Small galaxies likely played important role in evolution of the Universe

 A new study led by University of Minnesota astrophysicists shows that high-energy light from small galaxies may have played a key role in the early evolution of the Universe. The research gives insight into how the Universe became reionized, a problem that astronomers have been trying to solve for years.

The research is published in The Astrophysical Journal, a peer-reviewed scientific journal of astrophysics and astronomy.

After the Big Bang, when the Universe was formed billions of years ago, it was in an ionized state. This means that the electrons and protons floated freely throughout space. As the Universe expanded and started cooling down, it changed to a neutral state when the protons and electrons combined into atoms, akin to water vapor condensing into a cloud.

Now however, scientists have observed that the Universe is back in an ionized state. A major endeavor in astronomy is figuring out how this happened. Astronomers have theorized that the energy for reionization must have come from galaxies themselves. But, it's incredibly hard for enough high energy light to escape a galaxy due to hydrogen clouds within it that absorb the light, much like clouds in the Earth's atmosphere absorb sunlight on an overcast day.

Astrophysicists from the Minnesota Institute for Astrophysics in the University of Minnesota's College of Science and Engineering may have found the answer to that problem. Using data from the Gemini telescope, the researchers have observed the first ever galaxy in a "blow-away" state, meaning that the hydrogen clouds have been removed, allowing the high energy light to escape. The scientists suspect that the blow-away was caused by many supernovas, or dying stars, exploding in a short period of time.

"The star-formation can be thought of as blowing up the balloon," explained Nathan Eggen, the paper's lead author who recently received his master's degree in astrophysics from the University of Minnesota. "If, however, the star-formation was more intense, then there would be a rupture or hole made in the surface of the balloon to let out some of that energy. In the case of this galaxy, the star-formation was so powerful that the balloon was torn to pieces, completely blown-away."

The galaxy, named Pox 186, is so small that it could fit inside the Milky Way. The researchers suspect that its compact size, coupled with its large population of stars -- which amount to a hundred thousand times the mass of the sun -- made the blow-away possible.

The findings confirm that a blow-away is possible, furthering the idea that small galaxies were primarily responsible for the reionization of the Universe and giving more insight into how the Universe became what it is today.

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Move over CRISPR, the Retrons are coming

Researchers have created a new gene editing tool called Retron Library Recombineering (RLR) that can generate up to millions of mutations simultaneously, and 'barcodes' mutant bacterial cells so that the entire pool can be screened at once. It can be used in contexts where CRISPR is toxic or not feasible, and results in better editing rates.

While the CRISPR-Cas9 gene editing system has become the poster child for innovation in synthetic biology, it has some major limitations. CRISPR-Cas9 can be programmed to find and cut specific pieces of DNA, but editing the DNA to create desired mutations requires tricking the cell into using a new piece of DNA to repair the break. This bait-and-switch can be complicated to orchestrate, and can even be toxic to cells because Cas9 often cuts unintended, off-target sites as well.

Alternative gene editing techniques called recombineering instead perform this bait-and-switch by introducing an alternate piece of DNA while a cell is replicating its genome, efficiently creating genetic mutations without breaking DNA. These methods are simple enough that they can be used in many cells at once to create complex pools of mutations for researchers to study. Figuring out what the effects of those mutations are, however, requires that each mutant be isolated, sequenced, and characterized: a time-consuming and impractical task.

Researchers at the Wyss Institute for Biologically Inspired Engineering at Harvard University and Harvard Medical School (HMS) have created a new gene editing tool called Retron Library Recombineering (RLR) that makes this task easier. RLR generates up to millions of mutations simultaneously, and "barcodes" mutant cells so that the entire pool can be screened at once, enabling massive amounts of data to be easily generated and analyzed. The achievement, which has been accomplished in bacterial cells, is described in a recent paper in PNAS.

"RLR enabled us to do something that's impossible to do with CRISPR: we randomly chopped up a bacterial genome, turned those genetic fragments into single-stranded DNA in situ, and used them to screen millions of sequences simultaneously," said co-first author Max Schubert, Ph.D., a postdoc in the lab of Wyss Core Faculty member George Church, Ph.D. "RLR is a simpler, more flexible gene editing tool that can be used for highly multiplexed experiments, which eliminates the toxicity often observed with CRISPR and improves researchers' ability to explore mutations at the genome level."

Retrons: from enigma to engineering tool

Retrons are segments of bacterial DNA that undergo reverse transcription to produce fragments of single-stranded DNA (ssDNA). Retrons' existence has been known for decades, but the function of the ssDNA they produce flummoxed scientists from the 1980s until June 2020, when a team finally figured out that retron ssDNA detects whether a virus has infected the cell, forming part of the bacterial immune system.

While retrons were originally seen as simply a mysterious quirk of bacteria, researchers have become more interested in them over the last few years because they, like CRISPR, could be used for precise and flexible gene editing in bacteria, yeast, and even human cells.

