Astronomers using NASA’s Hubble Space Telescope have recorded a star’s final moments in detail as it gets gobbled up by a black hole.

These are termed “tidal disruption events.” But the wording belies the complex, raw violence of a black hole encounter. There is a balance between the black hole’s gravity pulling in star stuff, and radiation blowing material out. In other words, black holes are messy eaters. Astronomers are using Hubble to find out the details of what happens when a wayward star plunges into the gravitational abyss.

Hubble can’t photograph the AT2022dsb tidal event’s mayhem up close, since the munched-up star is nearly 300 million light-years away at the core of the galaxy ESO 583-G004. But astronomers used Hubble’s powerful ultraviolet sensitivity to study the light from the shredded star, which include hydrogen, carbon, and more. The spectroscopy provides forensic clues to the black hole homicide.

About 100 tidal disruption events around black holes have been detected by astronomers using various telescopes. NASA recently reported that several of its high-energy space observatories spotted another black hole tidal disruption event on March 1, 2021, and it happened in another galaxy. Unlike Hubble observations, data was collected in X-ray light from an extremely hot corona around the black hole that formed after the star was already torn apart.

“However, there are still very few tidal events that are observed in ultraviolet light given the observing time. This is really unfortunate because there’s a lot of information that you can get from the ultraviolet spectra,” said Emily Engelthaler of the Center for Astrophysics | Harvard & Smithsonian (CfA) in Cambridge, Massachusetts. “We’re excited because we can get these details about what the debris is doing. The tidal event can tell us a lot about a black hole.” Changes in the doomed star’s condition are taking place on the order of days or months.

For any given galaxy with a quiescent supermassive black hole at the center, it’s estimated that the stellar shredding happens only a few times in every 100,000 years.

This AT2022dsb stellar snacking event was first caught on March 1, 2022 by the All-Sky Automated Survey for Supernovae (ASAS-SN or “Assassin”), a network of ground-based telescopes that surveys the extragalactic sky roughly once a week for violent, variable, and transient events that are shaping our universe. This energetic collision was close enough to Earth and bright enough for the Hubble astronomers to do ultraviolet spectroscopy over a longer than normal period of time.

“Typically, these events are hard to observe. You get maybe a few observations at the beginning of the disruption when it’s really bright. Our program is different in that it is designed to look at a few tidal events over a year to see what happens,” said Peter Maksym of the CfA. “We saw this early enough that we could observe it at these very intense black hole accretion stages. We saw the accretion rate drop as it turned to a trickle over time.”

The Hubble spectroscopic data are interpreted as coming from a very bright, hot, donut-shaped area of gas that was once the star. This area, known as a torus, is the size of the solar system and is swirling around a black hole in the middle.

“We’re looking somewhere on the edge of that donut. We’re seeing a stellar wind from the black hole sweeping over the surface that’s being projected towards us at speeds of 20 million miles per hour (three percent the speed of light),” said Maksym. “We really are still getting our heads around the event. You shred the star and then it’s got this material that’s making its way into the black hole. And so you’ve got models where you think you know what is going on, and then you’ve got what you actually see. This is an exciting place for scientists to be: right at the interface of the known and the unknown.”

The results were reported at the 241st meeting of the American Astronomical Society in Seattle, Washington.

Researchers in Li Zhao’s lab studied mutations that occur during the production of sperm from germline cells, known as spermatogenesis. They found that mutations are common in the testes of both young and old fruit flies, but more abundant in older flies from the outset. Moreover, many of these mutations seem to be removed in younger fruit flies during spermatogenesis by the body’s genomic repair mechanisms — but they fail to be fixed in the testes of older flies.

“We were trying to test whether the older germline is less efficient at mutation repair, or whether the older germline just starts out more mutated,” says first author Evan Witt, a former graduate student in the lab and now a computational biologist at Biomarin Pharmaceuticals. “Our results indicate that it’s actually both. At every stage of spermatogenesis, there are more mutations per RNA molecule in older flies than in younger flies.”

Self-care at the genetic level

Genomes keep themselves tidy using a handful of repair mechanisms. When it comes to testes, they have to work overtime; testes have the highest rate of gene expression of any organ. Moreover, genes that are highly expressed in spermatogenesis tend to have fewer mutations than those that are not. This sounds counterintuitive, but it makes sense: One theory to explain why the testes express so many genes holds that it might be a sort of genomic surveillance mechanism — a way to reveal, and then weed out, problematic mutations.

But when it comes to older sperm, the researchers found, the weed-whacker apparently sputters out. Previous research suggests that a faulty transcription-coupled repair mechanism, which only fixes transcribed genes, could be to blame.

Inherited or new mutations?

To get these results, scientists in the Laboratory of Evolutionary Genetics and Genomics did single-cell sequencing on the RNA from the testes of about 300 fruit flies, roughly half of them young (48 hours old) and half old (25 days old), advancing a line of inquiry they began in 2019. In order to understand whether the mutations they detected were somatic, or inherited from the flies’ parents, or de novo — arising in the individual fly’s germline — they then sequenced the genome of each fly. They were able to document that each mutation was a true original. “We can directly say this mutation was not present in the DNA of that same fly in its somatic cells,” says Witt. “We know that it’s a de novo mutation.”

