Except this tale unfolded about 30 million years ago, just after the Eocene-Oligocene transition during which North America saw great cooling and drying, making the continent less hospitable to warmth-loving primates.

Today, paleontologists from the University of Kansas and the Institute of Vertebrate Paleontology and Paleoanthropology in Beijing have published evidence in the Journal of Human Evolution shedding light on the long-standing saga of Ekgmowechashala, based on fossil teeth and jaws found in both Nebraska and China.

To do so, the researchers first had to reconstruct its family tree, a job helped by the discovery of an even more ancient Chinese “sister taxon” of Ekgmowechashala the team has named Palaeohodites (or “ancient wanderer”). The Chinese fossil discovery resolves the mystery of Ekgmowechashala’s presence in North America, showing it was an immigrant rather than the product of local evolution.

“This project focuses on a very distinctive fossil primate known to paleontologists since the 1960s,” said lead author Kathleen Rust, a doctoral candidate in paleontology at KU’s Biodiversity Institute and Natural History Museum. “Due to its unique morphology and its representation only by dental remains, its place on the mammalian evolutionary tree has been a subject of contention and debate. There’s been a prevailing consensus leaning towards its classification as a primate. But the timing and appearance of this primate in the North American fossil record are quite unusual. It appears suddenly in the fossil record of the Great Plains more than 4 million years after the extinction of all other North American primates, which occurred around 34 million years ago.”

In the 1990s, Rust’s doctoral adviser and co-author Chris Beard, KU Foundation Distinguished Professor and senior curator of vertebrate paleontology, collected fossils from the Nadu Formation in the Baise Basin in Guangxi, China, that closely resembled the Ekgmowechashala material known from North America. By that time, Ekgmowechashala was notoriously enigmatic among North American paleontologists.

“When we were working there, we had absolutely no idea that we would find an animal that was closely related to this bizarre primate from North America, but literally as soon as I picked up the jaw and saw it, I thought, ‘Wow, this is it,'” Beard said. “It’s not like it took a long time, and we had to undertake all kinds of detailed analysis — we knew what it was. Here in KU’s collection, we have some critical fossils, including what is still by far the best upper molar of Ekgmowechashala known from North America. That upper molar is so distinctive and looks quite similar to the one from China that we found that it kind of seals the deal.”

Beard left it to Rust to conduct the morphological analysis that tied Ekgmowechashala and its cousin Palaeohodites from China in a phylogenetic tree to establish their evolutionary relationships.

In the course of the work, Rust was able to draw conclusions about how Ekgmowechashala came to be discovered in Nebraska, millions of years after its fellow primates died out in the continent’s fossil record.

“We collected a substantial amount of morphological data to create an evolutionary tree using a phylogenetic reconstruction software and algorithm,” Rust said. “This evolutionary tree suggests a close evolutionary relationship between North American Ekgmowechashala and Palaeohodites from China, which Chris and his colleagues discovered in the 1990s. The results from our analysis unequivocally supports this hypothesis.”

The KU researchers said their discovery is not only exciting in terms of discovering a new primate species from late Eocene China — but also in settling the origin story of Ekgmowechashala. Based on their investigation, Ekgmowechashala did not descend from an older North American primate that somehow survived the cooler and drier conditions that caused other North American primates to go extinct. Rather, its ancestors crossed over the Beringian region millions of years later, anticipating the route followed by the first Native Americans much later in time.

“Our analysis dispels the idea that Ekgmowechashala is a relic or survivor of earlier primates in North America,” Rust said. “Instead, it was an immigrant species that evolved in Asia and migrated to North America during a surprisingly cool period, most likely via Beringia.”

Species like Ekgmowechashala that show up suddenly in the fossil record long after their relatives have died off are referred to as “Lazarus taxa” after the biblical figure who was raised from the dead.

