The fossils include part of the Yutyrannus tail, and crucially, its skull. They reveal the sharp teeth and pointed head of a typical theropod – a carnivore that walked on its hind legs. Although smaller than its T.rex cousin, Yutyrannus weighed 1.4 tons and is by far the largest feathered dinosaur ever to have been discovered; 40 times heavier than Beipiaosaurus, the previously plumed record-holder.
The paper, published in Nature, raises intriguing questions as to why some of these scaly reptiles developed this ‘fuzzy down’-like plumage typical of a newly hatched duckling. The six inch long feathers of Yutyrannus were only simple filaments, certainly not adequate for flight, supporting the theory that they evolved for insulation. The surrounding soil dates back 125 million years to the mid-Cretaceous period; and this was thought to be a particularly chilly time. Although it is not known whether Yutyrannus was warm or cold blooded, even a thin insulating plumage could aid survival in these climates. Conversely, the feathers may have been used in mating displays, hinting at complex behaviours not traditionally associated with these terrifying lizards.
Feathers are notoriously hard to preserve in the fossil record, so the true extent of feathered dinosaurs may never be known. The sheer size of Yutyrannus however is decisive, as we can now say with confidence that feathers were not solely evolved for flight. Instead, evolution hijacked existing features of sexual selection or adaptations to the cold to propel dinosaurs into the skies.
Written by Zac Baynham-Herd
DOI:10.1038/nature10906










Feature: Coming of AGE – how molecular strategies may soon improve quality of life
The biological effects of aging are clear for all to see.
The average age of the British public is steadily rising. Life-expectancy has increased substantially in recent years, and this coupled to a decline in birth rate means that society now has more pensioners than teenagers.
The biological effects of aging are clear for all to see: the inevitable appearance of wrinkles, reduced mobility, increased incidence of arthritis and diabetes, reduced heart and kidney function and loss of sight. Most of these put a strain on global health services, as well as increasing dependence and the burden of care. But what if we could slow down the aging process? What if poor health did not have to go hand in hand with advancing years?
Many researchers have investigated the aging process and the ways in which it can be manipulated to better the quality of life in later years. A common feature of many of the afflictions associated with aging is reduced function in proteins that hold the cells and tissues of our body together. Many of these proteins have a life that spans tens of years. They are therefore subject to many chemical and enzymatic modifications that can affect their native function over time.
One such modification that is prevalent in old age is protein glycation. Glycation occurs when a sugar molecule – most frequently glucose – chemically reacts with a protein or its derivatives. The resulting protein modification is known as an Advanced Glycation End product (AGE). This AGE has the potential to chemically link itself to a second protein to form a cross-link that restricts flexibility and elasticity and thus reduces protein function.
The proteins that are most commonly damaged by glycation are those that are not recycled quickly by enzymes in the body. Protein recycling can keep cross-links in check as AGEs are destroyed with the protein. If this ‘turnover’ is very slow, however, glycation accumulates. The protein collagen is one such affected molecule as in some instances it may not be replaced within a lifetime. Collagen makes up 30 % of total protein in the body and forms the basis of many vital organs such as the heart, kidney and skin. Because of its ubiquity and age, collagen is very commonly subject to glycation in the elderly. Cross-linking of collagen can reduce elasticity of the skin or lead to the formation of cataracts in the eyes. It can also cause stiffness in the arteries and walls of the heart that may eventually lead to heart failure.
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