Origins of the Black Death identified

Yersinia pestis illustration

The Black Death, the biggest pandemic of our history, was caused by the bacterium Yersinia pestis and lasted in Europe between the years 1346 and 1353. Despite the pandemic's immense demographic and societal impacts, its origins have long been elusive. Now, a multidisciplinary team of scientists, including researchers from the Max Planck Institute for Evolutionary Anthropology in Leipzig, the University of Tübingen, in Germany, and the University of Stirling, in the United Kingdom, have obtained and studied ancient Y. pestis genomes that trace the pandemic's origins to Central Asia.

In 1347, plague first entered the Mediterranean via trade ships transporting goods from the territories of the Golden Horde in the Black Sea. The disease then disseminated across Europe, the Middle East and northern Africa claiming up to 60 percent of the population in a large-scale outbreak known as the Black Death. This first wave further extended into a 500-year-long pandemic, the so-called Second Plague Pandemic, which lasted until the early 19th century.

The origins of the Second Plague Pandemic have long been debated. One of the most popular theories has supported its source in East Asia, specifically in China. To the contrary, the only so-far available archaeological findings come from Central Asia, close to Lake Issyk Kul, in what is now Kyrgyzstan. These findings show that an epidemic devastated a local trading community in the years 1338 and 1339. Specifically, excavations that took place almost 140 years ago revealed tombstones indicating that individuals died in those years of an unknown epidemic or "pestilence." Since their first discovery, the tombstones inscribed in Syriac language, have been a cornerstone of controversy among scholars regarding their relevance to the Black Death of Europe.

In this study, an international team of researchers analysed ancient DNA from human remains as well as historical and archaeological data from two sites that were found to contain "pestilence" inscriptions. The team's first results were very encouraging, as DNA from the plague bacterium, Yersinia pestis, was identified in individuals with the year 1338 inscribed on their tombstones. "We could finally show that the epidemic mentioned on the tombstones was indeed caused by plague," says Phil Slavin, one of the senior authors of the study and historian at the University of Sterling, UK.

Researchers found the Black Death's source strain

But could this have been the origin of the Black Death? Researchers have previously associated the Black Death's initiation with a massive diversification of plague strains, a so-called Big Bang event of plague diversity. But the exact date of this event could not be precisely estimated, and was thought to have happened sometime between the 10th and 14th centuries. The team now pieced together complete ancient plague genomes from the sites in Kyrgyzstan and investigated how they might relate with this Big Bang event. "We found that the ancient strains from Kyrgyzstan are positioned exactly at the node of this massive diversification event. In other words, we found the Black Death's source strain and we even know its exact date [meaning the year 1338]," says Maria Spyrou, lead author and researcher at the University of Tübingen.

But where did this strain come from? Did it evolve locally or did it spread in this region from elsewhere? Plague is not a disease of humans; the bacterium survives within wild rodent populations across the world, in so-called plague reservoirs. Hence, the ancient Central Asian strain that caused the 1338-1339 epidemic around Lake Issyk Kul must have come from one such reservoir. "We found that modern strains most closely related to the ancient strain are today found in plague reservoirs around the Tian Shan mountains, so very close to where the ancient strain was found. This points to an origin of Black Death's ancestor in Central Asia," explains Johannes Krause, senior author of the study and director at the Max Planck Institute for Evolutionary Anthropology.

Story Source: Science Daily

 

 

Organic bipolar transistor developed

 Prof. Karl Leo has been thinking about the realization of this component for more than 20 years, now it has become reality: His research group at the Institute for Applied Physics at the TU Dresden has presented the first highly efficient organic bipolar transistor. This opens up completely new perspectives for organic electronics -- both in data processing and transmission, as well as in medical technology applications. The results of the research work have now been published in the leading specialist journal Nature.

