Enlarge (credit: Tanja Ivanova )

In the US, for orange juice to be labeled as such, it must be 90 percent sweet orange, or Citrus sinensis . Thus, citrus producers in the US have long planted 90 percent Citrus sinensis. But this cultivar is extremely susceptible to the bacteria that causes citrus greening disease, which has devastated the near-monocultural Florida crop. There is as yet no way to control the disease; the most effective way to deal with it would be to find citrus cultivars that are resistant to it and breed them with sweet orange to grant them disease resistance.

Sweet oranges are a hybrid of mandarin and pomelo and are not especially genetically diverse. Any disease-resistant citrus we know of, however, does not taste like sweet orange, so breeding with it will produce fruit and juice with off flavors. It has been difficult to define and quantify those off flavors, though, because it has been difficult to define and quantify the components essential for proper orange flavor.

Now, researchers at the USDA Agricultural Research Service performed a comprehensive chemical evaluation of 179 different citrus combinations—oranges, mandarins, and assorted hybrids—and cross-referenced their chemical compositions with evaluations of orange and mandarin flavors in juice samples performed by a “trained panel.”

Enlarge (credit: Xinhua Fu)

On one level, we have fireflies figured out. We know the enzyme they use to make light (called luciferase), as well as the chemicals they use in the light-generating reaction. We know them so well that we've turned them into useful tools for studying other aspects of biology, such that lots of people who have never even seen a firefly have used firefly luciferase in the lab.

But on another level, there's a lot we don't understand. Fireflies clearly exercise a level of control over when they light up, and they do so only in specialized organs. And there's nothing like that organ in other species. So, somehow, fireflies evolved an elaborate light-producing organ, and there's no sign of any potential precursors in related species. Which makes it a bit of a mystery.

Now, a pair of researchers from Wuhan, China, (Xinhua Fu and Xinlei Zhu) have started unraveling what's going on at the level of the genes responsible. And, while they haven't produced a complete picture of how evolution built the fireflies, they've brought us a lot closer.

Enlarge / A shopper looks at a meat display on June 20, 2022 at the Market 32 Supermarket in South Burlington, Vermont. Niacin can be found in foods such as red meat, poultry, fish, fortified cereals and breads, brown rice, nuts, legumes, and bananas. (credit: Getty | Robert Nickelsberg )

In the early 20th century, the deadliest nutrient-related disease in US history ravaged the American South. Pellagra, a disease caused by a deficiency in niacin and/or tryptophan , is marked by the four "D's" : diarrhea, dermatitis that leads to gruesome skin plaques, dementia, and death. At its peak during the Great Depression, pellagra killed nearly 7,000 Southerners a year . Between 1906 and 1940, researchers estimate that the epidemic struck roughly 3 million Americans, killing around 100,000 .

The deadly epidemic led to voluntary—and eventually mandatory—fortification of wheat and other cereals with niacin (aka Vitamin B3). By the middle of the century, pellagra nearly vanished from the US. But, decades later, the public health triumph may be backfiring. With Americans' diets more reliant than ever on processed, niacin-fortified foods, the average niacin intake in the US is now nearing what's considered the tolerable upper limit of the nutrient, according to a federal health survey. And an extensive study recently published in Nature Medicine suggests that those excess amounts of niacin may be exacerbating cardiovascular disease, increasing risks of heart attacks, strokes, and death.

The study, led by Stanley Hazen, chair of Cardiovascular and Metabolic Sciences at Cleveland Clinic's Lerner Research Institute, connected high blood levels of a breakdown product of niacin—and to a lesser extent, tryptophan—to an elevated risk of major adverse cardiovascular events (MACE). And this elevated risk appears to be independent of known risk factors for those events, such as high cholesterol.

Enlarge / A large family can come with some unfortunate downsides (in addition to that weird cousin). (credit: Oliver Rossi )

Analysis of genomic and behavioral data from the vast UK Biobank finally demonstrates that genes that promote reproductive behaviors come with the ultimate price.

Aging stinks. You get marks on your skin, you’re slower, you forget stuff, and everything hurts. Your joints crack and pop. Evolution has achieved so many remarkable things; how is it possible that we still have to put up with growing old?

