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Mongolia's 'Dragon Prince' dinosaur was forerunner of T. rex

Mongolia's 'Dragon Prince' dinosaur was forerunner of T. rex

The Star12-06-2025
This handout artist's illustration made available by University of Calgary on June 6, 2025, shows the newly discovered dinosaur species Khankhuuluu mongoliensis, an ancestor of Tyrannosaurus Rex. - AFP
WASHINGTON: A newly identified mid-sized dinosaur from Mongolia dubbed the "Dragon Prince" has been identified as a pivotal forerunner of Tyrannosaurus rex in an illuminating discovery that has helped clarify the famous predator's complicated family history.
Named Khankhuuluu mongoliensis, it lived roughly 86 million years ago during the Cretaceous Period and was an immediate precursor to the dinosaur lineage called tyrannosaurs, which included some of the largest meat-eating land animals in Earth's history, among them T. rex. Khankhuuluu predated Tyrannosaurus by about 20 million years.
It was about 4 metres long, weighed about 750 kg, walked on two legs and had a lengthy snout with a mouthful of sharp teeth. More lightly built than T. rex, its body proportions indicate Khankhuuluu was fleet-footed, likely chasing down smaller prey such as bird-like dinosaurs called oviraptorosaurs and ornithomimosaurs. The largest-known T. rex specimen is 12.3 metres.
Khankhuuluu means "Dragon Prince" in the Mongolian language. Tyrannosaurus rex means "tyrant king of the lizards."
"In the name, we wanted to capture that Khankhuuluu was a small, early form that had not evolved into a king. It was still a prince," said paleontologist Darla Zelenitsky of the University of Calgary in Canada, co-author of the study published on Wednesday in the journal Nature.
Tyrannosaurs and all other meat-eating dinosaurs are part of a group called theropods. Tyrannosaurs appeared late in the age of dinosaurs, roaming Asia and North America.
Khankhuuluu shared many anatomical traits with tyrannosaurs but lacked certain defining characteristics, showing it was a predecessor and not a true member of the lineage.
"Khankhuuluu was almost a tyrannosaur, but not quite. For example, the bone along the top of the snout and the bones around the eye are somewhat different from what we see in tyrannosaurs. The snout bone was hollow and the bones around the eye didn't have all the horns and bumps seen in tyrannosaurs," Zelenitsky said.
"Khankhuuluu had teeth like steak knives, with serrations along both the front and back edges. Large tyrannosaurs had conical teeth and massive jaws that allowed them to bite with extreme force then hold in order to subdue very large prey. Khankhuuluu's more slender teeth and jaws show this animal took slashing bites to take down smaller prey," Zelenitsky added.
The researchers figured out its anatomy based on fossils of two Khankhuuluu individuals dug up in the 1970s but only now fully studied. These included parts of its skull, arms, legs, tail and back bones.
The Khankhuuluu remains, more complete than fossils of other known tyrannosaur forerunners, helped the researchers untangle this lineage's evolutionary history. They concluded that Khankhuuluu was the link between smaller forerunners of tyrannosaurs and later true tyrannosaurs, a transitional animal that reveals how these meat-eaters evolved from speedy and modestly sized species into giant apex predators.
"What started as the discovery of a new species ended up with us rewriting the family history of tyrannosaurs," said University of Calgary doctoral student and study lead author Jared Voris. "Before this, there was a lot of confusion about who was related to who when it came to tyrannosaur species."
Some scientists had hypothesized that smaller tyrannosaurs like China's Qianzhousaurus - dubbed "Pinnochio-rexes" because of their characteristic long snouts - reflected the lineage's ancestral form. That notion was contradicted by the fact that tyrannosaur forerunner Khankhuuluu differed from them in important ways.
"The tyrannosaur family didn't follow a straightforward path where they evolved from small size in early species to larger and larger sizes in later species," Zelenitsky said.
Voris noted that Khankhuuluu demonstrates that the ancestors to the tyrannosaurs lived in Asia.
"Around 85 million years ago, these tyrannosaur ancestors crossed a land bridge connecting Siberia and Alaska and evolved in North America into the apex predatory tyrannosaurs," Voris said.
One line of North American tyrannosaurs later trekked back to Asia and split into two branches - the "Pinnochio-rexes" and massive forms like Tarbosaurus, the researchers said. These apex predators then spread back to North America, they said, paving the way for the appearance of T. rex. Tyrannosaurus ruled western North America at the end of the age of dinosaurs when an asteroid struck Earth 66 million years ago.
"Khankhuuluu was where it all started but it was still only a distant ancestor of T. rex, at nearly 20 million years older," Zelenitsky said. "Over a dozen tyrannosaur species evolved in the time between them. It was a great-great-great uncle, sort of." - Reuters
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Scientists use artificial intelligence to mimic the mind — warts and all

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Scientists use artificial intelligence to mimic the mind — warts and all

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Did a lab of AI 'scientists' design a possible Covid-19 treatment?
Did a lab of AI 'scientists' design a possible Covid-19 treatment?