The invention of the transistor in 1947 by Shockley, Bardeen and Brattain at Bell Laboratories ushered in the age of microelectronics and revolutionized our lives. First, so-called bipolar transistors were invented, in which negative and positive charge carriers contribute to the current transport, unipolar field effect transistors were only added later. The increasing performance due to the scaling of silicon electronics in the nanometer range has immensely accelerated the processing of data. However, this very rigid technology is less suitable for new types of flexible electronic components, such as rollable TV displays or for medical applications on or even in the body.

For such applications, transistors made of organic, i.e. carbon-based semiconductors, have come into focus in recent years. Organic field effect transistors were introduced as early as 1986, but their performance still lags far behind silicon components.

A research group led by Prof. Karl Leo and Dr. Hans Kleemann at the TU Dresden has now succeeded for the first time in demonstrating an organic, highly efficient bipolar transistor. Crucial to this was the use of highly ordered thin organic layers. This new technology is many times faster than previous organic transistors, and for the first time the components have reached operating frequencies in the gigahertz range, i.e. more than a billion switching operations per second. Dr Shu-Jen Wang, who co-led the project with Dr. Michael Sawatzki, explains: "The first realization of the organic bipolar transistor was a great challenge, since we had to create layers of very high quality and new structures. However, the excellent parameters of the component reward these efforts!" Prof. Karl Leo adds: "We have been thinking about this device for 20 years and I am thrilled that we have now been able to demonstrate it with the novel highly ordered layers. The organic bipolar transistor and its potential open up completely new perspectives for organic electronics, since they also make demanding tasks in data processing and transmission possible." Conceivable future applications are, for example, intelligent patches equipped with sensors that process the sensor data locally and wirelessly communicate to the outside.

Old skins cells reprogrammed to regain youthful function

Close-up of human skin

What is regenerative medicine?

As we age, our cells' ability to function declines and the genome accumulates marks of ageing. Regenerative biology aims to repair or replace cells including old ones. One of the most important tools in regenerative biology is our ability to create 'induced' stem cells. The process is a result of several steps, each erasing some of the marks that make cells specialised. In theory, these stem cells have the potential to become any cell type, but scientists aren't yet able to reliably recreate the conditions to re-differentiate stem cells into all cell types.

Turning back time

The new method, based on the Nobel Prize winning technique scientists use to make stem cells, overcomes the problem of entirely erasing cell identity by halting reprogramming part of the way through the process. This allowed researchers to find the precise balance between reprogramming cells, making them biologically younger, while still being able to regain their specialised cell function.

In 2007, Shinya Yamanaka was the first scientist to turn normal cells, which have a specific function, into stem cells which have the special ability to develop into any cell type. The full process of stem cell reprogramming takes around 50 days using four key molecules called the Yamanaka factors. The new method, called 'maturation phase transient reprogramming', exposes cells to Yamanaka factors for just 13 days. At this point, age-related changes are removed and the cells have temporarily lost their identity. The partly reprogrammed cells were given time to grow under normal conditions, to observe whether their specific skin cell function returned. Genome analysis showed that cells had regained markers characteristic of skin cells (fibroblasts), and this was confirmed by observing collagen production in the reprogrammed cells.

Age isn't just a number

To show that the cells had been rejuvenated, the researchers looked for changes in the hallmarks of ageing. As explained by Dr Diljeet Gill, a postdoc in Wolf Reik's lab at the Institute who conducted the work as a PhD student: "Our understanding of ageing on a molecular level has progressed over the last decade, giving rise to techniques that allow researchers to measure age-related biological changes in human cells. We were able to apply this to our experiment to determine the extent of reprogramming our new method achieved."

Researchers looked at multiple measures of cellular age. The first is the epigenetic clock, where chemical tags present throughout the genome indicate age. The second is the transcriptome, all the gene readouts produced by the cell. By these two measures, the reprogrammed cells matched the profile of cells that were 30 years younger compared to reference data sets.

