Two scientists have come up with a depressing new hypothesis that attempts to explain why cancer is so hard to stop.
Maybe, they suggest, cancer's not working against us. Maybe the disease is actually an evolutionary 'final checkpoint' that stops faulty DNA from being passed down to the next generation.
Throughout the history of life on Earth, multicellular life evolved from single cells numerous times, but explaining how this happened is one of the major evolutionary puzzles of our time. However, scientists have now completed a study of the complete DNA of one of the most important model organisms, Gonium pectorale, a simple green algae that comprises only 16 cells.
This microscopic organism is helping to fill the evolutionary gap in our understanding. The two year research project was a global collaboration between Kansas State University, Universities of Arizona and Tokyo, and Wits University. It is documented in the prestigious journal Nature Communications.
Pierre Durand, a researcher in the department of Molecular Medicine and Haematology and the Evolutionary Studies Institute at Wits University is one of the project collaborators.
"The evolution from unicellular to multicellular life was a big deal. It changed the way the planet would be forever. From worms to insects, the dinosaurs, grasses, flowering plants, hadedas and humans, you just have to look around and see the extraordinary forms of multicellular existence," says Durand.
"It has been difficult to explain how this occurred because it was not an easy thing to have happened. So questions like 'why did single cells live together in groups at the very beginning of multicellularity when it puts them at a fitness disadvantage?' challenged us for a long time," says Durand. We still don't know most of the answers but this project has certainly filled one of the gaps in our current understanding.
There are many model systems for studying multicellularity but nothing quite like the volvocine green algae, the group to which G. pectorale belongs.
"The evolutionary transition to multicellularity has occurred numerous times in all domains of life, yet the evolutionary history of this transition is not well understood. However, the volvocine green algae include a diverse variety of unicellular, colonial, and multicellular species," says Durand.
Bdelloid rotifers were believed to have persisted and diversified in the absence of sex. Two papers now show they exchange genes with each other, via horizontal gene transfers as known in bacteria and/or via other forms of non-canonical sex.
Reptile thermogenesis and the origins of endothermy
Author:
Tattersall
Abstract:
Extant endotherms have high rates of metabolism, elevated body temperatures, usually tight control over body temperature, and a reasonable scope for further increases in metabolism through locomotor activity. Vertebrate ectotherms, on the other hand, rely on behavioural thermoregulation and cardiovascular adjustments to facilitate warming, and generally lack specific biochemical and cellular mechanisms for sustained, elevated metabolism. Nevertheless, the ancestral condition to endothermy is thought to resemble that of many extant reptiles, which raises the question of the origins and selection pressures relevant to the transitional state. Numerous hypotheses have emerged to explain the multiple origins of endothermy in vertebrates, including thermoregulatory, locomotory, and reproductive activity as possible drivers for these sustained and elevated metabolic rates. In this article, I discuss recent evidence for facultative endothermy in an extant lepidosaur, the tegu lizard. Since lepidosaurs are a sister group to the archosaurs, understanding how a novel form of endothermy evolved will open up opportunities to test the compatibility or incompatibility of the various endothermy hypotheses, with potential to elucidate and resolve long contentious ideas in evolutionary physiology.
Science for a wilder Anthropocene: Synthesis and future directions for trophic rewilding research
Authors:
Svenning et al
Abstract:
Trophic rewilding is an ecological restoration strategy that uses species introductions to restore top-down trophic interactions and associated trophic cascades to promote self-regulating biodiverse ecosystems. Given the importance of large animals in trophic cascades and their widespread losses and resulting trophic downgrading, it often focuses on restoring functional megafaunas. Trophic rewilding is increasingly being implemented for conservation, but remains controversial. Here, we provide a synthesis of its current scientific basis, highlighting trophic cascades as the key conceptual framework, discussing the main lessons learned from ongoing rewilding projects, systematically reviewing the current literature, and highlighting unintentional rewilding and spontaneous wildlife comebacks as underused sources of information. Together, these lines of evidence show that trophic cascades may be restored via species reintroductions and ecological replacements. It is clear, however, that megafauna effects may be affected by poorly understood trophic complexity effects and interactions with landscape settings, human activities, and other factors. Unfortunately, empirical research on trophic rewilding is still rare, fragmented, and geographically biased, with the literature dominated by essays and opinion pieces. We highlight the need for applied programs to include hypothesis testing and science-based monitoring, and outline priorities for future research, notably assessing the role of trophic complexity, interplay with landscape settings, land use, and climate change, as well as developing the global scope for rewilding and tools to optimize benefits and reduce human–wildlife conflicts. Finally, we recommend developing a decision framework for species selection, building on functional and phylogenetic information and with attention to the potential contribution from synthetic biology.
