Bacteria in the sky may help to make it rain

Here's how they do it.

By Veronique Greenwood

PSEUDOMONAS SYRINGAE

This species of bacteria can cause ice to form, even at temperatures that are warmer than freezing.

James Kremer and Sheng Yang He via Howard Hughes Medical Institute

Microbes are everywhere—in your gut, on your skin, even in the sky. Along with water vapor and particles, clouds also contain living bacteria. And certain airborne species have a superpower: They can cause water to freeze into ice, which in turn prompts the heavens to open. Once frozen granules form around bits of dust, minerals, or tiny organisms, they fall, melting on the way down to become raindrops or forming flakes to make snow. This means the little life-forms might contribute to rainfall—but how much?

“If you loaded up a cloud with these microbes, it would create freezing and the processes that lead to precipitation,” confirms University of Florida’s Brent Christner, who studies atmospheric bacteria. “The unknown factor is, are there enough of them up there to matter?” Christner and other researchers are sending weather balloons and planes on sampling missions to try to answer the question—and shed light on what these citizens of the sky get out of the deal. They might use clouds to travel long distances before raining down on fresh new habitats.

In the image below, scroll over each red dot to learn more about the mechanisms behind this stormy process.

Illustration by Valerio Pellegrini

This article originally appeared in the Extreme Weather issue of Popular Science.

Having worms can be good for the gut

THE WORM TURNS  Intestinal parasites may have an upside. Researchers have discovered that people with whipworms (Trichuris trichiura, left) and mice with Heligmosomoides polygyrus (right) have fewer inflammation-provoking bacteria than they do without the worms. 

Parasites trigger immune reaction that can calm inflammation

BY 

TINA HESMAN SAEY

Parasitic worms may hold the secret to soothing inflamed bowels.

In studies of mice and people, parasitic worms shifted the balance of bacteria in the intestines and calmed inflammation, researchers report online April 14 in Science. Learning how worms manipulate microbes and the immune system may help scientists devise ways to do the same without infecting people with parasites.

Previous research has indicated that worm infections can influence people’s fertility (SN Online: 11/19/15), as well as their susceptibility to other parasite infections (SN: 10/5/13, p. 17) and to allergies (SN: 1/29/11, p. 26). Inflammatory bowel diseases also are less common in parts of the world where many people are infected with parasitic worms.

P’ng Loke, a parasite immunologist at New York University School of Medicine, and colleagues explored how worms might protect against Crohn’s disease. The team studied mice with mutations in the Nod2gene. Mutations in the human version of the gene are associated with Crohn’s in some people.

The mutant mice develop damage in their small intestines similar to that seen in some Crohn’s patients. Cells in the mice’s intestines don’t make much mucus, and more Bacteroides vulgatus bacteria grow in their intestines than in the guts of normal mice. Loke and colleagues previously discovered that having too much of that type of bacteria leads to inflammation that can damage the intestines.

In the new study, the researchers infected the mice with either a whipworm (Trichuris muris)or a corkscrew-shaped worm (Heligmosomoides polygyrus). Worm-infected mice made more mucus than uninfected mutant mice did. The parasitized mice also had less B. vulgatus and more bacteria from the Clostridiales family. Clostridiales bacteria may help protect against inflammation.

“Although we already knew that worms could alter the intestinal flora, they show that these types of changes can be very beneficial,” says Joel Weinstock, an immune parasitologist at Tufts University Medical Center in Boston.

Both the increased mucus and the shift in bacteria populations are due to what’s called the type 2 immune response, the researchers found. Worm infections trigger immune cells called T helper cells to release chemicals called interleukin-4 and interleukin-13. Those chemicals stimulate mucus production. The mucus then feeds the Clostridiales bacteria, allowing them to outcompete the Bacteroidales bacteria. It’s still unclear how the mucus encourages growth of one type of bacteria over another, Loke says.

Blocking interleukin-13 prevented the mucus production boost and the shift in bacteria mix, indicating that the worms work through the immune system. But giving interleukin-4 and interleukin-13 to uninfected mice could alter the mucus and bacterial balance without worms’ help, the researchers discovered.

Loke and colleagues also wanted to know if worms affect people’s gut microbes. So the researchers took fecal samples from people in Malaysia who were infected with parasitic worms.  

