Obliterating bacteria in the gut may hurt the brain, too.

In mice, a long course of antibiotics that wiped out gut bacteria slowed the birth of new brain cells and impaired memory, scientists write May 19 in Cell Reports. The results reinforce evidence for a powerful connection between bacteria in the gut and the brain (SN: 4/2/16, p. 23).

After seven weeks of drinking water spiked with a cocktail of antibiotics, mice had fewer newborn nerve cells in a part of the hippocampus, a brain structure important for memory. The mice’s ability to remember previously seen objects also suffered.
Further experiments revealed one way bacteria can influence brain cell growth and memory. Injections of immune cells called Ly6Chi monocytes boosted the number of new nerve cells. Themonocytes appear to carry messages from gut to brain, Susanne Wolf of the Max Delbrück Center for Molecular Medicine in Berlin and colleagues found.

Exercise and probiotic treatment with eight types of live bacteria also increased the number of newborn nerve cells and improved memory in mice treated with antibiotics. The results help clarify the toll of prolonged antibiotic treatment, and hint at ways to fight back, the authors write.

Forget it, peacocks. Nice try, elk. Sure, sexy feathers and antlers are showy, but the sperm of a fruit fly could be the most over-the-top, exaggerated male ornamentation of all.

In certain fruit fly species, such as Drosophila bifurca, males measuring just a few millimeters produce sperm with a tail as long as 5.8-centimeters, researchers report May 26 in Nature. Adjusted for body size, the disproportionately supersized sperm outdoes such exuberant body parts as pheasant display feathers, deer antlers, scarab beetle horns and the forward-grasping forceps of earwigs.
Fruit flies’ giant sperm have been challenging to explain, says study coauthor Scott Pitnick of Syracuse University in New York.

Now he and his colleagues propose that a complex interplay of male and female benefits has accelerated sperm length in a runaway-train scenario.

Males with longer sperm deliver fewer sperm, bucking a more-is-better trend. Yet, they still manage to transfer a few dozen to a few hundred per mating. And as newly arrived sperm compete to displace those already waiting in a female’s storage organ, longer is better. Fewer sperm per mating means females tend to mate more often, intensifying the sperm-vs.-sperm competition. Females that have the longest storage organs, which favor the longest sperm, benefit too: Males producing greater numbers of megasperm, the researchers found, tend to be the ones with good genes likely to produce robust offspring. “Sex,” says Pitnick, “is a powerful force.”
Among courtship-oriented body ornaments and weapons (red), the giant sperm of fruit flies (Drosophila) are the most disproportionately exaggerated, according to an index adjusted for body size. Higher numbers (bottom axis) indicate greater exaggeration.

When molecular biologist Kate Rubins blasts off from Kazakhstan on June 24, strapped into the Soyuz spacecraft bound for the International Space Station, the trip will cap off seven years of preparing — and 30 years of hoping.

As a child, Rubins plastered her Napa, Calif., bedroom with pictures of the space shuttle, proudly announcing her intention to be an astronaut. A week at Space Camp in Huntsville, Ala., in seventh grade cemented her vision. But by high school, she concluded that astronaut wasn’t “a realistic job,” she says.
Flash forward to 2009: Rubins is running a lab at the Whitehead Institute for Biomedical Research in Cambridge, Mass., focusing on virus-host interactions and viral genomics. A friend points out a NASA ad seeking astronaut candidates, and Rubins’ long-dormant obsession awakens. Since then, she has learned how to fly a T-38 jet, speak Russian to communicate with her cosmo-naut crewmates, conduct a spacewalk, operate the robotic arm on the ISS and even fix the habitable satellite’s toilet.

Joining NASA meant leaving her 14-person lab behind. But Rubins gained the rare opportunity to collaborate with dozens of scientists in fields as diverse as cell biology and astrophysics. On the space station, she’ll be “their hands, eyes and ears,” conducting about 100 experiments over five months.

She will, for instance, probe how heart cells behave when gravity doesn’t get in the way. And she’ll test a hand-held DNA sequencer, which reads out the genetic information stored in DNA and will be important to future missions looking for signatures of life on Mars.