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time4 days ago

  • The Star

Did a lab of AI 'scientists' design a possible Covid-19 treatment?

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Cancer's secret weapon to evade death
Cancer's secret weapon to evade death

The Star

time19-07-2025

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Cancer's secret weapon to evade death

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Studies have also found lipids are somehow involved in ferroptosis, a type of cell death discovered in 2012. A portmanteau of 'ferrous', the Latin word for iron, and apoptosis, the scientific word for programmed cell death, ferroptosis happens when a build-up of toxic molecules called oxidants and iron overwhelms a cell, causing it to essentially rust from the inside out. 'Oxidants damage the lipids that are forming the membranes (of) a cell,' Asst Prof Garcia-Bermudez said. 'What's interesting is that cancer cells tend to produce more oxidants than normal cells,' he added, noting that there's been interest in understanding why some cancers are more susceptible to this type of damage and in using ferroptosis to kill cancer cells. GAG-ging cancer cells The crafty masters of survival that they are, cancer cells have devised ways to dodge ferroptosis. Unraveling the reason why put Asst Prof Garcia-Bermudez and his lab on a four-year journey of scientific inquiry. One of the researchers' first findings, after screening 200 metabolic genes linked to cancer, was that an enzyme called glutathione peroxidase 4 was active in tumours. This wasn't a new discovery: Studies have shown that this enzyme, which can stop lipids from degrading, plays a pivotal role in controlling ferroptosis. When glutathione peroxidase 4 was erased from a cancer cell's genome, the tumour would die, unless it was given a drug blocking ferroptosis or fed lipoproteins. 'That was a clue that lipoproteins were somehow related to ferroptosis,' said study co-author and UT Southwestern Medical Center's Eugene McDermott Center for Human Growth and Development director Prof Dr Ralph DeBerardinis. In a battery of experiments that included depriving cancer cells in petri dishes of lipoproteins and exposing them to different antioxidants, the full picture began to be unveiled. Cancer cells were intercepting lipoproteins – particularly those bearing vitamin E, a fat-soluble antioxidant – from their surrounding environment. Like a fisherman with a fishing line, cancer cells accomplished this not with the usual reels used to catch lipoproteins, but with the long, flowy sugar chains known as GAGs. These molecules are attached to a cancer cell surface through another molecule called a ­proteoglycan. When the scientists blocked the biochemical pathway responsible for manufacturing GAGs, this limited a lab-grown cancer cell's access to vitamin E and made it more vulnerable to ferroptosis. In mice grafted with cancer cells, cutting off the pathway slowed tumour growth. The researchers also examined 20 tumours donated by patients with clear cell renal carcinoma, the most common type of kidney cancer. These tumours had higher levels of GAGs and vitamin E – about 15 times more of the latter – compared to normal kidney tissue. Disrupting the biochemical pathway producing GAGs prevented kidney cancer cells from devouring vitamin E-laden lipoproteins, resulting in them dying by the iron hand of ferroptosis. Much more to be done Asst Prof Garcia-Bermudez and Prof DeBerardinis caution that there is much more research to be done before their study's findings have any clinical application for treating cancer. 'We know that GAGS are on the surface, they speak to the lipoproteins and they affect the uptake of lipoproteins,' Asst Prof Garcia-Bermudez said. 'But how mechanistically this happens, especially in the cancer cell, hasn't been shown before. 'If we understand how this works and we find molecular targets that maybe we can treat with drugs and block, then we have a way to specifically deplete vitamin E in the tumour.' Prof DeBerardinis said that the research does not suggest any association between dietary vitamin E and cancer risk, or how vitamin E levels correlate with cancer patient outcomes. 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'Our study is really exciting, but at the same time, it's a very basic discovery,' Asst Prof Garcia-Bermudez said. 'It was incredible to discover something that people have not observed in cancer before, to understand why these tumours are so resistant. I'm super excited to keep working on this.' – By Miriam Fauzia/The Dallas Morning News/tca/dpa

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