“Our findings suggest that division of labor and political polarization — two social phenomena not typically considered together — may actually be driven by the same process,” said Tokita, a graduate student in ecology and evolutionary biology. “Division of labor is seen as a benefit to societies, while political polarization usually isn’t, but we found that the same dynamics could theoretically give rise to them both.”

In a paper published today in the Journal of the Royal Society Interface, Tokita and Tarnita examined two forces known to drive political polarization and added them to an existing model for how division of labor arises in ant communities. They found that a feedback between these two forces simultaneously resulted in division of labor and polarized social networks.

“It suggests that maybe there’s a common process underlying the organization of societies,” Tokita said.

The two forces are “social influence,” the tendency of individuals to become similar to those they interact with, and “interaction bias,” which leads us to interact with others who are already like us. The researchers combined those with a “response threshold” model of ant social dynamics, in which ants choose their activities based on which need meets a critical internal threshold.

In other words, if ants A and B have both checked community food stores recently and checked on their young recently, but A has a lower threshold for hunger while B has a lower threshold for worrying about the health of the larvae, A will head out foraging while B rushes back to the nursery. Over time, this leads A to interact with other hunger-sensitive ants, who become the foraging team, while B spends more time with other care providers, and they become the nurses. Combine that with social influence and interaction bias, and the gulf between the foragers and the nurses grows steadily wider.

When this leads to societies eating well and raising healthy young, it’s called division of labor and heralded as a cornerstone of civilization. When it leads to tribalism, it’s called a breakdown of civil discourse.

But the underlying forces might be the same, say the researchers.

“Social insect colonies thrive on the heterogeneity that leads to division of labor, but sometimes they need to make decisions that have to be embraced by the whole nest,” said Tarnita, an associate professor of ecology and evolutionary biology. “For example, when honeybees need to move their nest to a new location, it would be problematic if the colony couldn’t reach consensus and it ended up splitting,”

So what the researchers wondered next was how the social forces that polarized the ants into doing different tasks could be tamed to rebuild consensus when that was needed. Their model predicted a clear way back from polarization: fight the tendency to interact only with those who are similar, and be willing to let your internal thresholds shift a little.

“Our model predicts that if you interact with those who are different from you, over time, you’ll become similar to each other,” Tokita said. “It basically erases those differences.”

It even applies to scientists and sociologists, he added. “One of the things I hope comes from this project is that it causes people in different fields, coming at and thinking about social behavior from different perspectives, to talk to each other a little more. In this project, we learned a lot by borrowing theories from sociology and political science, and combining them with our biological model.”

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Malaria is caused by Plasmodium parasites spread to people by the bite of infected Anopheles mosquitoes.

“We don’t know what is inside malaria infections,” Dr. Cheeseman said. “We don’t know how many different genetically distinct strains of parasites there are. We don’t know how related they are to each other. We don’t know how many mosquitoes they came from.”

To help answer these questions, Dr. Cheeseman and his collaborators turned to single cell genome sequencing. Using this technology, individual malaria parasite cells are isolated and their genome amplified before being analyzed by a genome sequencer. Single cell sequencing allows researchers to capture the genetic mutations present in a single cell, and has been adopted by cancer researchers to understand how tumors evolve. This is the first time the technology was used to study malaria transmission.

Dr. Cheeseman and his international team studied single malaria-infected cells from malaria patients in Malawi, a country heavily burdened by this infectious disease. Malaria patients, who donated malaria-infected blood samples used in this study reside in Chikhwawa, a region with a large mosquito population. In this region, people may be bitten by a malaria-infected mosquito every 48 hours.

The single cell sequencing approach applied in this study provides a fresh picture of how often bites from an infected mosquito lead to a malaria infection. What researchers discovered went against conventional wisdom. Nearly all the infections they studied likely came from one mosquito bite.

“We found that complex malaria infections are predominantly caused by a single mosquito bite transmitting many genetically diverse but related parasites into the blood stream of a patient,” Dr. Standwell Nkhoma, lead author on the study and a Malawian national, stated.

Knowing this enables scientists to design more effective interventions to block mosquitoes from spreading malaria and build more sophisticated models to predict the spread of antimalarial drug resistance and malaria transmission patterns. The rise of antimalarial drug resistance is a major threat to malaria control globally as resistance to the antimalarial drugs artemisinin and piperaquine continue to spread.

Malaria infects an estimated 200 million people worldwide each year and kills more than 400,000 people, most of them children, according to the World Health Organization. “Any strides we can make in understanding this disease will make an enormous impact,” Dr. Cheeseman concluded.

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The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists.

The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.

Because these pathways are “conserved,” meaning that they have been passed down to humans through evolution, they have been the subject of intensive research. A number of drugs that extend healthy lifespan by altering these pathways are now under development. The discovery of the synergistic effect opens the door to even more effective anti-aging therapies.

The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.

“Despite the discovery in C. elegans of cellular pathways that govern aging, it hasn’t been clear how these pathways interact,” said Hermann Haller, M.D., president of the MDI Biological Laboratory. “By helping to characterize these interactions, our scientists are paving the way for much-needed therapies to increase healthy lifespan for a rapidly aging population.”

The elucidation of the cellular mechanisms controlling the synergistic response is the subject of a recent paper in the online journal Cell Reports entitled “Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity.” The authors include Jarod A. Rollins, Ph.D., and Aric N. Rogers, Ph.D., of the MDI Biological Laboratory.

“The synergistic extension is really wild,” said Rollins, who is the lead author with Jianfeng Lan, Ph.D., of Nanjing University. “The effect isn’t one plus one equals two, it’s one plus one equals five. Our findings demonstrate that nothing in nature exists in a vacuum; in order to develop the most effective anti-aging treatments we have to look at longevity networks rather than individual pathways.”

The discovery of the synergistic interaction could lead to the use of combination therapies, each affecting a different pathway, to extend healthy human lifespan in the same way that combination therapies are used to treat cancer and HIV, Pankaj Kapahi, Ph.D., of the Buck Institute, has said. Kapahi is a corresponding author of the paper with Rogers and Di Chen, Ph.D., of Nanjing University.

The synergistic interaction may also may explain why scientists have been unable to identify a single gene responsible for the ability of some people to live to extraordinary old ages free of major age-related diseases until shortly before their deaths.

The paper focuses on how longevity is regulated in the mitochondria, which are the organelles in the cell responsible for energy homeostasis. Over the last decade, accumulating evidence has suggested a causative link between mitochondrial dysregulation and aging. Rollins’ future research will focus on the further elucidation of the role of mitochondria in aging, he said.