Virus steals black widow poison gene to help it attack


 In one of the most unexpected genetic thefts ever, a virus that infects bacteria appears to have stolen the gene coding for the poison of the black widow spiders. The virus, called WO, probably uses the gene to help it attack its targets.

Wolbachia infected by viruses, enlarged in the inset (bottom left)


( from Michelle Marshall and Seth Bordenstein)

WO, however, faces a new and difficult challenge: its targets are Wolbachia bacteria living within the cells of insects, spiders, and some other animals. That means that for it to infect new bacterial cells, WO has to escape not only from its existing host, but also from the eukaryotic cell and, at end, the virus particles have infected a new host.

 Many viruses of eukaryotic cells co-opt genes from their hosts to help them do this. To verify if WO acts in the same way, Sarah and Seth Bordenstein, microbiologists at Vanderbilt University in Nashville, Tennessee, sequenced its genome and studied the provenance of its genes.

They found several genes closely related to ones found in eukaryotes, including the gene for latrotoxin, the poison used by black widow spiders. It kills by poking holes in cell membranes, making it a plausible tool for a virus needing to escape from a eukaryotic cell. WO also had other genes like those in eukaryotes, and these may help it evade the immune system.


This is the first time eukaryotic genes have turned up in a bacterial virus. What’s more, the eukaryote genes make up almost half of WO’s genome.

“For a phage to devote about half its genome to these eukaryotic-like genes, they must be important to the phage function,” says Sarah Bordenstein. WO probably picks up the eukaryote DNA after breaking out of a Wolbachia cell into the animal cell.


This unusual gene theft shows the evolutionary adaptability of phage viruses, says Ry Young, director of the Center for Phage Technology at Texas A&M University, College Station.

Their high mutation rate, rapid life cycle and vast numbers mean that almost any conceivable adaptation is likely to occur relatively quickly. “Phages are the most advanced form of life on Earth,” he says, only partly in jest. “They’ve evolved more than we have.”


Paper reference: Bordenstein, S. R. & Bordenstein, S. R. Eukaryotic association module in phage WO genomes from Wolbachia. Nat. Commun. 7, 13155 doi: 10.1038/ncomms13155 (2016).


One-celled life possessed tools for going multicellular


MOLECULAR TOOLKIT: Capsaspora owczarzaki, a unicellular organism closely related to animals, uses molecular tools shared by multicellular organisms to move through its different life stages.


Scaling up from one cell to many may have been a small step rather than a giant leap for early life on Earth. A single-celled organism closely related to animals controls its life cycle using a molecular toolkit much like the one animals use to give their cells different roles, scientists report October 13 in Developmental Cell.

“Animals are regarded as this very special branch, as in, there had to be so many innovations to be an animal,” says David Booth, a biologist at the University of California, Berkeley who wasn’t part of the study. But this research shows “a lot of the machinery was there millions of years before animals evolved.”


Multicellular organisms need to be able to send messages between their cells and direct them to particular roles within the body. That requires a great deal of cell-to-cell coordination — something that unicellular organisms don’t have to deal with. But an amoeba (Capsaspora owczarzaki) employs many of those same tricks to switch its single-celled body between different life stages. That means that the earliest animals were probably “recycling mechanisms that were already present before,” says study coauthor Iñaki Ruiz-Trillo, a biologist at the Institute for Evolutionary Biology in Barcelona.


  1. owczarzaki goes through three different life stages, acting independently in some stages and aggregating with other amoebas in others. Ruiz-Trillo and colleagues analyzed C. owczarzaki’s proteome — its complete set of proteins — during each life stage.


This study suggests that the unicellular common ancestor of today’s animals and C. owczarzaki probably used these same tricks, too, paving the way for multicellular life. That’s not to say animals don’t get any credit, says Sabidó — they’ve expanded this toolkit further over time. But the perceived chasm between a simple single-celled existence and a complex multicellular one might not have required a flying leap to cross.  “This gap,” Sabidó says, “maybe isn’t such a gap.”


Paper Reference: A. Sebé-Pedrós et al. High-Throughput Proteomics Reveals the Unicellular Roots of Animal Phosphosignaling and Cell Differentiation. Developmental Cell. Vol. 39, October 24, 2016, p. 1. doi:10.1016/j.devcel.2016.09.019.




Placenta protectors no match for toxic Strep B pigment

MICROBIAL MACHETE: A toxic pigment made by Strep B bacteria destroys infection-fighting cells called neutrophils (healthy neutrophil, left; one exposed to a pigmented strain of Strep B, middle; one exposed to a hyperpigmented strain, right).


A type of bacteria that can cause stillbirth and fatal illness in newborns attacks with an unlikely weapon: an orange pigment made of fat.


This pigment mutilates infection-fighting immune system cells, enabling the bacteria — Group B Streptococcus — to quickly cross the placenta and invade the amniotic sac, a new study in monkeys shows. In one case, it took as little as 15 minutes for the bacteria to cross the protective membrane, researchers report October 14 in Science Immunology.


“That’s shocking,” says study coauthor Kristina Adams Waldorf, a specialist in obstetrics and gynecology at the University of Washington in Seattle. “The poor placenta has no time to control the invasion.”

Strep B bacteria are an often harmless part of the gastrointestinal tract and vaginal flora of healthy women. But during pregnancy, the bacteria can cause serious problems, including preterm labor, stillbirth and life-threatening infections.


Previous work led by study coauthor Lakshmi Rajagopal, a microbiologist at Seattle Children’s Research Institute and the University of Washington, found that strains of Strep B isolated from the amniotic fluid of women who went into preterm labor made an orange pigment. Experiments in lab dishes revealed that these pigmented strains were especially good at invading the placenta.


The researchers studied the progression of infection in macaques, whose pregnancy closely mimics human pregnancy. Ten pregnant monkeys got a strain of Strep B that makes a lot of pigment or a strain that couldn’t make the pigment. (Five additional monkeys got saline solution as a control.)

Only one monkey in the group exposed to pigment-free Strep B had a problematic pregnancy. But pregnancies in all the monkeys exposed to pigmented Strep B had problems. Four went into early preterm labor; the fifth had an emergency C-section after researchers found discolored amniotic fluid indicating an infection.

Pathogen-fighting neutrophils flooded the site of infection, but to no avail, the researchers found. Strep B’s pigment, a long chain of fat attracted to cell membranes, quickly poked holes in the neutrophils. Unlike some bacterial weaponry, the pigment “doesn’t make a nice defined hole,” says Rajagopal. “It inserts in random places, disfiguring the membrane.” Neutrophils are known to expel their innards, ensnaring invaders in a mess of DNA and chromatin, but those traps were ineffective against the pigment.


“This is a beautiful, elegant study,” says Maria Gloria Dominguez-Bello of the New York University School of Medicine. The work raises lots of questions, such as how Strep B can go from harmless to dangerous. “Why can we live with such a potential enemy? And how can we avoid the virulent strains?” Dominguez-Bello asks.


Paper Reference: E. Boldenow et al. Group B streptococcus circumvents neutrophils and neutrophil extracellular traps during amniotic cavity invasion and preterm labor. Science Immunology. Published online October 14, 2016.  doi: 10.1126/sciimmunol.aah4576.

Written by: Federico Dona