The antagonistic pleiotropy hypothesis states that your body falls apart when you’re old to pay the cost of being reproductively fit when you’re young. If the same gene has different effects (called pleiotropy) at different times of life—if it enhances your chances of reproduction when you’re young but is deleterious somehow once you get older—that gene will still undergo positive selection and remain in the population because reproduction is that important.

Enlarge / Drawing of a trade expedition to Punt during the reign of Queen Hatshepsut. Note the presence of baboons on board the lower ship. (credit: Nastasic )

One of the most enduring mysteries within archaeology revolves around the identity of Punt, an otherworldly “land of plenty” revered by the ancient Egyptians. Punt had it all—fragrant myrrh and frankincense, precious electrum (a mixed alloy of gold and silver) and malachite, and coveted leopard skins, among other exotic luxury goods.

Despite being a trading partner for over a millennium, the ancient Egyptians never disclosed Punt’s exact whereabouts except for vague descriptions of voyages along what’s now the Red Sea. That could mean anywhere from southern Sudan to Somalia and even Yemen.

Now, according to a recent paper published in the journal eLife, Punt may have been the same as another legendary port city in modern-day Eritrea, known as Adulis by the Romans. The conclusion comes from a genetic analysis of a baboon that was mummified during ancient Egypt’s Late Period (around 800 and 500 BCE). The genetics indicate the animal originated close to where Adulis would be known to come into existence centuries later.

Enlarge / Fish-eating kingfishers execute plunging dives into the water to capture prey, yet never seem to get concussed. (credit: Richard Towell)

There are many different species of kingfisher, and those that eat fish hunt by repeatedly diving head-first into the water when they spot tasty prey without suffering brain injuries like concussions. It turns out that diving kingfishers have several modified genes associated with diet and brain structure, according to a new paper published in the journal Communications Biology—notably mutations in genes related to the tau proteins that help stabilize neuron structure, although they can be harmful if too many build up.

“I learned a lot about tau proteins when I was the concussion manager of my son’s hockey team,” said co-author Shannon Hackett , associate curator of birds at the Field Museum. “I started to wonder, why don’t kingfishers die because their brains turn to mush? There’s gotta be something they're doing that protects them from the negative influences of repeatedly landing on their heads on the water’s surface.”

It's not the first time scientists have pondered this question, not just for kingfishers, but for other birds like gannets and woodpeckers . For instance, physicists at Virginia Tech studied diving gannets back in 2014 (publishing their conclusions in 2016 ), which fold their wings back as they dive, hitting the water with their whole body to snag underwater prey. From a physics standpoint, we're talking about an elastic body hitting the surface of water as fast as 55 MPH. The stress of moving from the medium of air to the much denser medium of water exerts a huge force on the bird's body, with an impact akin to tornadoes hitting the water. Yet despite the stress on their bodies, gannets (like the kingfisher) manage the feat again and again without injury, especially concussions.

Enlarge (credit: Liu Yang )

On an island off the coast of New Zealand, in the shadows of a primeval forest, an eerie sound resonates through the night. It's a deep boom that can sometimes be heard from miles away. This is the mating call of one of the strangest and most intriguing creatures in the region. Meet the critically endangered kākāpō .

Kākāpō (its name means “night parrot” in Māori) are large flightless parrots endemic to New Zealand. In 1894, conservationist Richard Henry relocated mainland birds to a supposedly safe island, but they were met by unsuspected predators. More kākāpō were found on the mainland and some surrounding islands in the 1970s. Though the mainland birds were later moved to those islands, only one survived. He was appropriately named Richard Henry.

The peculiar parrots now roam five islands free of predators, and their population has risen from a precarious 51 in 1995 to 252 in 2022. Still, the limited genetic diversity of such a small population has made breeding problematic. Breeding programs have found that most kākāpō are severely inbred and susceptible to disease and infertility. In an unprecedented move to conserve the species, researchers from the University of Otago have now sequenced the genome of nearly all existing birds in an effort to find out whether there are genetic variants in the population that could help keep the kākāpō from vanishing.