The potential applications of this technique are dependent on the cells not only appearing younger, but functioning like young cells too. Fibroblasts produce collagen, a molecule found in bones, skin tendons and ligaments, helping provide structure to tissues and heal wounds. The rejuvenated fibroblasts produced more collagen proteins compared to control cells that did not undergo the reprogramming process. Fibroblasts also move into areas that need repairing. Researchers tested the partially rejuvenated cells by creating an artificial cut in a layer of cells in a dish. They found that their treated fibroblasts moved into the gap faster than older cells. This is a promising sign that one day this research could eventually be used to create cells that are better at healing wounds.

In the future, this research may also open up other therapeutic possibilities; the researchers observed that their method also had an effect on other genes linked to age-related diseases and symptoms. The APBA2 gene, associated with Alzheimer's disease, and the MAF gene with a role in the development of cataracts, both showed changes towards youthful levels of transcription.

The mechanism behind the successful transient reprogramming is not yet fully understood, and is the next piece of the puzzle to explore. The researchers speculate that key areas of the genome involved in shaping cell identity might escape the reprogramming process.

 

Warming oceans are getting louder

 Climate change will significantly alter how sound travels underwater, potentially affecting natural soundscapes as well as accentuating human-generated noise, according to a new global study that identified future ocean "acoustic hotspots." These changes to ocean soundscapes could impact essential activities of marine life.

In warmer water, sound waves propagate faster and last longer before dying away.

"We calculated the effects of temperature, depth and salinity based on public data to model the soundscape of the future," said Alice Affatati, an bioacoustics researcher at the Memorial University of Newfoundland and Labrador in St. John's, Canada, and lead author of the new study, published today in Earth's Future, AGU's journal for interdisciplinary research on the past, present and future of our planet and its inhabitants. It is the first global-scale estimate of ocean sound speed linked to future climate.

Two hotspots, in the Greenland Sea and a patch of the northwestern Atlantic Ocean east of Newfoundland, can expect the most change at 50 and 500 meter depths, the new study projected. The average speed of sound is likely to increase by more than 1.5%, or approximately 25 meters per second (55 miles per hour) in these waters from the surface to depths of 500 meters (1,640 feet), by the end of the century, given continued high greenhouse gas emissions (RCP8.5).

"The major impact is expected in the Arctic, where we know already there is amplification of the effects of climate change now. Not all the Arctic, but one specific part where all factors play together to give a signal that, according to the model predictions, overcomes the uncertainty of the model itself," said author Stefano Salon, a researcher at the National Institute of Oceanography and Applied Geophysics in Trieste, Italy.

The ocean soundscape is a cacophony of vibrations produced by living organisms, natural phenomena like waves and cracking ice, and ship traffic and resource extraction. Sound speed at 50 meters depth ranges from 1,450 meters per second in the polar regions to 1,520 meters per second in equatorial waters (3,243 to 3,400 miles per hour, respectively).

Many marine animals use sound to communicate with each other and navigate their underwater world. Changing the sound speed can impact their ability to feed, fight, find mates, avoid predators and migrate, the authors said.

Changing soundscapes

In addition to the notable hotpots around Greenland and in the northwestern Atlantic Ocean, the new study found a 1% sound speed increase, more than 15 meters per second, at 50 m in the Barents Sea, northwestern Pacific, and in the Southern Ocean (between 0 and 70E), and at 500 m in the Arctic Ocean, Gulf of Mexico, and southern Caribbean Sea.

Temperature, pressure with increasing depth and salinity all affect how fast and how far sound travels in water. In the new study, the researchers focused on hotspots where the climate signal stood out clearly from the model uncertainty and was larger than seasonal variability.

The new study also modeled common vocalizations, under the projected future conditions, of the North Atlantic right whale, a critically endangered species inhabiting both north Atlantic acoustic hotspots. The whales' typical "upcall" at 50 Hertz is likely to propagate farther in a warmer future ocean, the researchers found.