"For a long time, CRISPR was just considered a weird thing that bacteria did, and figuring out how to harness it for genome engineering changed the world. Retrons are another bacterial innovation that might also provide some important advances," said Schubert. His interest in retrons was piqued several years ago because of their ability to produce ssDNA in bacteria -- an attractive feature for use in a gene editing process called oligonucleotide recombineering.

Recombination-based gene editing techniques require integrating ssDNA containing a desired mutation into an organism's DNA, which can be done in one of two ways. Double-stranded DNA can be physically cut (with CRISPR-Cas9, for example) to induce the cell to incorporate the mutant sequence into its genome during the repair process, or the mutant DNA strand and a single-stranded annealing protein (SSAP) can be introduced into a cell that is replicating so that the SSAP incorporates the mutant strand into the daughter cells' DNA.

"We figured that retrons should give us the ability to produce ssDNA within the cells we want to edit rather than trying to force them into the cell from the outside, and without damaging the native DNA, which were both very compelling qualities," said co-first author Daniel Goodman, Ph.D., a former Graduate Research Fellow at the Wyss Institute who is now a Jane Coffin Childs Postdoctoral Fellow at UCSF.

Another attraction of retrons is that their sequences themselves can serve as "barcodes" that identify which individuals within a pool of bacteria have received each retron sequence, enabling dramatically faster, pooled screens of precisely-created mutant strains.

To see if they could actually use retrons to achieve efficient recombineering with retrons, Schubert and his colleagues first created circular plasmids of bacterial DNA that contained antibiotic resistance genes placed within retron sequences, as well as an SSAP gene to enable integration of the retron sequence into the bacterial genome. They inserted these retron plasmids into E. coli bacteria to see if the genes were successfully integrated into their genomes after 20 generations of cell replication. Initially, less than 0.1% of E. coli bearing the retron recombineering system incorporated the desired mutation.

To improve this disappointing initial performance, the team made several genetic tweaks to the bacteria. First, they inactivated the cells' natural mismatch repair machinery, which corrects DNA replication errors and could therefore be "fixing" the desired mutations before they were able to be passed on to the next generation. They also inactivated two bacterial genes that code for exonucleases -- enzymes that destroy free-floating ssDNA. These changes dramatically increased the proportion of bacteria that incorporated the retron sequence, to more than 90% of the population.

Name tags for mutants

Now that they were confident that their retron ssDNA was incorporated into their bacteria's genomes, the team tested whether they could use the retrons as a genetic sequencing "shortcut," enabling many experiments to be performed in a mixture. Because each plasmid had its own unique retron sequence that can function as a "name tag," they reasoned that they should be able to sequence the much shorter retron rather than the whole bacterial genome to determine which mutation the cells had received.

First, the team tested whether RLR could detect known antibiotic resistance mutations in E coli. They found that it could -- retron sequences containing these mutations were present in much greater proportions in their sequencing data compared with other mutations. The team also determined that RLR was sensitive and precise enough to measure small differences in resistance that result from very similar mutations. Crucially, gathering these data by sequencing barcodes from the entire pool of bacteria rather than isolating and sequencing individual mutants, dramatically speeds up the process.

Then, the researchers took RLR one step further to see if it could be used on randomly-fragmented DNA, and find out how many retrons they could use at once. They chopped up the genome of a strain of E. coli highly resistant to another antibiotic, and used those fragments to build a library of tens of millions of genetic sequences contained within retron sequences in plasmids. "The simplicity of RLR really shone in this experiment, because it allowed us to build a much bigger library than what we can currently use with CRISPR, in which we have to synthesize both a guide and a donor DNA sequence to induce each mutation," said Schubert.

This library was then introduced into the RLR-optimized E coli strain for analysis. Once again, the researchers found that retrons conferring antibiotic resistance could be easily identified by the fact that they were enriched relative to others when the pool of bacteria was sequenced.

"Being able to analyze pooled, barcoded mutant libraries with RLR enables millions of experiments to be performed simultaneously, allowing us to observe the effects of mutations across the genome, as well as how those mutations might interact with each other," said senior author George Church, who leads the Wyss Institute's Synthetic Biology Focus Area and is also a Professor of Genetics at HMS. "This work helps establish a road map toward using RLR in other genetic systems, which opens up many exciting possibilities for future genetic research."

Another feature that distinguishes RLR from CRISPR is that the proportion of bacteria that successfully integrate a desired mutation into their genome increases over time as the bacteria replicate, whereas CRISPR's "one shot" method tends to either succeed or fail on the first try. RLR could potentially be combined with CRISPR to improve its editing performance, or could be used as an alternative in the many systems in which CRISPR is toxic.

