UC Berkeley
2021 Stories
The evolution of tuskless elephants foils poachers, but at a cost
Between 1977 and 1992, a civil war in Mozambique killed over a million people, displaced five million more, and destroyed roads, schools, and hospitals. It also killed a lot of elephants. Armies need money to fight, and ivory from elephant tusks was a way to get it. The protected elephant population in Gorongosa National Park in Mozambique was decimated by ivory poachers. Before the war in 1972, the park was home to 2542 elephants. By the year 2000, that number had fallen to just 242. Now, recent research shows that poaching during this period caused rapid evolution in the elephant population, specifically, the rise of tuskless elephants.
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A decade of change, a decade of Evo in the News
In science, explanations like evolution are accepted or rejected based on evidence — and in that sphere, evolutionary theory has more than proven its worth. Experiments, field studies, observations, and fossils — all of it lines up behind the idea that different species evolved from shared ancestors and that natural selection and other evolutionary processes shape the traits of lineages. However, in the public sphere, particularly in the United States, evolutionary theory has not fared so well. Between around 1950 and 2007, surveys suggest that less than half of American adults accepted evolution. But that is changing. Researchers just announced that, over the last decade, we crossed over the halfway mark: the majority of American adults surveyed now report accepting evolution as an explanation for humans. The new research delves into factors that might help explain this shift, such as a rise in number of people enrolling in four-year college degree programs and college-level science courses. Here, we’ll focus on the evolutionary science that accompanied this uptick in acceptance.
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Pantry staples from the genetic swap meet
To many people, genetically engineered food feels unnatural and repellent: Fish genes in strawberries? No thanks. Opponents often call them “Frankenfoods,” suggesting that only a mad scientist could combine genes from different species in this way. But in recent decades, biologists have found that nature itself often plays fast and loose with DNA. The more we’ve looked, the more examples we’ve found where a gene from one species has made its way into another, sometimes distantly related, species. Now, new research shows how important this inter-species genetic swap meet has been in grasses, a group that includes food staples like rice, corn, wheat, and sugar cane.
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The genetic toolkit for evolving a venomous bite
If you scrolled past the non-stop coronavirus reporting in science news last month, you might have been hooked by some obvious clickbait “Humans will probably evolve to be venomous.” Uh…they will? Well, of course not. We needn’t worry about (or eagerly anticipate) becoming a lineage of fanged mutants. However, a look at the new research that inspired that extreme headline does provide a fascinating glimpse into how (and how easily) venom evolves in some situations.
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Viruses, variation, and vaccines
Last month, we discussed new strains of SARS-CoV-2 and how they evolved, despite the relatively slow pace of coronavirus evolution. Since then, the new strains have continued to spread and more have popped up. This month, with over 15% percent of the US at least partially vaccinated, we all want to know how effective the existing vaccines will be against those new strains. Will we need another shot for the new viral varieties in six months? And then again in a year? And so on indefinitely? As we face down a future that almost certainly means learning to coexist with the virus in some way, it’s worth asking a big-picture question: why do some vaccines successfully beat back a disease year after year and others do not?
Read more »Virus, variabilidad y vacunas
El mes pasado, hablamos sobre las nuevas cepas del SARS-CoV-2 y sobre cómo habían evolucionado, aunque su ritmo de evolución sea relativamente lento. Desde entonces, las cepas nuevas han seguido propagándose y algunas más han aparecido. Este mes, con cerca del 15% de la población de US, al menos, parcialmente vacunada, todos queremos saber la efectividad que tendrán las vacunas existentes contra estas nuevas cepas. ¿Dentro de seis meses necesitaremos otro pinchazo contra las nuevas variedades del virus? ¿Y al cabo de un año otra? ¿Y así indefinidamente? Mientras nos enfrentamos a un futuro que seguramente nos llevará a coexistir con el virus, vale la pena hacerse una pregunta general tiene sentido preguntarse sobre el gran escenario: ¿por qué algunas vacunas tienen éxito contra unas enfermedades año tras año, mientras que otras no?