At times, Rubins will be both experimenter and subject. In one study, she will observe bone cells in a lab dish, comparing their behavior with what happens in a simulated gravity-free environment on the ground. Because astronauts in space are vulnerable to rapid bone loss, CT scanning before and after the mission will also document changes in Rubins’ own hip bone.

Rubins is particularly eager to examine how liquid behaves in microgravity on a molecular scale. In 2013, Canadian astronaut Chris Hadfield created an Internet sensation when he demonstrated that wringing out a wet washcloth in space caused water to form a bubble that enveloped the cloth and his hands. “It’s incredibly bizarre,” Rubins says. Understanding how fluids move in test tubes in space will help NASA plan for Mars exploration, among other applications.
Before any of the research can begin, Rubins has to get off the ground. As treacherous as accelerating to 17,500 miles per hour may sound, she’s not worried.

“An important part of the training experience is making all the information and skills routine,” she says. She predicts that sitting down in the Soyuz spacecraft, pulling out her procedures and getting ready to launch will feel a lot like going into the lab and picking up a pipette — “a normal day at the office.”

Until the engines turn on, anyway. “I think it’s going to feel different when there’s a rocket underneath.”

When Francis Crick was 31, he decided he needed to change his luck. As a graduate student in physics during World War II, his research hadn’t gone so well; his experiment was demolished by a bomb. To beat the war, he joined it, working on naval warfare mines for the British Admiralty.

After the war, he sought a new direction.

“There are lots of ways of being unlucky,” Crick told me in an interview in 1998. “One is sticking to things too long. Another is not adventuring at all.”

He decided to adventure.

Molecular biologists everywhere will celebrate that decision on June 8, the centennial of Crick’s birth, in Weston Favell, Northampton, England, in 1916.

“Crick was one of the central figures, one might say the central figure, in the molecular revolution that swept through biology in the latter half of the 20th century,” science historian Robert Olby wrote in a biographical sketch.

In 1953, at the University of Cambridge, Crick and his collaborator James Watson figured out how life’s most important molecule, deoxyribonucleic acid, was put together. DNA, the stuff that genes are made of, became the most famous of biological molecules. Today the image of its double helix structure symbolizes biology itself. It would be easy to make the case that discovering DNA’s structure was the single greatest event in the history of biology — and always will be. In 1962, Watson and Crick won the Nobel Prize for their work (which was, of course, greatly aided by X-ray diffraction imagery from Rosalind Franklin, who unfortunately died before the Nobel was awarded).

Crick’s DNA adventure began at a time when molecular biology was ripe for revolution. But Crick didn’t know that. His choice was lucky.
“I had no idea when I started that molecular biology would advance so fast,” he said. “No idea at all.”

In fact, Crick very nearly chose a different path. His interest in genes was equaled by his curiosity about the brain. Both were topics that he liked to gossip about.

“But I didn’t know enough about either subject,” he said. He just knew a little bit more about biochemistry.

“I thought ‘Well look, I have a training in physics and I know a bit of chemistry, I don’t know anything about the brain.’” So he decided it would be more sensible to start with genes.

“I thought that problem of what genes were and how they replicate and what they did would last me the rest of my life,” he said.

As it happened, genes did occupy him for a couple of decades. Crick made major contributions to elucidating the genetic code during that time. But he never forgot his interest in the brain, and more specifically, consciousness. In the 1970s, he moved from England to California, where he began consciousness research in San Diego at the Salk Institute for Biological Studies.

Consciousness turned out to be a much tougher problem than understanding genes. In retrospect, Crick could see why.

With genetics, “what really made the thing was the simplicity of the double helix. It wrote the whole research program,” he said. “It probably goes back to near the origin of life, when things had to be simple.” Consciousness appeared on the scene only much later, after the evolution of the brain’s vast complexity.

Nevertheless, Crick perceived parallels between genetics and consciousness as subjects for scientific inquiry. As the 20th century came to an end, he mused that consciousness as a concept remained vague — researchers did not all agree about what the word meant. The situation with genes had at one time been similar.

“In a sense people were just as vague about what genes were in the 1920s as they are now about consciousness,” Crick said. “It was exactly the same. The more professional people in the field, which was biochemistry at that time, thought that it was a problem that was too early to tackle. And I think they were right in the ’20s.”