More work remains to be done on RLR to improve and standardize editing rate, but excitement is growing about this new tool. RLR's simple, streamlined nature could enable the study of how multiple mutations interact with each other, and the generation of a large number of data points that could enable the use of machine learning to predict further mutational effects.

"This new synthetic biology tool brings genome engineering to an even higher levels of throughput, which will undoubtedly lead to new, exciting, and unexpected innovations," said Don Ingber, M.D., Ph.D., the Wyss Institute's Founding Director. Ingber is also the Judah Folkman Professor of Vascular Biology at HMS and Boston Children's Hospital, and Professor of Bioengineering at the Harvard John A. Paulson School of Engineering and Applied Sciences.

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Asteroid that hit Botswana in 2018 likely came from Vesta, scientists say

An international team of researchers searched for pieces of a small asteroid tracked in space and then observed to impact Botswana on June 2, 2018. Guided by SETI Institute meteor astronomer Peter Jenniskens, they found 23 meteorites deep inside the Central Kalahari Game Reserve and now have published their findings online in the journal Meteoritics and Planetary Science.

"Combining the observations of the small asteroid in space with information gleaned from the meteorites shows it likely came from Vesta, second largest asteroid in our Solar System and target of NASA's DAWN mission," said Jenniskens. "Billions of years ago, two giant impacts on Vesta created a family of larger, more dangerous asteroids. The newly recovered meteorites gave us a clue on when those impacts might have happened."

The asteroid

The small asteroid that impacted Botswana, called 2018 LA, was first spotted by the University of Arizona's Catalina Sky Survey as a faint point of light moving among the stars. The Catalina Sky Survey searches for Earth-crossing asteroids as part of NASA's Planetary Defense program.

"Small meter-sized asteroids are no danger to us, but they hone our skills in detecting approaching asteroids," said Eric Christensen, director of the Catalina Sky Survey program.

The team recovered archival data from the SkyMapper Southern Survey program in Australia that showed the asteroid spinning in space, rotating once every 4 minutes, alternatingly presenting a broad and a narrow side to us while reflecting the sunlight.

On its journey to Earth, cosmic rays bombarded the asteroid and created radioactive isotopes. By analyzing those isotopes, the researchers determined that 2018 LA was a solid rock about 1.5 m in size, which reflected about 25% of sunlight.

The recovery

"This is only the second time we have spotted an asteroid in space before it hit Earth over land," said Jenniskens. "The first was asteroid 2008 TC3 in Sudan ten years earlier." Jenniskens also guided the search for fragments of 2008 TC3.

This time, fewer observations led to more uncertainty in the asteroid's position in its orbit. Davide Farnocchia of NASA JPL's Center for Near-Earth Object Studies combined astronomical observations of the asteroid with US Government Satellite data of the fireball to calculate the fall area. Esko Lyytinen of the Ursa Finnish Fireball Network made a parallel effort.

"When Jenniskens first arrived in Maun, he needed our help narrowing down the fall area," says Oliver Moses of the Okavango Research Institute. "We subsequently tracked down more video records in Rakops and Maun and were able to triangulate the position of the fireball."

After confirming the fall area, Moses and Jenniskens joined geologist Alexander Proyer of the Botswana International University of Science and Technology (BIUST) in Palapye and geoscientist Mohutsiwa Gabadirwe of the Botswana Geoscience Institute (BGI) in Lobatse and their colleagues to search for the meteorites.

"On the fifth day, our last day of searching, Lesedi Seitshiro of BIUST found the first meteorite only 30 meters from camp," said Jenniskens. "It was 18 grams and about 3 cm in size."

The search area was in the Central Kalahari Game Reserve, home to diverse wildlife, including leopards and lions. Researchers were kept safe by the staff of the Botswana Department of Wildlife and National Parks. BGI coordinated the search with the Department of National Museum and Monuments in Botswana.

"The meteorite is named 'Motopi Pan' after a local watering hole," said Gabadirwe, now the curator of this rare sample of an asteroid observed in space before impacting Earth. "This meteorite is a national treasure of Botswana."

The meteorite type

Non-destructive analysis at the University of Helsinki, Finland, showed that Motopi Pan belongs to the group of Howardite-Eucrite-Diogenite (HED) meteorites, known to have likely originated from the giant asteroid Vesta, which was recently studied in detail by NASA's DAWN mission.

"We managed to measure metal content as well as secure a reflectance spectrum and X-ray elemental analysis from a thinly crusted part of the exposed meteorite interior," said Tomas Kohout of the University of Helsinki. "All the measurements added well together and pointed to values typical for HED type meteorites."

Dynamical studies show that the orbit of 2018 LA is consistent with an origin from the inner part of the asteroid belt where Vesta is located. The asteroid was delivered into an Earth-impacting orbit via the resonance situated in the asteroid belt's inner side.

"Another HED meteorite fall we investigated in Turkey in 2015, called Sariçiçek, impacted on a similarly short orbit and produced mostly smallish 2 to 5-gram meteorites," said Jenniskens.