From Pleistocene to trophic rewilding: A wolf in sheep’s clothing
Authors:
Rubenstein et al
Abstract:
Nearly 10 y ago, we (1) critiqued the idea of Pleistocene rewilding (2), a misguided attempt to resurrect bygone ecosystems. Much has happened to the Earth’s biodiversity over the decade since the term “Pleistocene rewilding” was coined, most of it bad. More than half a billion people have been added to the world’s population, and ecosystems continue to be degraded at an alarming rate. A sixth mass extinction is underway, and poaching of megafauna has increased across sub-Saharan Africa. Unfortunately, one thing that has not happened is any serious attempt to scientifically study Pleistocene rewilding. Despite a number of publicized Pleistocene rewilding projects (Oostvaardersplassen in The Netherlands and Pleistocene Park in Siberia), we have yet to see any quantitative data concerning the impacts of megafauna reintroductions.
Reply to Rubenstein and Rubenstein: Time to move on from ideological debates on rewilding
Authors:
Svenning et al
Abstract:
In their comment (1) on our review and perspective on trophic rewilding science (2), Rubenstein and Rubenstein launch a critique not so much directed at our study as at trophic rewilding as a conservation approach. They first lament that Pleistocene rewilding has not been scientifically studied since the term was introduced. This is much in line with our study, where we conclude that empirical research on trophic rewilding is rare, fragmented, and geographically biased, with the literature dominated by essays and opinion pieces, and follow this up by providing recommendations for research opportunities and priorities. Rubenstein and Rubenstein (1) then claim that we repackage the concept of Pleistocene rewilding (3) under the new term “trophic rewilding,” defined as species introductions to restore top–down trophic interactions and associated trophic cascades to promote self-regulating biodiverse ecosystems (2). However, the two concepts are not identical. Notably, with the name and definition of trophic rewilding we provide emphasis on a clear, testable functional objective rather than on a certain time frame.
To unravel the link between past climates and animal faunas requires an exceptional fossil record. Chew, an associate professor at Western University of Health Sciences, California, used fossils from the Bighorn Basin of Wyoming, a nearly complete record of around 5 million years of mammalian evolution, to study responses of mammal communities through time. "The Bighorn Basin fossil record, particularly from this part of the basin, is one of the best early Cenozoic terrestrial records in the world." remarks Chew. "My colleagues have been assembling the fossil samples on which this work is based for more than 30 years. Their efforts have produced a superb, highly resolved, thoroughly studied record that is unparalleled. This record allows us to examine more sophisticated questions about faunal response to climate and environmental change than was previously possible."
Information on past climate in the Bighorn basin comes from the structure of carbon atoms, known as isotopes, preserved in the rock. This technique revealed three global warming events. The first occurred 55 million years ago, and has been previously linked to decreasing body-size. However, data from the next two events, occurring two million years later, is required to test if this forms part of a larger evolutionary pattern. "No other terrestrial record exists with the density of fossils necessary to test faunal response to the later hyperthermals [climatic warming]. The central Bighorn Basin record essentially documents a set of repeated, natural experiments in climate warming." Chew explains.