At the end of the 20th century, research on consciousness found itself in much the same state.

“Everybody agrees that it’s an interesting question,” Crick said, “but there are two points of view among scientists: One is that it isn’t a scientific question and is best left to philosophers. And the other one is that, even if it’s a scientific question, it’s too early to tackle it now.”

Crick tackled it anyway. Until his death in 2004, he worked vigorously on the subject with his collaborator Christof Koch, making substantial inroads into identifying the brain activity associated with conscious awareness. Crick was not lucky enough to solve the problem of consciousness, but he perhaps brought the arrival of that solution a little closer.

When plankton on the high seas catch a cold, the whole ocean may sneeze. Viruses hijacking these microbes could be an important overlooked factor in tracing how living things trap — or in this case, fail to trap — the climate-warming gas carbon dioxide.

Plants and other organisms that photosynthesize use energy from the sun to capture CO2 for food. The most abundant of these photosynthesizers on the planet are marine cyanobacteria with hardly any name recognition: Synechococcus and Prochlorococcus.
Now, for the first time, a study looks in detail at what happens when some of the abundant viruses found in the sea infect these microbes. Two viruses tested in the lab hijacked cell metabolism, allowing photosynthesis to continue but shunting the captured energy to virus reproduction. The normal use of that energy, capturing CO2, largely shuts down, David Scanlan of the University of Warwick in England and colleagues report online June 9 in Current Biology. As a result, people could be overestimating by 10 percent the amount of CO2 that photosynthesis in the oceans captures.

On any given day, 1 to 60 percent of these plankton may have picked up a viral infection, researchers have estimated. That means that between 0.02 and 5.39 petagrams of carbon — up to 5.39 billion metric tons — may not be captured by marine organisms a year. The high end of that scenario is equivalent to 2.8 times the CO2 routinely captured annually by all the planet’s salt marshes, coral reefs, estuaries, sea grass meadows and seaweeds put together.

Synechococcus and Prochlorococcus plankton “are organisms that you’ve never heard of but you really should have,” says Adam Martiny of the University of California, Irvine. He studies the same kinds of plankton but wasn’t involved in the new virus research, and what he appreciates about it is the intriguing biology of viral manipulation the new work has uncovered.

Until now, Scanlan says, the prevailing view was that while infected plankton were still alive, they were probably carrying on normal photosynthesis. As early as 2003, researchers had clues that the viruses attacking these tiny marine organisms might manipulate photosynthesis in some way, perhaps keeping the process running in an infected cell. These viruses have genes for proteins used in photosynthesis, even though a virus doesn’t even have its own cell much less a way to photosynthesize.

What the viruses are doing, Scanlan and his colleagues have now shown, is subverting their victim’s photosynthesis. Energy capture, the part of photosynthesis directly involved with light, goes on as usual; the cells carry out the routine electron transport for catching energy. But instead of using those sizzling electrons to capture CO2 and turn it into carbohydrates for basic cell metabolism, the viruses shut down this process (called carbon fixation). The light reactions are the ones that researchers normally measure to estimate how much carbon photosynthesis captures in the oceans, but the covert viral shunting means that estimate could be too high.

Scanlan cautions that this is just the beginning of working out the numbers and possible climate effects of virus diseases for these organisms. Whatever the current effects of this takeover turn out to be outside the lab, they may intensify as the climate changes. Synechococcus and Prochlorococcus are “projected to be winners in the new, warmer oceans” and may become even more numerous, Martiny says. And what’s good for them may also increase the abundance of the viral pirates that hijack them.

Since 1973, eight spacecraft have flown past or orbited Jupiter. On July 4, NASA’s Juno probe will become the planet’s ninth visitor.

Juno’s trajectory is different than all others, as seen in the plot above and in the video. For 20 months, Juno will repeatedly skim the cloud tops, looping over the poles on orbits that are almost perpendicular to Jupiter’s equator.

Most other spacecraft zipped by, using the planet’s gravity to speed them along to other destinations. Only Galileo, which arrived in 1995, stuck around; it spent nearly eight years circling Jupiter’s equator, repeatedly buzzing the four largest moons.