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The new coronavirus strains and evolution’s “I told you so” moment
It seems like new coronavirus strains are suddenly popping up everywhere. These include the “UK” strain, a variant discovered in South Africa, two in Brazil, and now one in California, inspiring many anxious questions. Do these new strains spread more easily? At least some of them seem to. Are they more deadly? Evidence is just coming in but the British variant, at least, may be. Will our vaccines work against them? To varying degrees. Moderna is developing a booster shot to make its vaccine more effective against the strain from South Africa. As researchers try to sort out answers to these key questions, it’s worth taking a step back to ask how we got here. What’s the force behind all these new strains? Of course, the answer is evolution.
Read more »2020 Stories
Have long wings, will travel
This year, many Americans are refraining from holiday travel to slow the spread of COVID-19. While we are stuck at home, though, many of us can look out the window or take a walk to appreciate a different sort of annual trek, one that continues in full swing … or, in this case, full wing. During their annual migration in the fall, monarch butterflies travel from their summer range across North America to warmer sites in Mexico and the southern United States, where their food plant (the milkweed Asclepia) is available even in the dead of winter. They make the return trip in the spring. In the last few weeks, monarchs have been spotted in most southern U.S. states and in central Mexico as they leave the cold weather behind. This trip is a true family affair. No single butterfly will live long enough to make the entire return trip; instead they breed en route. However, some monarchs skip the family vacation entirely. Over the last 200 years, monarchs have spread around the world, seeding populations that stay put and don’t migrate at all. Now, new research reveals the evolution that accompanied and follows these colonizations.
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Human evolutionary history impacts our COVID-19 risk
One more COVID story, and then next month we promise to bring you something different. Evolution underlies much research on SARS-CoV-2 so it keeps popping up in important and fascinating ways:
Since the beginning of the pandemic, scientists have wondered why SARS-CoV-2 affects people so differently. Some wind up on life support or die, while others don’t even notice they are infected. Most factors that tip this balance turned out to be more environmental than evolutionary. We now know that smoking, obesity, and conditions like cancer and diabetes can make COVID-19 more dangerous. Other research highlights how social inequalities and racial disparities contribute to higher infection, hospitalization, and death rates in some groups (e.g., Black and Hispanic Americans). However, studies have also revealed gene variants associated with increased risk, and one set of these has a deep evolutionary history among not just humans, but our ancient relatives: Neanderthals.
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La historia evolutiva del ser humano afecta nuestro riesgo de padecer COVID-19
Les compartimos un relato más sobre el COVID, y el mes próximo prometemos traerles algo diferente. La evolución es la base de muchas investigaciones sobre el SARS-COV-2, que sigue emergiendo presentando contenido importante y apunta a caminos fascinantes de investigación.
Desde el principio de la pandemia, los científicos se han preguntado por qué el SARS-CoV-2 afecta a la gente de forma tan diferente. Algunos sobreviven con ayuda de soporte vital para el resto de sus vidas, otros mueren, mientras que otros ni siquiera se enteran de que han sido infectados. La mayoría de factores que desequilibran este balance parecen estar relacionados con factores más ambientales que evolutivos. Sabemos que fumar, estar sobrepeso, o padecer de condiciones como cáncer o diabetes pueden hacer al Covid-19 más peligroso. Otras investigaciones señalan que las desigualdades sociales y las disparidades raciales o étnicas contribuyen a agravar la infección, la hospitalización, y la tasa de mortalidad en algunos grupos (ej.: lafroamericanos o hispanos/latinxs). A pesar de todo, los estudios también revelan variantes genéticas asociadas a un incremento del riesgo, y un conjunto de estas variaciones remontan a nuestra profunda historia evolutiva no entre los humanos sino entre nuestros antiguos parientes, los neandertales.
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Is the coronavirus’ ability to spread evolving…or not?