If you have diabetes, or cancer or even heart problems, maybe you should blame it on your dad's behaviour or environment. Or even your grandfather's. That's because, in recent years, scientists have shown that, before his offspring are even conceived, a father's life experiences involving food, drugs, exposure to toxic products and even stress can affect the development and health not only of his children, but even of his grandchildren.
But, despite a decade of work in the area, scientists haven't been able to understand much about how this transmission of environmental memories over several generations takes place. McGill researchers and their Swiss collaborators think that they have now found a key part of the molecular puzzle. They have discovered that proteins known as histones, which have attracted relatively little attention until now, may play a crucial role in the process.
They believe that this finding, which they describe in a paper just published in Science, has the potential to profoundly change our understanding of how we inherit things. That's because the researchers show that there is something apart from DNA that plays an important role in inheritance in general, and could determine whether a father's children and grandchildren will be healthy or not.
Caltech biologists have developed a nonsurgical method to deliver long-term contraception to both male and female animals with a single shot. The technique--so far used only in mice--holds promise as an alternative to spaying and neutering feral animals.
The approach was developed in the lab of Bruce Hay, professor of biology and biological engineering at Caltech, and is described in the October 5 issue of Current Biology. The lead author on the paper is postdoctoral scholar Juan Li.
Hay's team was inspired by work conducted in recent years by David Baltimore and others showing that an adeno-associated virus (AAV)--a small, harmless virus that is unable to replicate on its own, that has been useful in gene-therapy trials--can be used to deliver sequences of DNA to muscle cells, causing them to produce specific antibodies that are known to fight infectious diseases, such as HIV, malaria, and hepatitis C.
Li and her colleagues thought the same approach could be used to produce infertility. They used an AAV to deliver a gene that directs muscle cells to produce an antibody that neutralizes gonadotropin-releasing hormone (GnRH) in mice. GnRH is what the researchers refer to as a "master regulator of reproduction" in vertebrates--it stimulates the release of two hormones from the pituitary that promote the formation of eggs, sperm, and sex steroids. Without it, an animal is rendered infertile.
In the past, other teams have tried neutralizing GnRH through vaccination. However, the loss of fertility that was seen in those cases was often temporary. In the new study, Hay and his colleagues saw that the mice--both male and female--were unable to conceive after about two months, and the majority remained infertile for the remainder of their lives.
"Inhibiting GnRH is an ideal way to inhibit fertility and behaviors caused by sex steroids, such as aggression and territoriality," says Hay. He notes that in the study, his team also shows that female mice can be rendered infertile using a different antibody that targets a binding site for sperm on the egg. "This target is ideal when you want to inhibit fertility but want to leave the individual otherwise completely normal in terms of reproductive behaviors and hormonal cycling."
Hay's team has dubbed the new approach "vectored contraception" and says that there are many other proteins that are thought to be important for reproduction that might also be targeted by this technique.
You might expect that little happens in the Arctic Ocean during the cold and dark winter. But that just isn't so, according to researchers who have sampled the activities of many different species during three consecutive winters in Kongsfjorden, Svalbard. Their findings are published in the Cell Press journal Current Biology on September 24.
"This once and for all changes the way we think of marine ecosystems during the polar night," says Jørgen Berge of UiT The Arctic University of Norway and the University Centre in Svalbard.
"The dark polar night is not a period without any biological activity [as had been assumed]. Concealed behind the curtain of darkness is a world of activity, beauty, and ecosystem importance."
Berge says the researchers were inspired to look more closely at what happens during the polar night based on a chance encounter they had on a small boat in the middle of a Svalbard fjord.
"Above us was a starry, winter night and below us were countless blue-green 'stars' in the deep" produced by bioluminescent organisms, Berge says. "The beauty of it was stunning, and the fact that so many organisms were producing light was a strong indication that the system was not in a resting mode."