Young zebra finches (Taeniopygia guttata) learn to sing from a teacher, usually dad. Remembering dad’s tunes may even be hardwired into the birds’ brains.

Researchers at the Okinawa Institute of Science and Technology in Japan measured activity in the brains of male juvenile birds listening to recordings of singing adult males, including their fathers. The team focused its efforts on neurons in a part of the brain called the caudomedial nidopallium that’s thought to influence song learning and memory.

A subset of neurons in the caudomedial nidopallium lit up in response to songs performed by dad but not those of strangers, the team reports June 21 in Nature Communications. The more baby birds heard songs, the more their neurons responded and the clearer their own songs became. Sleep and a neurotransmitter called GABA influenced this selectivity.

The researchers suggest that this particular region of the brain stores song memories as finches learn to sing, and GABA may drive the storage of dad’s songs over others.
Researchers played a variety of sounds for young zebra finches: their own song, dad’s song and songs and calls from other adult finches. Over time, their songs became more and more similar to that of their father.

Hair, scales and feathers arose from one ancestral structure, a new study finds.

Studies in fetal Nile crocodiles, bearded dragon lizards and corn snakes appear to have settled a long-standing debate on the rise of skin coverings. Special skin bumps long known to direct the development of hair in mammals and feathers in birds also turn out to signal scale growth in reptiles, implying all three structures evolved from a shared ancestor, scientists report online June 24 in Science Advances.
In embryonic birds and mammals, some areas of the skin thicken into raised bumps. Since birds evolved from ancient reptiles, scientists expected that modern snakes, lizards and crocodiles would have the same structures. A study at Yale University last year found that one protein already known to be important in hair and feather development is also active in the skin of developing alligators. But the team did not find the telltale skin thickening. Without that evidence from modern reptiles, scientists weren’t sure if the bumps had been lost in reptiles, or if birds and mammals had evolved them independently, using the same set of genes.
The new results are “a relief,” says Michel Milinkovitch, whose lab led the new study at the University of Geneva. Scientists had come up with a variety of complicated ideas to explain how birds and mammals could share a structure that reptiles lack. But, he says, “the reality is much simpler.”

Clues from a mutant lizard inspired Milinkovitch’s team to probe the mystery. Nicolas Di-Poï, a coauthor of the new study who is now at the University of Helsinki, found that a hair-development gene called EDA was present, but disrupted, in scaleless, or “silky,” bearded dragons. Di-Poï and Milinkovitch searched for similar molecular signals in normal reptile embryos and found genes and proteins associated with hair and feather growth studding the skin. Cell staining revealed characteristic skin thickening at those signal centers.

Reptilian skin bumps eluded previous researchers because they are tiny, appear briefly and don’t all come in at once as they do in mammals, Milinkovitch speculates. “You have to look in the right place at the right time to see them,” he says. “Then boom, you see them, and you’re like, ‘Whoa, they are exactly the same.’”

This study “addresses a fundamental question about identity for skin structures,” says paleontologist Marcelo Sánchez of the University of Zurich, who was not involved in the new research. It’s especially important that the team used crocodiles, lizards and snakes, which are far from typical lab animals, he says. Using nonmodel organisms “gives new insight into evolution we wouldn’t get otherwise.”

The next step is to understand how hairs, feathers and scales diversified from the same ancestral structure. That primordial body covering wasn’t necessarily a scale, says evolutionary biologist Günter Wagner, an author of the 2015 Yale study. “Even though intuitively you would think reptilian-like skin is ancestral, compared to mammals,” he says “it’s entirely unclear what kind of structure the scales and feathers on the one side and hair on the other has evolved from.”

A gaping wound in Earth’s atmosphere is definitively healing. Since 2000, the average size of the Antarctic ozone hole in September has shrunk by about 4.5 million square kilometers, an area larger than India, researchers report online June 30 in Science. While the hole won’t close completely until at least midcentury, the researchers say the results are a testament to the success of the Montreal Protocol. That international treaty, implemented in 1989, banned ozone-depleting chemicals called chlorofluorocarbons worldwide.