When Jenniskens returned to Botswana in October of 2018, the team found 22 more small meteorites. Gabadirwe was the first to spot another out-of-this-world rock. Surprisingly, subsequent meteorite finds showed a lot of diversity in their outward appearance.

"We studied the petrography and mineral chemistry of five of these meteorites and confirmed that they belong to the HED group," said Roger Gibson of Witts University in Johannesburg, South Africa. "Overall, we classified the material that asteroid 2018 LA contained as being Howardite, but some individual fragments had more affinity to Diogenites and Eucrites."

Other studies also confirmed the surprising diversity of the team's finds, such as reflection spectroscopy and the content of polyaromatic hydrocarbons in the sample. The asteroid was a breccia, a mixture of cemented rock pieces from different parts on Vesta.

Origin of the meteorites

A previous hypothesis proposed that Sariçiçek originated from Vesta in the collision that created the Antonia impact crater imaged by DAWN. Still showing a visible ejecta blanket, that young crater was formed about 22 million years ago. One-third of all HED meteorites that fall on Earth were ejected 22 million years ago. Did Motopi Pan originate from the same crater?

"Noble gas isotopes measurements at ETH in Zürich, Switzerland, and radioactive isotopes measured at Purdue University showed that this meteorite too had been in space as a small object for about 23 million years," said Kees Welten of UC Berkeley, "but give or take 4 million years, so it could be from the same source crater on Vesta."

Researchers found Motopi Pan and Sariçiçek to be similar in some ways but different in others. Like Motopi Pan, Sariçiçek exploded at 27.8 km altitude, but produced less light in that breakup.

"The infrasound shockwave measured in South Africa was not as strong as expected from US Government sensor detections of the bright light," said Peter Brown of the University of Western Ontario, Canada.

From lead isotopes in zircon minerals, researchers found that both Sariçiçek and Motopi Pan solidified at Vesta's surface about 4563 million years ago. But phosphate grains in Motopi Pan experienced another melting event more recently. Sariçiçek did not.

"About 4234 million years ago, the material in Motopi Pan was close to the center of a large impact event," said Qing-zhu Yin of UC Davis, "Sariçiçek was not."

Vesta experienced two significant impact events that created the Rheasilvia impact basin and the underlying, and therefore older, Veneneia impact basin.

"We now suspect that Motopi Pan was heated by the Veneneia impact, while the subsequent Rheasilvia impact scattered this material around," said Jenniskens. " If so, that would date the Veneneia impact to about 4234 million years ago. On top of Rheasilvia impact ejecta is the 10.3-km diameter Rubria impact crater, slightly smaller than the 16.7-km Antonia crater, and slightly younger at 19 +/- 3 million years, but a good candidate for the origin crater of Motopi Pan."

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Molecular biologists travel back in time 3 billion years

A research group working at Uppsala University has succeeded in studying 'translation factors' -- important components of a cell's protein synthesis machinery -- that are several billion years old. By studying these ancient 'resurrected' factors, the researchers were able to establish that they had much broader specificities than their present-day, more specialised counterparts.

In order to survive and grow, all cells contain an in-house protein synthesis factory. This consists of ribosomes and associated translation factors that work together to ensure that the complex protein production process runs smoothly. While almost all components of the modern translational machinery are well known, until now scientists did not know how the process evolved.

The new study, published in the journal Molecular Biology and Evolution, took the research group led by Professor Suparna Sanyal of the Department of Cell and Molecular Biology on an epic journey back into the past. A previously published study used a special algorithm to predict DNA sequences of ancestors of an important translation factor called elongation factor thermo-unstable, or EF-Tu, going back billions of years. The Uppsala research group used these DNA sequences to resurrect the ancient bacterial EF-Tu proteins and then to study their properties.

The researchers looked at several nodes in the evolutionary history of EF-Tu. The oldest proteins they created were approximately 3.3 billion years old.

"It was amazing to see that the ancestral EF-Tu proteins matched the geological temperatures prevailing on Earth in their corresponding time periods. It was much warmer 3 billion years ago and those proteins functioned well at 70°C, while 300 million year old proteins were only able to withstand 50°C," says Suparna Sanyal.

The researchers were able to demonstrate that the ancient elongation factors are compatible with various types of ribosome and therefore can be classified as 'generalists', whereas their modern descendants have evolved to fulfil 'specialist' functions. While this makes them more efficient, they require specific ribosomes in order to function properly. The results also suggest that ribosomes probably evolved their RNA core before the other associated translation factors.

"The fact that we now know how protein synthesis evolved up to this point makes it possible for us to model the future. If the translation machinery components have already evolved to such a level of specialisation, what will happen in future, for example, in the case of new mutations?" ponders Suparna Sanyal.