After taking a deworming drug, the people had less Clostridiales and more Bacteriodales bacteria than before. That shift in bacteria was associated with a drop in the number ofTrichuris trichiura whipworm eggs in the people’s feces, indicating that getting rid of worms may have negative consequences for some people.

Having data from humans is important because sometimes results in mice don’t hold up in people, says Aaron Blackwell, a human biologist at the University of California, Santa Barbara. “It’s nice to show that it’s consistent in humans.”

Worms probably do other things to limit inflammation as well, Weinstock says. If scientists can figure out what those things are, “studying these worms and how they do it may very well lead to the development of new drugs.” 

Gut reaction

In normal mice (top), the cells lining the intestines form fingers reaching toward the hollow center. In mice with a mutation in the Nod2 gene (middle), the intestinal lining is often swollen and damaged (an abscess shown). But infecting mutant mice with a whipworm (Trichuris muris) can restore the gut to health (bottom) by promoting mucus production and shifting the mix of bacteria that live the intestines.

Citations

D. Ramanan et al. Helminth infection promotes colonization resistance via type 2 immunity.Science. Published online April 14, 2016. doi: 10.1126/science.aaf3229. 

D. RAMANAN ET AL/SCIENCE 2016

SOME VIRUSES HAVE THEIR OWN IMMUNE SYSTEMS

Mimivirus

A large virus, called a mimivirus, under an electron microscope.

AND IT WORKS KIND OF LIKE CRISPR

By Alexandra Ossola

Just like bacteria, giant viruses need to protect themselves from invasive microbes, and they do so with the help of an immune system that works quite similar to the CRISPR system found in bacteria (and now borrowed by human geneticists) according to a study published today in Nature.

In 2003, researchers Didier Raoult and Bernard La Scola of Aix-Marseille University in France discovered something strange lurking in amoebas: giant viruses, visible under a typical microscope, and about four times larger than the ones we often see infecting human cells. Collectively they’re called mimiviruses because they appear to mimic bacteria.

In the intervening years, these researchers have discovered 150 different types of these large viruses, according to Stat News, such as megaviruses andpandoraviruses. Many of these challenge the traditional definition of a virus; Raoult has controversially claimed that mimiviruses make up a new branch of the tree of life, according to Nature News.

One way these mimiviruses have proven different is that they themselves can be attacked by smaller viruses. But in 2014, the researchers realized that viruses can invade only certain types of mimiviruses. They hypothesized that these large viruses had immune systems much like bacteria's, in which they would incorporate little bits of their attackers’ DNA into their own genetic code. That way, if the same virus tried to invade again, the host would be able to identify the unwanted attacker and kill it. Those bits of invaders’ genetic code in an organism’s DNA are called CRISPR; by taking advantage of this unique pattern and of its accompanying gene-snipping enzyme, Cas9, researchers have been working to create more robust crops and eliminatediseases in humans.

The researchers wanted to test these large viruses to see if they did in fact have a CRISPR-like immune system. So they analyzed the genomes of 60 strains of mimiviruses looking for the telltale snips of DNA from a much smaller virus (or virophage) called Zamilon, known to attack many of them. As they expected, the researchers found that mimiviruses immune to Zamilon had bits of its genetic code lodged in their own. The researchers also found that the mimiviruses contain enzymes capable of degrading foreign DNA, just as CRISPR does. The researchers named this viral immune system the MIMIVIRE, which stands for “mimivirus virophage resistance element.”

As The Atlantic points out, the MIMIVIRE isn’t the same as CRISPR—it’s just a good example of convergent evolution. But it does provide more evidence that mimiviruses are different from other, simpler viruses, possibly shifting the discussion about their evolutionary origins or whether they’re alive. In the future, the researchers hope to better understand the mechanisms that drive the MIMIVIRE.

Year in review: Fluke extinction surprises lab

CAUSE OF DEATH  Researchers previously believed that the extinction in one flask of bacteria in a long-term evolution experiment was the result of survival of the fittest. This year, scientists discovered the bacteria's demise was more likely an accident. 

Accident, not competition, wiped out E. coli

BY 

TINA HESMAN SAEY 

A die-off of bacteria that had been growing for thousands of generations in a carefully controlled lab experiment offered an evolutionary lesson this year: Survival depends not only on fitness but also on luck.