Ozone helps shield life on Earth from hazardous ultraviolet radiation. Tracking the ozone layer’s recovery process is tricky because natural phenomena such as volcanic eruptions and weather variations can alter the size of the ozone hole. While some earlier studies suggested that the ozone had already begun healing (SN: 6/4/11, p. 15), many scientists questioned whether the work had been detailed enough to separate out the effects of natural variability.

MIT atmospheric scientist Susan Solomon and colleagues used a sophisticated 3-D atmospheric simulation to distinguish between the forces acting on atmospheric ozone. The work suggests that about half of the ozone hole’s recent shrinkage resulted from a drop in chlorofluorocarbons in the atmosphere; the remainder stemmed from weather changes.

Volcanic eruptions obscure healing signs. Last October, the ozone hole reached a record-setting average size of 25.3 million square kilometers — an area larger than Russia — thanks to the April 2015 eruption of Chile’s Calbuco volcano. That large size doesn’t disprove that the ozone hole is healing in the long run, though. Without the temporary 4.2-million-square-kilometer boost from the volcano, the hole’s average size would have peaked at a more modest 21.1 million square kilometers, the researchers estimate.

For a “three-parent baby,” getting disease-free mitochondrial DNA from a surrogate may do more than just avert disease: For better or for worse, a donor’s mitochondria could also affect the course of aging, new research shows.

Two strains of mice – genetically identical except for the source of their mitochondria, the energy centers of cells – aged very differently, researchers report online July 6 in Nature. Even though both mouse strains had healthy mitochondrial DNA, the mice with mitochondria that did not come from the same source as the rest of their DNA fared better later in life: After two years, these mice showed fewer signs of aging and had a lower incidence of tumors.
The results don’t necessarily mean that a mitochondria transplant leads to a healthier life. This is just one case, researchers caution. Other DNA mixes and matches could turn out differently. But the study’s finding does point to a larger relationship between mitochondrial DNA and aging and raises new questions about the long-term effects of creating three-parent babies.

What the new results mean for people is still unclear, says Michio Hirano, a neurologist at Columbia University who was not involved in the study. But if the findings do apply to humans, he says, “you can blame your mother for how you age.”

Mitochondrial DNA is passed down from mother to child. Three-parent babies are created through an in-vitro fertilization technique that substitutes a mother’s diseased mitochondria for the healthy mitochondria of a surrogate (SN: 11/17/12, p. 5). In the procedure, which is legal in the United Kingdom and deemed ethical by a U.S. panel of experts this year (SN Online: 2/3/16), a baby inherits its nuclear DNA — the majority of its genetic fingerprint — from mom and dad. But a small amount of DNA — just 37 genes — comes from the mitochondria of a second, healthy woman.

Mitochondria do more than just power cells; they also play big roles in cell-to-cell communication and metabolism. Over the last two decades, mitochondria have also been implicated in aging but without conclusive evidence. The new research, Hirano says, “adds fuel to this debate.”

In the study, José Enríquez of the Spanish National Center for Cardiovascular Research in Madrid and colleagues bred two strains of mice. The original strain was called C57/Black 6. A second strain of C57/Black 6 carried mitochondria from another kind of mouse called NZB. This mismatch mimicked the effects of a mitochondrial transplant. Early in life, normal C57 mice bulked up faster than those carrying NZB mitochondria and had 11 percent longer telomeres (protective caps at the ends of chromosomes that get shorter over time, so are used as a proxy for aging). But later in life, the mice with NZB mitochondria had longer telomeres, less fat in their muscles and lower risk of having liver tumors at the end of their lives.
Young C57 mice “tend to be stronger,” Enríquez says, probably because their mitochondrial and nuclear DNA are a good match and make efficient mitochondria. The weaker batteries in the mice with mismatched mitochondria may cause more cellular stress early on, he says, which may toughen up these mice to age more gracefully.

Since the study was done in mice, researchers don’t know how mitochondrial substitution would affect aging in humans. To avoid unforeseen and unwanted consequences, Enríquez urges caution. “Before we understand it better,” a mitochondrial transplant should mimic natural conditions, he says: “Why don’t we match the mitochondrial DNA of the donor and receptor?”