“The ‘Lazarus effect’ in paleontology is when we find evidence in the fossil record of animals apparently going extinct — only to reappear after a long hiatus, seemingly out of nowhere,” Beard said. “This is the grand pattern of evolution that we see in the fossil record of North American primates. The first primates came to North America about 56 million years ago at the beginning of the Eocene, and they flourished on this continent for more than 20 million years. But they went extinct when climate became cooler and drier near the Eocene-Oligocene boundary, about 34 million years ago. Several million years later Ekgmowechashala shows up like a drifting gunslinger in a Western movie, only to be a flash in the pan as far as the long trajectory of evolution is concerned. After Ekgmowechashala is gone for more than 25 million years, Clovis people come to North America, marking the third chapter of primates on this continent. Like Ekgmowechashala, humans in North America are a prime example of the Lazarus effect.”

Rust and Beard were joined in the work by co-authors Xijun Ni of the Chinese Academy of Sciences, Beijing, and Kristen Tietjen, scientific illustrator with the KU Biodiversity Institute and Natural History Museum.

According to Rust, the tale of Ekgmowechashala is worth people’s attention because it happened in an era of profound environmental and climatic changes, much like our own that’s driven by human activity.

“It’s crucial to comprehend how past biota reacted to such shifts,” she said. “In such situations, organisms typically either adapt by retreating to more hospitable regions with available resources or face extinction. Around 34 million years ago, all of the primates in North America couldn’t adapt and survive. North America lacked the necessary conditions for survival. This underscores the significance of accessible resources for our non-human primate relatives during times of drastic climatic change.”

The study is also a part of a larger story that represents the earliest chapters of our own evolutionary journey that ultimately led to our own species, Rust said.

“Understanding this narrative is not only humbling, but also helps us appreciate the depth and complexity of the dynamic planet we inhabit,” she said. “It allows us to grasp the intricate workings of nature, the power of evolution in giving rise to life and the influence of environmental factors.”

“PACs are an ecological surprise arriving late to the scene of widespread ecosystem degradation of coral reefs in the Anthopocene epoch,” writes the team, led by Peter Edmunds of California State University, Northridge. “Within this seascape, PACs may serve as an ecological catalyst that could hasten the global demise of corals on reefs under accelerating climate change.”

One of the most challenging aspects of the emerging PAC threat is that the algae can be incredibly hard to identify. There are an estimated 48 different species of PACs, and they can be difficult to tell apart from harmless species like seaweeds because their morphology varies significantly when it comes to color, shape, and structure.

“PAC outbreaks appear to be a rapidly developing crisis on coral reefs throughout the world, where they are exploiting the ecological legacies of decades of reef degradation,” write the authors.

Already, between 2012 and 2019, PACs took over 47%-64% of the shallow reefs in St. John, US Virgin Islands. And given the fact that PACs appear to be much more resilient than other related species to the impacts of climate change, including ocean acidification and extreme weather events like hurricanes, the researchers predict that PACs will eventually dominate reefs worldwide. “The recent increases in cover and distribution of PACs on tropical reefs demonstrate their capacity to accelerate the restructuring of tropical benthic habitats,” they write.

To slow the spread of PACs and protect the reefs, the authors stress the importance of detecting PAC outbreaks as early as possible. They also encourage researchers to look into the transformative impact of PACs on benthic communities and learn more about tropical reef resilience against PAC outbreaks.

“Suitable progress in these areas will only be obtained by a well-funded synergy of ecological, phylogenetic, and multi-omic studies that must start with the ability to quickly and accurately identify the taxa driving the global advance of PACs,” write the researchers.

“Looking at recent, natural climate anomalies helps to understand the processes and mechanisms that human-induced global warming may trigger,” says Dr Anastasia Zhuravleva, lead author of the study. She was a PhD student at GEOMAR and received the Annette Barthelt Prize for her dissertation in 2019. She then worked as a post-doctoral researcher at GEOMAR and Dalhousie University, where the study was completed.