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New law of physics helps humans and robots grasp the friction of touch

Although robotic devices are used in everything from assembly lines to medicine, engineers have a hard time accounting for the friction that occurs when those robots grip objects -- particularly in wet environments. Researchers have now discovered a new law of physics that accounts for this type of friction, which should advance a wide range of robotic technologies.

"Our work here opens the door to creating more reliable and functional haptic and robotic devices in applications such as telesurgery and manufacturing," says Lilian Hsiao, an assistant professor of chemical and biomolecular engineering at North Carolina State University and corresponding author of a paper on the work.

At issue is something called elastohydrodynamic lubrication (EHL) friction, which is the friction that occurs when two solid surfaces come into contact with a thin layer of fluid between them. This would include the friction that occurs when you rub your fingertips together, with the fluid being the thin layer of naturally occurring oil on your skin. But it could also apply to a robotic claw lifting an object that has been coated with oil, or to a surgical device that is being used inside the human body.

One reason friction is important is because it helps us hold things without dropping them.

"Understanding friction is intuitive for humans -- even when we're handling soapy dishes," Hsiao says. "But it is extremely difficult to account for EHL friction when developing materials that controls grasping capabilities in robots."

To develop materials that help control EHL friction, engineers would need a framework that can be applied uniformly to a wide variety of patterns, materials and dynamic operating conditions. And that is exactly what the researchers have discovered.

"This law can be used to account for EHL friction, and can be applied to many different soft systems -- as long as the surfaces of the objects are patterned," Hsiao says.

In this context, surface patterns could be anything from the slightly raised surfaces on the tips of our fingers to grooves in the surface of a robotic tool.

The new physical principle, developed jointly by Hsiao and her graduate student Yunhu Peng, makes use of four equations to account for all of the physical forces at play in understanding EHL friction. In the paper, the research team demonstrated the law in three systems: human fingers; a bio-inspired robotic fingertip; and a tool called a tribo-rheometer, which is used to measure frictional forces. Peng is first author of the paper.

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How does the brain flexibly process complex information?

Human decision-making depends on the flexible processing of complex information, but how the brain may adapt processing to momentary task demands has remained unclear. In a new article published in the journal Nature Communications, researchers from the Max Planck Institute for Human Development have now outlined several crucial neural processes revealing that our brain networks may rapidly and flexibly shift from a rhythmic to a "noisy" state when the need to process information increases.

Driving a car, deliberating over different financial options, or even pondering different life paths requires us to process an overwhelming amount of information. But not all decisions pose equal demands. In some situations, decisions are easier because we already know which pieces of information are relevant. In other situations, uncertainty about which information is relevant for our decision requires us to get a broader picture of all available information sources. The mechanisms by which the brain flexibly adapts information processing in such situations were previously unknown.

To reveal these mechanisms, researchers from the Lifespan Neural Dynamics Group (LNDG) at the Max Planck Institute for Human Development and the Max Planck UCL Centre for Computational Psychiatry and Ageing Research designed a visual task. Participants were asked to view a moving cloud of small squares that differed from each other along the four visual dimensions: color, size, brightness, and movement direction. Participants were then asked a question about one of the four visual dimensions. For example, "Were more squares moving to the left, or right?." Prior to seeing the squares, the study authors manipulated "uncertainty" by informing participants which feature(s) they could be asked about; the more features that were relevant, the more uncertain participants were expected to become about which features to focus upon. Throughout the task, brain activity was measured using electroencephalography (EEG) and functional magnetic resonance imaging (fMRI).

First, the authors found that when participants were more uncertain about the relevant feature in the upcoming choice, participants' EEG signals shifted from a rhythmic mode (present when participants could focus on a single feature) to a more arrhythmic, "noisy" mode. "Brain rhythms may be particularly useful when we need to select relevant over irrelevant inputs, while increased neural 'noise' could make our brains more receptive to multiple sources of information. Our results suggest that the ability to shift back and forth between these rhythmic and 'noisy' states may enable flexible information processing in the human brain," says Julian Q. Kosciessa, LNDG post-doc and the article's first author.

Additionally, the authors found that the extent to which participants shifted from a rhythmic to a noisy mode in their EEG signals was dominantly coupled with increased fMRI activity in the thalamus, a deep brain structure largely inaccessible by EEG. The thalamus is often thought of primarily as an interface for sensory and motor signals, while its potential role in flexibility has remained elusive. The findings of the study may thus have broad implications for our current understanding of the brain structures required for us to adapt to an ever-changing world. "When neuroscientists think about how the brain enables behavioral flexibility, we often focus exclusively on networks in the cortex, while the thalamus is traditionally considered a simple relay for sensorimotor information. Instead, our results argue that the thalamus may support neural dynamics in general and could optimize brain states according to environmental demands, allowing us to make better decisions," says Douglas Garrett, senior author of the study and LNDG group leader.

