeri Mukherjee told Nature.

With contributions from Hannah Richter and Adrian Cho

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