Joanna Monti-Masel and Noah Whiteman, both researchers in the University of Arizona's Department of Ecology and Evolutionary Biology, each have received research grants from the John Templeton Foundation. The scientists' separate projects in evolutionary biology will address the origins of new genes and the diversity of life on Earth, questions that have puzzled biologists for centuries.
The John Templeton Foundation aims to serve as a catalyst for discoveries relating to questions of human purpose and understanding of ultimate reality, funding research projects on topics such as complexity, evolution, creativity, forgiveness and free will.
Happy Accidents Leading to New Genes
"A big question in evolution is the origin of new stuff. Where does new stuff come from?" says Masel, an associate professor in the Department of Ecology and Evolutionary Biology and a member of the UA's Bio5 Institute.
"One example of that is where do genes come from? The original idea that had been common in evolutionary biology was that new genes come from old genes, but then you have a kind of chicken and egg problem: If new genes come from old genes, where did those old genes come from? And so on.
"I didn’t find this very credible, and there is now increasing evidence that new genes are actually appearing all the time," Masel said.
Masel will study the evolution of new genes with a grant from the John Templeton Foundation.
Masel and her team will investigate theories of how new genes could occur as well as look for instances in which they do occur in DNA, and study the possible biochemical effects of new genes in organisms.
"We look at things that are new genes, and things that might become new genes in the future," Masel said. "There's lots of DNA that could become a gene. Genomes are full of what we often call junk DNA."
Biologists believe that so-called junk DNA, sections of an organism's genome that have no apparent function, may play an important role in development of new genetic material, when some of that disused DNA becomes functional.
"That junk DNA just needs a few little elements to make a protein, but if you made a protein out of random amino acids jumbled together it would probably be really toxic, so there's a biochemistry question of how does this ever happen in a way that's benign enough to lead to a functional gene?
"The central idea is that things happen in stages," Masel said. "There's an early stage where it's just trying out being a gene, sort of a playground for evolution. We believe a lot of important things happen in that playground stage."
In order for genetic material such as junk DNA to change to develop new function, mistakes have to be made in the process by which DNA is copied and reproduced, Masel explained. These mutation errors lead to changes in the genetic material, some of which can be good, some of which are bad, and some of which have no effect at all. Before these mutations happen, other errors can happen – not in the DNA, but in the processes that turn DNA into proteins. These two kinds of errors can have similar effects.
"We have mathematical models of these error rates and how that can help this playground idea, and then we're doing analyses of genome sequences to see if we find evidence that these error rates are in fact acting on genomes before they become new genes," Masel said.
Masel's hypothesis is that higher error rates lead to more rapid evolution, or greater capacity for evolution, simply because there will be more potential for new functional genes to arise.
"One of the things we're interested in is what sets the error rate," Masel said. "For this theory for the evolution of novelty to be plausible, the error rates have to be pretty high."
Fortunately for her team's studies, they are. "When you add up everything that could go wrong in the process of copying genetic material, it's possible that a serious 20 or 30 percent of the total proteins that are made have something wrong with them."
Driving the Diversity of Life
"Most named species of life on Earth are plants and the insects that feed on them," says Noah Whiteman, an assistant professor in the department of ecology and evolutionary biology with joint appointments in the Department of Neuroscience, and the Department of Entomology and School of Plant Sciences in the College of Agriculture and Life Sciences.
"One hypothesis to explain how this tremendous diversity arose is called coevolution. In that scenario, the ability of insects to overcome toxins in plants generates insect diversity because it forces insects to become specialized, and then at the same time plants evolve new defenses that overcome insect colonization, which is followed in turn by an escape from insect herbivory and more plant diversification, followed by another bout of insect specialization and diversification, ad ininitum," which could lead to the tremendous diversity in plant and insect species that we see today, Whiteman said.
Many insects develop the same or similar strategies to combat plant defenses in a process known as convergent evolution, Whiteman explained. "Convergent evolution is a hallmark of adaptive evolution and is defined by the independent evolution of a similar trait or phenotype in distantly related species, due to a common selective agent, so one observes the same or similar phenotype."
Bat wings and bird wings are an excellent example of convergent evolution: Both are physical structures that enable the animals to fly, but the traits evolved independently in species that are only distantly related.
Whiteman received more than $300,000 from the John Templeton Foundation to study the genetic basis of convergent evolution in insects that have independently evolved resistance to digitoxin and other cardenolides, a potent chemical toxin produced by plants in the milkweed family, probably as a defense against being eaten.
"Digitoxin binds to animal sodium potassium ATP-ase, a protein that controls the pumping of sodium potassium in and out of cells and controls heart rate," Whiteman said. "Digitoxin binds to that protein and prevents the pump from working."
Digitoxin has been used medically to treat conditions like tachycardia, or abnormally fast heart rate, in humans by decreasing heart rate through its interaction with the sodium potassium pump.
Many insects that feed on milkweed independently have evolved the same amino acid substitution in their genomes that gives them resistance to the effects of digitoxin, Whiteman said.
"They're unrelated, so that suggests that there's one target for natural selection in the genomes of these insects, and that's the sodium potassium pump. They responded by coming up with the same solution to digitoxin independently," he said.
The exception is in insects that have two copies of the gene that controls the sodium potassium pump, Whiteman said. "There you see new solutions that you never see in species that have only one copy of the gene."
"One model to explain this is this classic idea of neofunctionalization," in which a gene develops new functions, Whiteman said. "In species that have two copies of the gene you see unique changes that we know confer resistance to digitoxin, but you never see these changes in species where there's a single copy."
Whiteman believes that evolution of new abilities to combat toxins produced by plants could be made possible by gene duplication events in the genomes of insects, in which some insects develop two copies of the same gene. This frees one copy of the gene for new functions while the other still performs the original, and necessary, function controlling the sodium potassium pump in cells and heart rate.
Whiteman's lab team, with collaborators Anurag Agrawal at Cornell University and Susanne Dobler at the University of Hamburg, will test this hypothesis by introducing two copies of the same gene into the genomes of fruit flies, with one copy of the gene altered to give a new function, to find out if the duplication of genes drives the diversity in insects and potentially other organisms as well.