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Black hole-neutron star collisions may help settle dispute over Universe's expansion

Studying the violent collisions of black holes and neutron stars may soon provide a new measurement of the Universe's expansion rate, helping to resolve a long-standing dispute, suggests a new simulation study led by researchers at UCL (University College London).

Our two current best ways of estimating the Universe's rate of expansion - measuring the brightness and speed of pulsating and exploding stars, and looking at fluctuations in radiation from the early Universe - give very different answers, suggesting our theory of the Universe may be wrong.

A third type of measurement, looking at the explosions of light and ripples in the fabric of space caused by black hole-neutron star collisions, should help to resolve this disagreement and clarify whether our theory of the Universe needs rewriting.

The new study, published in Physical Review Letters, simulated 25,000 scenarios of black holes and neutron stars colliding, aiming to see how many would likely be detected by instruments on Earth in the mid- to late-2020s.

The researchers found that, by 2030, instruments on Earth could sense ripples in space-time caused by up to 3,000 such collisions, and that for around 100 of these events, telescopes would also see accompanying explosions of light.

They concluded that this would be enough data to provide a new, completely independent measurement of the Universe's rate of expansion, precise and reliable enough to confirm or deny the need for new physics.

Lead author Dr Stephen Feeney (UCL Physics & Astronomy) said: "A neutron star is a dead star, created when a very large star explodes and then collapses, and it is incredibly dense - typically 10 miles across but with a mass up to twice that of our Sun. Its collision with a black hole is a cataclysmic event, causing ripples of space-time, known as gravitational waves, that we can now detect on Earth with observatories like LIGO and Virgo.

"We have not yet detected light from these collisions. But advances in the sensitivity of equipment detecting gravitational waves, together with new detectors in India and Japan, will lead to a huge leap forward in terms of how many of these types of events we can detect. It is incredibly exciting and should open up a new era for astrophysics."

To calculate the Universe's rate of expansion, known as the Hubble constant, astrophysicists need to know the distance of astronomical objects from Earth as well as the speed at which they are moving away. Analysing gravitational waves tells us how far away a collision is, leaving only the speed to be determined.

To tell how fast the galaxy hosting a collision is moving away, we look at the "redshift" of light - that is, how the wavelength of light produced by a source has been stretched by its motion. Explosions of light that may accompany these collisions would help us pinpoint the galaxy where the collision happened, allowing researchers to combine measurements of distance and measurements of redshift in that galaxy.

Dr Feeney said: "Computer models of these cataclysmic events are incomplete and this study should provide extra motivation to improve them. If our assumptions are correct, many of these collisions will not produce explosions that we can detect - the black hole will swallow the star without leaving a trace. But in some cases a smaller black hole may first rip apart a neutron star before swallowing it, potentially leaving matter outside the hole that emits electromagnetic radiation."

Co-author Professor Hiranya Peiris (UCL Physics & Astronomy and Stockholm University) said: "The disagreement over the Hubble constant is one of the biggest mysteries in cosmology. In addition to helping us unravel this puzzle, the spacetime ripples from these cataclysmic events open a new window on the universe. We can anticipate many exciting discoveries in the coming decade."

Gravitational waves are detected at two observatories in the United States (the LIGO Labs), one in Italy (Virgo), and one in Japan (KAGRA). A fifth observatory, LIGO-India, is now under construction.

Our two best current estimates of the Universe's expansion are 67 kilometres per second per megaparsec (3.26 million light years) and 74 kilometres per second per megaparsec. The first is derived from analysing the cosmic microwave background, the radiation left over from the Big Bang, while the second comes from comparing stars at different distances from Earth - specifically Cepheids, which have variable brightness, and exploding stars called type Ia supernovae.

Dr Feeney explained: "As the microwave background measurement needs a complete theory of the Universe to be made but the stellar method does not, the disagreement offers tantalising evidence of new physics beyond our current understanding. Before we can make such claims, however, we need confirmation of the disagreement from completely independent observations - we believe these can be provided through black hole-neutron star collisions."

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Major advance enables study of genetic mutations in any tissue

For the first time, scientists are able to study changes in the DNA of any human tissue, following the resolution of long-standing technical challenges by scientists at the Wellcome Sanger Institute. The new method, called nanorate sequencing (NanoSeq), makes it possible to study how genetic changes occur in human tissues with unprecedented accuracy.

The study, published today (28 April) in Nature, represents a major advance for research into cancer and ageing. Using NanoSeq to study samples of blood, colon, brain and muscle, the research also challenges the idea that cell division is the main mechanism driving genetic changes. The new method is also expected to allow researchers to study the effect of carcinogens on healthy cells, and to do so more easily and on a much larger scale than has been possible up until now.

The tissues in our body are composed of dividing and non-dividing cells. Stem cells renew themselves throughout our lifetimes and are responsible for supplying non-dividing cells to keep the body running. The vast majority of cells in our bodies are non-dividing or divide only rarely. They include granulocytes in our blood, which are produced in the billions every day and live for a very short time, or neurons in our brain, which live for much longer.