This unconventional approach — inferring genomic mutations from single-cell RNA sequencing and then comparing them to the genomic data — allowed the researchers to match mutations to the cell type in which they occurred. “It’s a good way to compare mutational load between cell types, because you can follow them throughout spermatogenesis,” Witt says.

The human connection

The next step is to expand the analysis to more age groups of flies and test whether or not this transcription repair mechanism can occur — and if it does, identify the pathways responsible, Witt says. “What genes,” he wonders, “are really driving the difference between old and young flies in terms of mutation repair?”

Because fruit flies have a high reproductive rate, investigating their mutation patterns can offer new insights into the effect of new mutations in human health and evolution, says Zhao.

Witt adds, “It’s largely unknown whether a more mutated male germline is more or less fertile than a less mutated one. There’s not been very much research on it except for at a population level. And if people inherit more mutations from aging fathers, that increases the odds of de novo genetic disorders or certain types of cancers.”

When clothing made from plastic fibers, such as polyester and nylon, are laundered, the fabric sheds microscopic fibers that eventually end up in wastewater and the environment. Though researchers have investigated the amount and types of microplastic fibers shed while laundering clothing, most studies have focused on washing machines. In many countries, however, it is still common to manually launder clothing. A team has previously reported on the effects of washing fabric by hand, but the study was not comprehensive. So, Wang, Zhao, Xing and colleagues wanted to systematically investigate microplastic fiber release from synthetic textiles with different methods of hand washing in contrast to machine washing.

The team cleaned two types of fabric swatches made from 100% polyester and a 95% polyester-5% spandex blend with hand washing methods and a washing machine. The researchers found that:

• Manual methods released far fewer fibers. For example, the 100% polyester fabric shed an average of 1,853 microplastic pieces during hand washing compared with an average of 23,723 pieces from the same fabric that was machine laundered.
• By weight, machine laundering released over five times more microplastics than the traditional method.
• The fibers released from hand washing tended to be longer.
• Adding detergent, pre-soaking the fabrics and using a washboard increased the number of released fibers with manual methods, but still not to the same extent as using a machine.
• In contrast, they found that temperature, detergent type, wash time and the amount of water used had no meaningful effects on the amount of microplastics shed while hand washing.

The researchers say that these results will help clarify the sources of microplastic pollution in the environment and can provide guidance for “greener” laundering methods.

The authors acknowledge funding from the Zhejiang Provincial Natural Science Foundation of China, the National Natural Science Foundation of China and the Scientific Research Foundation of Hangzhou Dianzi University.

If accurate, such an estimator could computationally demonstrate binding affinity and thus prevent experimental researchers from needing to investigate millions of chemical compounds. The work could substantially reduce the cost and time associated with developing new drugs.

“We developed a theoretical framework for estimating ligand-protein binding,” said Mahmoud Moradi, associate professor of chemistry and biochemistry in the Fulbright College of Arts and Sciences. “The proposed method assigns an effective energy to the ligand at every grid point in a coordinate system, which has its origin at the most likely location of the ligand when it is in its bound state.”

A ligand is a substance — an ion or molecule — such as a drug that binds to another molecule, such as a protein, to form a complex system that may cause or prevent a biological function.

Moradi’s research focuses on computational simulations of diseases, including coronavirus. For this project, he collaborated with Suresh Thallapuranam, professor of biochemistry and the Cooper Chair of Bioinformatics Research.

Moradi and Thallapuranam used biased simulations — as well as non-parametric re-weighting techniques to account for the bias — to create a binding estimator that was computationally efficient and accurate. They then used a mathematically robust technique called orientation quaternion formalism to further describe the ligand’s conformational changes as it bound to targeted proteins.

The researchers tested this approach by estimating the binding affinity between human fibroblast growth factor 1 — a specific signaling protein — and heparin hexasaccharide 5, a popular medication.

The project was conceived because Moradi and Thallapuranam were studying human fibroblast growth factor 1 protein and its mutants in the absence and presence of heparin. They found strong qualitative agreement between simulations and experimental results.

“When it came to binding affinity, we knew that the typical methods we had at our disposal would not work for such a difficult problem,” Moradi said. “This is why we decided to develop a new method. We had a joyous moment when the experimental and computational data were compared with each other, and the two numbers matched almost perfectly.”

The researchers’ work was published in Nature Computational Science.

Moradi previously received attention for developing computational simulations of the behavior of SARS-CoV-2 spike proteins prior to fusion with human cell receptors. SARS-CoV-2 is the virus that causes COVID-19.

