- Gondwanatherians were mammals that roamed present-day Madagascar.
- The new species likely resembled a badger and was about the size of a cat, which was relatively big for its time.
- The discovery highlights how isolation often leads to strange, evolutionarily distinct creatures.
After discovering an extraordinarily well-preserved fossil, scientists have classified a new species of extinct mammal: Adalatherium hui, or "crazy beast."
It's likely the most complete Gondwanatherian skeleton that's ever been discovered. Gondwanatheria is an extinct group of mammals that roamed the ancient supercontinent of Gondwana in the Southern Hemisphere 70 million years ago, during the Maastrichtian age of the Late Cretaceous.
Today, the land that was Gondwana is Madagascar. Like many large and isolated islands, Madagascar is known for its unique flora and fauna that have evolved over the ages since it separated from the Indian Plate about 88 million years ago.
Krause et al
The newly reported "crazy beast" species is unique, in part, for its weight: about 3 kilograms, or 6.6 pounds. That may seem small. But this badger-like creature would've been relatively big for its time, when most mammals that coexisted with dinosaurs were about the size of a mouse.
"Long isolated places produce very unique results in biology," Guillermo Rougier, a paleontologist at the University of Louisville and co-author of the paper, said in a press release. "These fossils keep reminding us of the unexpected forms and shapes that evolution can take over long periods of time in an isolated place."
ANDREY ATUCHIN
One such unexpected feature: a bone in its snout that had disappeared millions of years earlier in the ancestors of modern mammals.
"Knowing what we know about the skeletal anatomy of all living and extinct mammals, it is difficult to imagine that a mammal like Adalatherium could have evolved," vertebrate palaeontologist David Krause from the Denver Museum of Nature & Science, who helped discover the skeleton during an expedition in Madagascar in 1999, told Science Alert.
"It bends and even breaks a lot of rules."
Krause et al.
Adalatherium hui is also distinct for its teeth, which are arranged backward compared to all other mammals, suggesting the creature evolved from a remote ancestor uncommon to similar species.
Gondwanatherians were once thought to be related to modern sloths, anteaters and armadillos. But as lead study author Dr. David Krause told the New York Institute of Technology, this group of mammals is "now known to have been part of a grand evolutionary experiment doing their own thing, an experiment that failed and was snuffed out in the Eocene, about 45 million years ago."- Scientists Suspect Genetic Underpinnings to Human Monogamy ›
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Reactive oxygen species (ROS) accumulate in the gut of sleep-deprived fruit flies, one (left), seven (center) and ten (right) days without sleep.
- A study provides further confirmation that a prolonged lack of sleep can result in early mortality.
- Surprisingly, the direct cause seems to be a buildup of Reactive Oxygen Species in the gut produced by sleeplessness.
- When the buildup is neutralized, a normal lifespan is restored.
We don't have to tell you what it feels like when you don't get enough sleep. A night or two of that can be miserable; long-term sleeplessness is out-and-out debilitating. Though we know from personal experience that we need sleep — our cognitive, metabolic, cardiovascular, and immune functioning depend on it — a lack of it does more than just make you feel like you want to die. It can actually kill you, according to study of rats published in 1989. But why?
A new study answers that question, and in an unexpected way. It appears that the sleeplessness/death connection has nothing to do with the brain or nervous system as many have assumed — it happens in your gut. Equally amazing, the study's authors were able to reverse the ill effects with antioxidants.
The study, from researchers at Harvard Medical School (HMS), is published in the journal Cell.
An unexpected culprit
The new research examines the mechanisms at play in sleep-deprived fruit flies and in mice — long-term sleep-deprivation experiments with humans are considered ethically iffy.
What the scientists found is that death from sleep deprivation is always preceded by a buildup of Reactive Oxygen Species (ROS) in the gut. These are not, as their name implies, living organisms. ROS are reactive molecules that are part of the immune system's response to invading microbes, and recent research suggests they're paradoxically key players in normal cell signal transduction and cell cycling as well. However, having an excess of ROS leads to oxidative stress, which is linked to "macromolecular damage and is implicated in various disease states such as atherosclerosis, diabetes, cancer, neurodegeneration, and aging." To prevent this, cellular defenses typically maintain a balance between ROS production and removal.
"We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation," says senior study author Dragana Rogulja, admitting, "We were surprised to find it was the gut that plays a key role in causing death." The accumulation occurred in both sleep-deprived fruit flies and mice.
"Even more surprising," Rogulja recalls, "we found that premature death could be prevented. Each morning, we would all gather around to look at the flies, with disbelief to be honest. What we saw is that every time we could neutralize ROS in the gut, we could rescue the flies." Fruit flies given any of 11 antioxidant compounds — including melatonin, lipoic acid and NAD — that neutralize ROS buildups remained active and lived a normal length of time in spite of sleep deprivation. (The researchers note that these antioxidants did not extend the lifespans of non-sleep deprived control subjects.)
Image source: Tomasz Klejdysz/Shutterstock/Big Think
The experiments
The study's tests were managed by co-first authors Alexandra Vaccaro and Yosef Kaplan Dor, both research fellows at HMS.
You may wonder how you compel a fruit fly to sleep, or for that matter, how you keep one awake. The researchers ascertained that fruit flies doze off in response to being shaken, and thus were the control subjects induced to snooze in their individual, warmed tubes. Each subject occupied its own 29 °C (84F) tube.
For their sleepless cohort, fruit flies were genetically manipulated to express a heat-sensitive protein in specific neurons. These neurons are known to suppress sleep, and did so — the fruit flies' activity levels, or lack thereof, were tracked using infrared beams.
Starting at Day 10 of sleep deprivation, fruit flies began dying, with all of them dead by Day 20. Control flies lived up to 40 days.
The scientists sought out markers that would indicate cell damage in their sleepless subjects. They saw no difference in brain tissue and elsewhere between the well-rested and sleep-deprived fruit flies, with the exception of one fruit fly.
However, in the guts of sleep-deprived fruit flies was a massive accumulation of ROS, which peaked around Day 10. Says Vaccaro, "We found that sleep-deprived flies were dying at the same pace, every time, and when we looked at markers of cell damage and death, the one tissue that really stood out was the gut." She adds, "I remember when we did the first experiment, you could immediately tell under the microscope that there was a striking difference. That almost never happens in lab research."
The experiments were repeated with mice who were gently kept awake for five days. Again, ROS built up over time in their small and large intestines but nowhere else.
As noted above, the administering of antioxidants alleviated the effect of the ROS buildup. In addition, flies that were modified to overproduce gut antioxidant enzymes were found to be immune to the damaging effects of sleep deprivation.
The research leaves some important questions unanswered. Says Kaplan Dor, "We still don't know why sleep loss causes ROS accumulation in the gut, and why this is lethal." He hypothesizes, "Sleep deprivation could directly affect the gut, but the trigger may also originate in the brain. Similarly, death could be due to damage in the gut or because high levels of ROS have systemic effects, or some combination of these."
The HMS researchers are now investigating the chemical pathways by which sleep-deprivation triggers the ROS buildup, and the means by which the ROS wreak cell havoc.
"We need to understand the biology of how sleep deprivation damages the body so that we can find ways to prevent this harm," says Rogulja.
Referring to the value of this study to humans, she notes,"So many of us are chronically sleep deprived. Even if we know staying up late every night is bad, we still do it. We believe we've identified a central issue that, when eliminated, allows for survival without sleep, at least in fruit flies."