Genetic changes, known as somatic mutations, occur in our cells as we age. This is a natural process, with cells acquiring around 15-40 mutations per year. Most of these mutations will be harmless, but some of them can start a cell on the path to cancer.

Since the advent of genome sequencing in the late twentieth century, cancer researchers have been able to better understand the formation of cancers and how to treat them by studying somatic mutations in tumour DNA. In recent years, new technologies have also enabled scientists to study mutations in stem cells taken from healthy tissue.

But until now, genome sequencing has not been accurate enough to study new mutations in non-dividing cells, meaning that somatic mutation in the vast majority of our cells has been impossible to observe accurately.

In this new study, researchers at the Wellcome Sanger Institute sought to refine an advanced sequencing method called duplex sequencing1. The team searched for errors in duplex sequence data and realised that they were concentrated at the ends of DNA fragments, and had other features suggesting flaws in the process used to prepare DNA for sequencing.

They then implemented improvements to the DNA preparation process, such as using specific enzymes to cut DNA more cleanly, as well as improved bioinformatics methods. Over the course of four years, accuracy was improved until they achieved fewer than five errors per billion letters of DNA.

Dr Robert Osborne, an alumnus of the Wellcome Sanger Institute who led the development of the method, said: "Detecting somatic mutations that are only present in one or a few cells is incredibly technically challenging. You have to find a single letter change among tens of millions of DNA letters and previous sequencing methods were simply not accurate enough. Because NanoSeq makes only a few errors per billion DNA letters, we are now able to accurately study somatic mutations in any tissue."

The team took advantage of NanoSeq's improved sensitivity to compare the rates and patterns of mutation in both stem cells and non-dividing cells in several human tissue types.

Surprisingly, analysis of blood cells found a similar number of mutations in slowly dividing stem cells and more rapidly dividing progenitor cells2. This suggested that cell division is not the dominant process causing mutations in blood cells. Analysis of non-dividing neurons and rarely dividing cells from muscle also revealed that mutations accumulate throughout life in cells without cell division, and at a similar pace to cells in the blood.

Dr Federico Abascal, the first author of the paper from the Wellcome Sanger Institute, said: "It is often assumed that cell division is the main factor in the occurrence of somatic mutations, with a greater number of divisions creating a greater number of mutations. But our analysis found that blood cells that had divided many times more than others featured the same rates and patterns of mutation. This changes how we think about mutagenesis and suggests that other biological mechanisms besides cell division are key."

The ability to observe mutation in all cells opens up new avenues of research into cancer and ageing, such as studying the effects of known carcinogens like tobacco or sun exposure, as well as discovering new carcinogens. Such research could greatly improve our understanding of how lifestyles choices and exposures to carcinogens can lead to cancer.

A further benefit of the NanoSeq method is the relative ease with which samples can be collected. Rather than taking biopsies of tissue, cells can be collected non-invasively, such as by scraping the skin or swabbing the throat.

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Two compounds can make chocolate smell musty and moldy

Chocolate is a beloved treat, but sometimes the cocoa beans that go into bars and other sweets have unpleasant flavors or scents, making the final products taste bad. Surprisingly, only a few compounds associated with these stinky odors are known. Now, researchers reporting in ACS' Journal of Agricultural and Food Chemistry have identified the two compounds that cause musty, moldy scents in cocoa -- work that can help chocolatiers ensure the quality of their products.

Cocoa beans, when fermented correctly, have a pleasant smell with sweet and floral notes. But they can have an off-putting scent when fermentation goes wrong, or when storage conditions aren't quite right and microorganisms grow on them. If these beans make their way into the manufacturing process, the final chocolate can smell unpleasant, leading to consumer complaints and recalls. So, sensory professionals smell fermented cocoa beans before they are roasted, detecting any unwanted musty, moldy, smoky or mushroom-like odors. Even with this testing in place, spoiled beans can evade human noses and ruin batches of chocolate, so a more objective assessment is needed for quality control. In previous studies, researchers used molecular techniques to identify the compounds that contribute to undesirable smoky flavors, but a similar method has not clarified other volatile scent compounds. So, Martin Steinhaus and colleagues wanted to determine the principal compounds that cause musty and moldy odors in tainted cocoa beans.