“Researchers often consider an increase in sea ice extent and desalination in the subpolar North Atlantic as possible triggers for past cold periods, but processes in the tropical Atlantic appear to be equally important,” says Dr Zhuravleva. “In fact, in contrast to the northern and mid-latitudes, there is little information on these recent climate events from the subtropical-tropical Atlantic and their impact on regions in the Northern Hemisphere,” adds Dr Henning Bauch, paleoclimatologist at AWI and GEOMAR, co-initiator and co-author of the study. “This is where our research comes in.”

So, what happened in the tropical Atlantic during historical climate anomalies, and how might potential changes there have affected ocean circulation and climate much further north? To answer these questions, the team worked on a sediment profile from the southern Caribbean and reconstructed the salinity and temperature of the surface water over the last 1700 years. Among other things, the researchers determined the isotopic and elemental composition of the calcareous shells of plankton.

The results show a cooling of about 1°C during the Little Ice Age. “It is a significant temperature change for this region,” says Dr Mahyar Mohtadi, co-author of the study and head of the Low Latitude Climate Variability group at MARUM. “Particularly noteworthy is the occurrence of another pronounced cooling for the 8th-9th centuries. Colder temperatures in the otherwise warm tropical ocean led to lower regional rainfall, which coincided with severe droughts in the Yucatan Peninsula and the decline of the Classic Maya culture.”

In addition, the researchers found that the cold climate anomalies in the subpolar North Atlantic and Europe were accompanied by weaker ocean circulation and increased salinity in the Caribbean. “Advection, or the movement of tropical salt to high northern latitudes, is essential for maintaining high surface densities in the subpolar North Atlantic. This is a prerequisite for the overall stability of the large-scale ocean circulation, including the transfer of warm Gulf Stream water, which is responsible for our mild temperatures in Europe,” says Dr Bauch.

The data on the historical past thus allow a reconstruction of the connection across the North Atlantic. Initial cooling can be caused by volcanic eruptions, low solar activity and feedbacks between sea ice and the ocean in the north. The new study provides evidence that a decrease in salt movement to high northern latitudes will amplify and prolong these climate events. Conversely, the slow movement of positive salinity anomalies from the tropics will eventually increase the density at the surface of the subpolar North Atlantic. This may favour the northward transport of heat by ocean currents, resulting in milder temperatures over Europe and North America.

“Such a salinity feedback is known from models and has been assumed for the Little Ice Age. However, in the absence of tropical ocean data, these assumptions have been based on less direct precipitation records,” says Dr Zhuravleva.

There is evidence that the Gulf Stream is weakening and that human-induced warming is a likely cause. What is certain is that the consequences of this change will be global. The extent to which the different climate mechanisms interact has been an open question. This study now confirms that the south-north transport of salt is a key factor in the processes involved.

Now, a new Harvard Medical School study published Nov. 3 in Science Immunology may offer a molecular explanation behind this century-old observation.

The study, done in mice, suggests that the beneficial effects of exercise may be driven, at least partly, by the immune system. It shows that muscle inflammation caused by exertion mobilizes inflammation-countering T cells, or Tregs, which enhance the muscles’ ability to use energy as fuel and improve overall exercise endurance.

Long known for their role in countering the aberrant inflammation linked to autoimmune diseases, Tregs now also emerge as key players in the body’s immune responses during exercise, the research team said.

“The immune system, and the T cell arm in particular, has a broad impact on tissue health that goes beyond protection against pathogens and controlling cancer. Our study demonstrates that the immune system exerts powerful effects inside the muscle during exercise,” said study senior investigator Diane Mathis, Morton Grove-Rasmussen Professor of Immunology in the Blavatnik Institute at HMS.

Mice are not people, and the findings remain to be replicated in further studies, the researchers cautioned. However, the study is an important step toward detailing the cellular and molecular changes that occur during exercise and confer health benefits.

Understanding the molecular underpinnings of exercise

Protecting from cardiovascular disease, reducing the risk of diabetes, shielding against dementia. The salutary effects of exercise are well established. But exactly how does exercise make us healthy? The question has intrigued researchers for a long time.