"We chose to talk about one megafauna species, but many trophic levels in the ocean are affected by the soundscape or use sound," Affatati said. "All these hotspots are locations of great biodiversity."

Future work will combine the global soundscape with other maps of anthropogenic impacts in the oceans to pinpoint areas of combined stressors, or direct needed observational research

Scientists reveal how Venus fly trap plants snap shut

 

Venus fly trap

Scientists at Scripps Research have revealed the three-dimensional structure of Flycatcher1, an aptly named protein channel that may enable Venus fly trap plants to snap shut in response to prey. The structure of Flycatcher1, published February 14 in Nature Communications, helps shed light on longstanding questions about the remarkably sensitive touch response of Venus fly traps. The structure also gives the researchers a better understanding of how similar proteins in organisms including plants and bacteria, as well as proteins in the human body with similar functions (called mechanosensitive ion channels), might operate.

"Despite how different Venus fly traps are from humans, studying the structure and function of these mechanosensitive channels gives us a broader framework for understanding the ways that cells and organisms respond to touch and pressure," says co-senior author and Scripps Research professor Andrew Ward, PhD.

"Every new mechanosensitive channel that we study helps us make progress in understanding how these proteins can sense force and translate that to action and ultimately reveal more about human biology and health," adds co-senior author Ardem Patapoutian, PhD, a Scripps Research professor who won the Nobel Prize in Physiology or Medicine for research on the mechanosensitive channels that allow the body to sense touch and temperature.

Mechanosensitive ion channels are like tunnels that span the membranes of cells. When jostled by movement, the channels open, letting charged molecules rush across. In response, cells then alter their behavior -- a neuron might signal its neighbor, for instance. The ability for cells to sense pressure and movement is important for people's senses of touch and hearing, but also for many internal body processes -- from the ability of the bladder to sense that it's full to the ability of lungs to sense how much air is being breathed.

Previously, scientists had homed in on three ion channels in Venus fly traps thought to be related to the ability of the carnivorous plant to snap its leaves shut when its sensitive trigger hairs get touched. One, Flycatcher1, caught researchers' attention because its genetic sequence looked similar to a family of mechanosensitive channels, MscS, found in bacteria.

"The fact that variants of this channel are found throughout evolution tells us that it must have some fundamental, important functions that have been maintained in different types of organisms," says co-first author Sebastian Jojoa-Cruz, a graduate student at Scripps Research.

In the new study, the researchers used cryo-electron microscopy -- a cutting-edge technique that reveals the locations of atoms within a frozen protein sample -- to analyze the precise arrangement of molecules that form the Flycatcher1 protein channel in Venus fly trap plants. They found that Flycatcher1 is, in many ways, similar to bacterial MscS proteins -- seven groups of identical helices surrounding a central channel. But, unlike other MscS channels, Flycatcher1 has an unusual linker region extending outward from each group of helices. Like a switch, each linker can be flipped up or down. When the team determined the structure of Flycatcher1, they found six linkers in the down position, and just one flipped up.

"The architecture of Flycatcher1's channel core was similar to other channels that have been studied for years, but these linker regions were surprising," says Kei Saotome, PhD, a former postdoctoral research associate at Scripps Research and co-first author of the new paper.

To help elucidate the function of these switches, the researchers altered the linker to disrupt the up position. Flycatcher1, they found, no longer functioned as usual in response to pressure; the channel remained open for a longer duration when it would normally close upon removal of pressure.

"The profound effect of this mutation tells us that the conformations of these seven linkers is likely relevant for how the channel works," says co-senior author Swetha Murthy, PhD, of Vollum Institute at Oregon Health and Science University, a former postdoctoral research associate at Scripps Research.

Now that they solved the molecular structure, the research team is planning future studies on the function of Flycatcher1 to understand how different conformations affect its function. More work is also needed to determine whether Flycatcher1 is solely responsible for the snapping shut of Venus fly trap leaves, or whether other suspected channels play complementary roles.