The researchers identified 57 molecules that made up the scent profiles of both normal and musty/moldy smelling cocoa beans using gas chromatography in combination with olfactometry and mass spectrometry. Of these compounds, four had higher concentrations in off-smelling samples. Then, these four compounds were spiked into unscented cocoa butter, and the researchers conducted smell tests with 15-20 participants. By comparing the results of these tests with the molecular content of nine samples of unpleasant fermented cocoa beans and cocoa liquors, the team determined that (-)-geosmin -- associated with moldy and beetroot odors -- and 3-methyl-1H-indole -- associated with fecal and mothball odors -- are the primary contributors to the musty and moldy scents of cocoa beans. Finally, they found that (-)-geosmin was mostly in the beans' shells, which are removed during processing, while 3-methyl-1H-indole was primarily in the bean nib that is manufactured into chocolate. The researchers say that measuring the amount of these compounds within cocoa beans could be an objective way to detect off-putting scents and flavors, keeping future batches of chocolate smelling sweet.

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Stress slows the immune response in sick mice

The neurotransmitter noradrenaline, which plays a key role in the fight-or-flight stress response, impairs immune responses by inhibiting the movements of various white blood cells in different tissues, researchers report April 28th in the journal Immunity. The fast and transient effect occurred in mice with infections and cancer, but for now, it's unclear whether the findings generalize to humans with various health conditions.

"We found that stress can cause immune cells to stop moving and prevents immune cells from protecting against disease," says senior study author University of Melbourne's Scott Mueller (@SMuellerLab) of the Peter Doherty Institute for Infection and Immunity (Doherty Institute). "This is novel because it was not known that stress signals can stop immune cells from moving about in the body and performing their job."

One main function of the sympathetic nervous system (SNS) is to coordinate the fight-or-flight stress response -- a group of changes that prepare the body to fight or take flight in stressful or dangerous situations to protect itself from possible harm. Most tissues, including the lymph nodes and spleen, are innervated by SNS fibers. Stress-induced activation of the SNS can suppress immune responses, but the underlying mechanisms have been poorly characterized. "We hypothesized that SNS signals might modify the movement of T cells in tissues and lead to compromised immunity," Mueller says.

White blood cells, also known as leukocytes, travel constantly throughout the body and are highly motile within tissues, where they locate and eradicate pathogens and tumors. Although the movement of leukocytes is critical for immunity, it has not been clear how these cells integrate various signals to navigate within tissues. "We also speculated that neurotransmitter signals might be a rapid way to modulate leukocyte behavior in tissues, in particular during acute stress that involves increased activation of the SNS," Mueller says.

To test this idea, the researchers used advanced imaging to track the movements of T cells in mouse lymph nodes. Within minutes of being exposed to noradrenaline, T cells that had been rapidly moving stopped in their tracks and retracted their arm-like protrusions. This effect was transient, lasting between 45 and 60 minutes. Localized administration of noradrenaline in the lymph nodes of live mice also rapidly halted the cells. Similar effects were observed in mice that received noradrenaline infusions, which are used to treat patients with septic shock -- a life-threatening condition that occurs when infection leads to dangerously low blood pressure. This finding suggests that therapeutic treatment with noradrenaline might impair leukocyte functions.

"We were very surprised that stress signals had such a rapid and dramatic effect on how immune cells move," Mueller says. "Since movement is central to how immune cells can get to the right parts of the body and fight infections or tumors, this rapid movement off-switch was unexpected."

Other experiments revealed that SNS signals inhibit the migration of distinct immune cells, including B cells and dendritic cells, exerting these effects in different tissues such as skin and liver. Additional results suggest that the effects of SNS activation on cell motility may be mediated by the constriction of blood vessels, reduced blood flow, and oxygen deprivation in tissues, resulting in an increase in calcium signaling in leukocytes.

"Our results reveal that an unanticipated consequence of modulation of blood flow in response to SNS activity is the rapid sensing of changes in oxygen by leukocytes and the inhibition of motility," Mueller says. "Such rapid paralysis of leukocyte behavior identifies a physiological consequence of SNS activity that explains, at least in part, the widely observed relationship between stress and impaired immunity."

Moreover, SNS signals impaired protective immunity against pathogens and tumors in various mouse models, decreasing the proliferation and expansion of T cells in the lymph nodes and spleen. For example, treatment with SNS-stimulating molecules rapidly stopped the movements of T cells and dendritic cells in mice infected with herpes simplex virus 1 and reduced virus-specific T cell recruitment to the site of the skin infection. Similar effects were observed in mice with melanoma and in mice infected with a malarial parasite.

"Our data suggest that SNS activity in tissues could impact immune outcomes in diverse diseases," Mueller says. "Further insight into the impact of adrenergic receptor signals on cellular functions in tissues may inform the development of improved treatments for infections and cancer."

The degree to which SNS activation affects leukocyte behavior or disease outcomes in humans remains to be determined. Notably, increased SNS activity is prominent in patients with obesity and heart failure, while psychological stress can cause blood vessel constriction in patients with heart disease. An unappreciated impact of increased SNS activity, particularly in individuals with underlying health conditions, might be impaired leukocyte behavior and functions. The findings may also have important health implications for patients who use SNS-activating drugs to treat diseases such as heart failure, sepsis, asthma, and allergic reactions.

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