For more than a quarter century, evolutionary biologist Richard Lenski and colleagues have been growing 12 flasks of E. coli at Michigan State University. About 31,000 generations in, some of the bacteria in one flask evolved the ability to use a chemical called citrate as an energy source. Bacteria in that flask that couldn’t eat citrate went extinct, seemingly because they had been outcompeted, the scientists thought.

But when Lenski and his team replayed evolution, reviving samples stored before the non-citrate eaters vanished, these bacteria survived 40 out of 40 times in a mixed population. An unknown lab accident probably finished them off the first time around, the team concluded this year (SN: 9/19/15, p. 11). Unlike in the real world, these bacteria are getting another shot at survival. A 13th flask has been added to the experiment.

Year in review: Microbe discoveries spur rethink of treetop of life

LIFE STORIES  DNA samples of microbes discovered near hydrothermal vents like this one in the Arctic Mid-Ocean Ridge may be the closest kin yet known to complex life.

Scientists consider deep history of eukaryotes

BY 

SUSAN MILIUS

Microbes discovered in Arctic mud could be the closest relatives yet found to the single-celled ancestor that swallowed a bacterium and made life so complicated. Biologists have proposed that this swallowing event, perhaps 1.8 billion years ago, led to complex cells with membrane-wrapped organelles, the hallmark of all eukaryotes from amoebas to zebras.

Researchers discovered the new phylum of microbes, dubbed Lokiarchaeota, by screening DNA from sediment (SN: 5/30/15, p. 6). Though no one has identified an actual cell yet, the new phylum appears to mingle genes similar to those in modern eukaryotes and genes from archaea, the sister group to bacteria. Analyses suggest the cells have dynamic structures that could have engulfed bacteria long ago. (Biologists have proposed representing that merger as a ring of life, rather than a tree.) What happened next in the tale is clearer but still a puzzle.

Forget the split

Unlike the three-domain tree, the ring conveys that bacteria and archaea merged to give rise to eukaryotes.

SOURCE: W. MARTIN AND T.M. EMBLEY/NATURE 2004, J.O. MCINERNEY ET AL/NATURE REVIEWS MICROBIOLOGY 2014

“We don’t have all the existing pieces right now because a lot of the diversity of microbial eukaryotes remains unexplored,” says Patrick Keeling of the University of British Columbia in Vancouver, who studies early eukaryote history. But what scientists have found has radically reshaped the old multicellular-biased tree of life learned by generations of schoolchildren.

This year marked the 10th anniversary of a paper, in the Journal of Eukaryotic Microbiology, that served as an obituary for that tree (SN: 8/8/15, p. 22). Old textbooks had drawn a eukaryote treetop that branched into three kingdoms of mostly multicellular organisms (plants, animals and fungi) and one hodgepodge kingdom of single-celled beasts called Protista. Beginning in the late 1980s, though, new genetic studies relegated the multicelled kingdoms to mere side branches on five to seven much bigger branches of mostly single-celled protists.

This new scheme has held up “pretty well,” says Sina Adl of the University of Saskatchewan in Saskatoon, a coauthor on the 2005 paper. In the May 22 Science, for example, the Tara Oceans consortium, which surveyed plankton worldwide, classified diversity using the new divisions: SAR, Amoebozoa, Archaeplastida, Excavata and Opisthokonta (to which humans belong). These aren’t exactly house-hold names, though — at least not yet.

Microbes show up on schedule after death

MICROBIAL CLOCK  Telltale crews of microbes (including bacteria from a group called Enterobacteria, shown here) colonize the soil beneath a decomposing body during different stages of decay.

BY MEGHAN ROSEN

Dead people tell no tales — but dead people’s microbes do.

Bacteria, fungi and worms living in the soil beneath a decomposing body can help reveal the time — and place — of death, scientists report December 10 in Science.

Researchers have tracked the comings and goings of cadaver microbes before, but the new study is the mostcomprehensive survey yet. For months, microbial ecologist Jessica Metcalf of the University of Colorado Boulder and colleagues tallied up microbes on and near dead mice and humans.

As bodies decayed, similar microbes cropped up like clockwork, even on different soil types and during different seasons of the year, the team found. The microbes were so predictable that researchers could estimate the time of death (within a few days) of a body that had been dead for about a month.

And because telltale microbes stayed in the soil long after a body had been moved, they could offer investigators clues about potential crime scenes, the team suggests.