Like all living organisms, pathogens want to thrive. Aside from cellular reproduction, though, the best future for them lies in moving from host to host. Think of each host as Stevenson’s eggs, unwittingly waiting to be, if not broken, certainly cracked. Meaning ill. That’s why pathogens — from conjunctivitis, commonly known as pink eye, or a common cold or a disease as severe as COVID-19 — make their hosts sick: Spread is sometimes only made possible by expulsion via swollen red eyes; ,coughing or sneezing, or passing through bodily fluids, according to Virginia Tech biologist Dana Hawley.

“For a pathogen, ‘spreading’ is their key form of reproduction. And when we think about why pathogens make their hosts sick, it’s long been a mystery, because making a host sick or making your host die is superficially not a good way for a pathogen to be able to spread. A very sick host will stay home and not interact as much as others, which means less spread potential for a pathogen,” said Hawley, a professor in the Department of Biological Sciences, part of the Virginia Tech College of Science.

But here’s the caveat: “Making your hosts feel ill can be important for getting some of the copies of yourself out of the host you are infecting and into another. So there is a trade-off for the pathogen,” Hawley said. “Making your host feel sick means that host may not interact with as many other hosts as they normally would — this is bad for the pathogen — but when they do have interactions, a very sick host that is coughing or has swollen eyes is going to be much more likely to spread whatever pathogen it has in its body. This isgoodfor the pathogen.”

Using songbirds, a type known as finches, whose populations are affected by a pink-eye disease in nature, Hawley and a team of researchers from Virginia Tech and the University of Memphis in Tennessee have shown just how easily these pathogens — in this case, a form of conjunctivitis common in birds, but harmless to humans — spread. And they did it without having the pink eye pathogen itself spread from bird to bird.

Instead, the team used UV fluorescent powder coatings and tracked thatand not the pathogen. During the experiment, birds were divided up into three groups: not ill, mildly ill, and strongly ill, all with conjunctivitis, and each bird was housed with four healthy flockmates. By applying a powder coating around the outer eye of each bird, but not inside the eye, the researchers could track how much powder was spread to flockmates from birds that were strongly, mildly, or not ill with pink eye.

“We weren’t actually tracing the spread of conjunctivitis. We were tracing the spread of powder as a model for the likely spread of conjunctivitis,” said Hawley, who is also an affiliated member of the Virginia Tech Fralin Life Sciences Institute’s Global Change Center and its Center for Emerging, Zoonotic, and Arthropod-borne Pathogens, about the study, published today in the journal Royal Society Open Science.

During the study, birds were kept in large-flight cages, sharing feeders and potentially spreading powder to cage mates. Feeder surfaces are one main avenue of the powder’s travel, according to the study.

There were some surprises along the way, Hawley said. The finches experiencing the strongest conjunctivitis symptoms were far less likely to eat but nonetheless spread the powder at a higher rate than the mildly ill birds who spent more time feeding.

“In our study system, the benefits of making your host sicker by increasing eye swelling outweighed the cost of making the finches feed and interact less,” Hawley said. “So overall, this pathogen is going to likely evolve to causemore harm to birds in nature so that it can spread at a higher rate, but up to some limit, because if the pathogen kills a bird immediately, the pathogen doesn’t have a chance to spread at all.”

The human factor

What does all this mean for humans and the spread of a common cold or COVID-19 at a doctor’s office or the cinema, or the spread of conjunctivitis amongst young children at a nursery school or day care?

The mantra of “stay home if you’re sick” still applies more than ever, according to Hawley. This study suggests that symptoms will make the spread of anything you are infected with much more likely. And wear a face mask — and not just for potential spread of COVID. “Wearing masks when you are coughing from any illness can likely go a long way in preventing disease spread,” Hawley said. “For pink eye, keeping kids isolated is going to be key because young children are just not going to be able to wash their hands or avoid touching each other — speaking from experience as a parent.”

Evolution plays another part. Again, pathogens are living organisms and prone to the rules of life, including evolution. “This goes back to the idea that everyone hoped that COVID would evolve to become milder over time,” Hawley said. “Our study shows that the pressures on pathogens are complicated. On the one hand, being mild is good for pathogens if it keeps your host out and about and in others’ company — good for spread, but on the other hand, being mild may mean that none of the pathogen makes it out of the host and into another because your host isn’t coughing or depositing as much pathogen onto hands or other surfaces. So pathogens are in many cases going to be favored to make us sick.”

In other words, for humans, common sense actions can prevent us from being those proverbial eggs spoken of by Stevenson.

Co-authors on the paper include Courtney A. Thomason, a former postdoctoral associate at Virginia Tech from January 2015 to October 2017, who is now at the Tennessee Department of Environment and Conservation; Matt Aberle, who earned a master’s degree in biological sciences in 2018 and is now a wildlife biologist with Oregon Department of Forestry; and Richard Brown, who graduated with a bachelor’s degree in wildlife conservation from the Virginia Tech College of Natural Resources and Environment in 2017 and is now a master’s student at George Mason University; as well as James S. Adelman, an assistant professor at the University of Memphis.

Funding for the study came from two National Science Foundation grants and additional funding from the National Institute of General Medical Sciences, the latter part of the National Institutes for Health.