Early in the pandemic, a particular mutation in the virus that causes COVID-19 (SARS-CoV-2) caught scientists’ attention. The mutation, known as D614G, makes a small change to the virus, causing a single amino acid in the spike proteins of the virus to be swapped for a different amino acid. After the mutation arose (likely in China), it spread, and lineages carrying this mutation came to dominate many outbreaks. This left scientists wondering if the D614G mutation is an adaptation that helped the virus along as it spread around the world. Since then, every month brings a new slew of studies on the mutation, along with alarming headlines. September 2020 was no exception. The Washington Post declared about a recent D614G investigation, “Massive genetic study shows coronavirus mutating and potentially evolving amid rapid U.S. spread.” And yet, many scientists question whether D614G is anything notable. Here, we’ll briefly explain the lines of evidence and a few different evolutionary explanations for what’s going on.
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Evolution explains mosquitoes’ taste for human blood
This summer the coronavirus pandemic forced many residents of the northern hemisphere out of air-conditioned spaces and into the great outdoors for socially distanced get-togethers, barbecues, playdates, drive-in movies, and dining. There, we became the de facto buffet for biting insects. While we balanced our drinks, mosquitoes also had a sip … of human blood. New research published this summer explains why some mosquitoes just can’t leave humans alone, while others prefer a nice, juicy guinea pig. The answer, of course, comes down to evolution…
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Tracking COVID-19 outbreaks with evolution
Earlier this month, an autopsy revealed that COVID-19 began killing people in the United States weeks before we noticed. The earliest COVID-19 death now appears to be a Californian who died on February 6, 2020, not the Washington State residents who died 20 days later, the previous “first” deaths. The newly discovered coronavirus victims had not traveled recently and probably caught it from someone in the community. This suggests that the virus was spreading person-to-person in the U.S. earlier than previously believed. The revised timeline also fits well with new evidence collected by scientists who use evolutionary techniques to unveil the sources and course of COVID-19 outbreaks.
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The deep evolutionary history of the new coronavirus
For the past month, news of the pandemic coronavirus, known as COVID-19, has rattled people across the U.S. and around the globe. Internationally, the nearly 1.2 million cases have resulted in more than 60,000 deaths. Businesses have shuttered, jobs have disappeared, large swaths of the population have been asked to shelter in their homes, and many others have been left homeless, hungry, and scared. Our last Evo in the news story explained how evolutionary theory helps answer important questions about the origin of the pandemic. This month we’ll dig even deeper into the virus’s evolutionary history and how those deep relationships relate to prospects for a vaccine.
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Evolution of an outbreak
For the past month, each day has brought worrisome news: more cases of the new coronavirus popping up around the world. This virus was first identified in Wuhan China, just two months ago. Since then it has spread to Southeast Asia, Australia, Europe, and North America. While the virus is no Ebola — its symptoms are much like those of the flu — it is much more transmissible than Ebola and still deadly, killing around 3% of those sickened. New diseases, like this coronavirus, Ebola, SARS, and MERS, might seem to appear out of nowhere. But in fact, these diseases are merely new to us humans. They have all been infecting other species for a long time and only recently made the evolutionary leap to humans.
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A “new mode” of evolution?
In the age of clickbait, headlines are best consumed with more than a grain of salt. Is Thailand really in for a “Viral Rampage!” of the new coronavirus? Is Kim Jong-un’s aunt actually “Back from the Dead?” Did the United States literally cut a deal with killer pirates? Possibly…but more often than not, the truth is less sensational. So when a science news site exclaims over the “new mode of evolution” recently uncovered by scientists (as the website LiveScience did last month), it’s worth digging deeper…
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Experimenting with evolution to fight bacteria
Pseudomonas aeruginosa is a killer. This bacterium causes thousands of deaths each year in the United States and was recently placed on the World Health Organization’s list of 12 antibiotic resistant pathogens that pose the most serious threats to human health. P. aeruginosa tends to hit people when they are down — already in the hospital recovering from some other injury or disease. In this setting, the bacterium is exposed to many different drugs, encouraging the evolution of antibiotic resistance. There, it also encounters many different bacteria, allowing the microbe to acquire from these other lineages bits of DNA that contain genes for resistance to still other antiobiotics. The result is deadly pathogen that is extremely difficult to fight. But scientists have not given up hope. Now, new research suggests that we may be able to exploit the bacterium’s own evolutionary tendencies to beat it.
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