The new findings come amid intensifying efforts to understand the molecular underpinnings of exercises. Untangling the immune system’s involvement in this process is but one aspect of these research efforts.

“We’ve known for a long time that physical exertion causes inflammation, but we don’t fully understand the immune processes involved,” said study first author Kent Langston, a postdoctoral researcher in the Mathis lab. “Our study shows, at very high resolution, what T cells do at the site where exercise occurs, in the muscle.”

Most previous research on exercise physiology has focused on the role of various hormones released during exercise and their effects on different organs such as the heart and the lungs. The new study unravels the immunological cascade that unfolds inside the actual site of exertion — the muscle.

T cell heroes and inflammation-fueling villains

Exercise is known to cause temporary damage to the muscles, unleashing a cascade of inflammatory responses. It boosts the expression of genes that regulate muscle structure, metabolism, and the activity of mitochondria, the tiny powerhouses that fuel cell function. Mitochondria play a key role in exercise adaptation by helping cells meet the greater energy demand of exercise.

In the new study, the team analyzed what happens in cells taken from the hind-leg muscles of mice that ran on a treadmill once and animals that ran regularly. Then, the researchers compared them with muscle cells obtained from sedentary mice.

The muscle cells of the mice that ran on treadmills, whether once or regularly, showed classic signs of inflammation — greater activity in genes that regulate various metabolic processes and higher levels of chemicals that promote inflammation, including interferon.

Both groups had elevated levels of Treg cells in their muscles. Further analyses showed that in both groups, Tregs lowered exercise-induced inflammation. None of those changes were seen in the muscle cells of sedentary mice.

However, the metabolic and performance benefits of exercise were apparent only in the regular exercisers — the mice that had repeated bouts of running. In that group, Tregs not only subdued exertion-induced inflammation and muscle damage, but also altered muscle metabolism and muscle performance, the experiments showed. This finding aligns with well-established observations in humans that a single bout of exercise does not lead to significant improvements in performance and that regular activity over time is needed to yield benefits.

Further analyses confirmed that Tregs were, indeed, responsible for the broader benefits seen in regular exercisers. Animals that lacked Tregs had unrestrained muscle inflammation, marked by the rapid accumulation of inflammation-promoting cells in their hindleg muscles. Their muscle cells also had strikingly swollen mitochondria, a sign of metabolic abnormality.

More importantly, animals lacking Tregs did not adapt to increasing demands of exercise over time the way mice with intact Tregs did. They did not derive the same whole-body benefits from exercise and had diminished aerobic fitness.

These animals’ muscles also had excessive amounts of interferon, a known driver of inflammation. Further analyses revealed that interferon acts directly on muscle fibers to alter mitochondrial function and limit energy production. Blocking interferon prevented metabolic abnormalities and improved aerobic fitness in mice lacking Tregs.

“The villain here is interferon,” Langston said. “In the absence of guardian Tregs to counter it, interferon went on to cause uncontrolled damage.”

Interferon is known to promote chronic inflammation, a process that underlies many chronic diseases and age-related conditions and has become a tantalizing target for therapies aimed at reducing inflammation. Tregs have also captured the attention of scientists and industry as treatments for a range of immunologic conditions marked by abnormal inflammation.

The study findings provide a glimpse into the cellular innerworkings behind exercise’s anti-inflammatory effects and underscore its importance in harnessing the body’s own immune defenses, the researchers said.

There are efforts afoot to design interventions targeting Tregs in the context of specific immune-mediated diseases. And while immunologic conditions driven by aberrant inflammation require carefully calibrated therapies, exercise is yet another way to counter inflammation, the researchers said.

“Our research suggests that with exercise, we have a natural way to boost the body’s immune responses to reduce inflammation,” Mathis said. “We’ve only looked in the muscle, but it’s possible that exercise is boosting Treg activity elsewhere in the body as well.”