Epigenetic regulation of the nuclear-coded GCAT and SHMT2 genes confers human age-associated mitochondrial respiration defects
Authors:
Hashizume et al
Abstract:
Age-associated accumulation of somatic mutations in mitochondrial DNA (mtDNA) has been proposed to be responsible for the age-associated mitochondrial respiration defects found in elderly human subjects. We carried out reprogramming of human fibroblast lines derived from elderly subjects by generating their induced pluripotent stem cells (iPSCs), and examined another possibility, namely that these aging phenotypes are controlled not by mutations but by epigenetic regulation. Here, we show that reprogramming of elderly fibroblasts restores age-associated mitochondrial respiration defects, indicating that these aging phenotypes are reversible and are similar to differentiation phenotypes in that both are controlled by epigenetic regulation, not by mutations in either the nuclear or the mitochondrial genome. Microarray screening revealed that epigenetic downregulation of the nuclear-coded GCAT gene, which is involved in glycine production in mitochondria, is partly responsible for these aging phenotypes. Treatment of elderly fibroblasts with glycine effectively prevented the expression of these aging phenotypes.
It's the world's most popular building material, and ever since the Romans built the pantheon from it some 2,000 years ago, we've been trying to find ways to make concrete more durable.
No matter how carefully it is mixed or reinforced, all concrete eventually cracks, and under some conditions, those cracks can lead to collapse.
"The problem with cracks in concrete is leakage," explains professor Henk Jonkers, of Delft University of Technology, in the Netherlands.
"If you have cracks, water comes through -- in your basements, in a parking garage. Secondly, if this water gets to the steel reinforcements -- in concrete we have all these steel rebars -- if they corrode, the structure collapses."
But Jonkers has come up with an entirely new way of giving concrete a longer life.
"We have invented bioconcrete -- that's concrete that heals itself using bacteria," he says.
In a study published in the January 2015 issue of The American Naturalist, Gustavo A. Londoño, Duván Garcia, and Manuel Sánchez MartÃnez report a novel nesting strategy observed in a tropical lowland bird that inhabits an area with very high losses to nest predators.
How can tropical birds cope with the high rates of nest predation that are typical in most tropical habitats? Are there nesting strategies that allow tropical birds to escape predators such as birds, mammals, and snakes that regularly eat eggs and nestlings?
During the fall of 2012, while working on a long-term avian ecological study, the researchers discovered the second nest ever described for the cinereous mourner (Laniocera hypopyrra) at Pantiacolla Lodge in the upper Madre de Dios River in southeastern Peru. They observed that upon hatching, the chicks had downy feathers with long orange barbs with white tips, which was very different from any other nestling they had observed in the area. The peculiar downy feathers attracted their attention, but the nestling behavior provided a more important cue. While researchers were collecting morphological measurements, the nestling started moving its head very slowly from side to side in a way typical of many hairy caterpillars. While working in the area, the investigators found a poisonous caterpillar with similar size and hair coloration as the nestling. Therefore, the researchers suggest that this is an example of Batesian mimicry in which the nestling tricks predators into thinking that it is a toxic, spiny caterpillar rather than a highly edible nestling.
That humans and the cities we build affect the ecosystem and even drive some evolutionary change in species' traits is already known. The signs are small but striking: Spiders in cities are getting bigger and salmon in rivers smaller; birds in urban areas are growing tamer and bolder, outcompeting their country cousins.
What's new is that these evolutionary changes are happening much more quickly than previously thought, and have potential impacts on ecosystem function on a contemporary scale. Not in the distant future, that is -- but now.
A new paper by Marina Alberti of the University of Washington College of Built Environments' Urban Ecology Research Lab published this month in the journal Trends in Ecology & Evolution suggests that if human-driven evolutionary change affects the functioning of ecosystems -- as evidence is showing -- it "may have significant implications for ecological and human well-being."
Alberti, a professor of urban design and planning, said that until recently it was assumed that evolutionary change would take too long to affect ecological processes quite so immediately. Such thinking has prevented evidence from coming together "in a way that can only emerge through a cross-disciplinary lens," she said, observing the interactions between humans and natural processes.
"We now have evidence that there is rapid evolution. These changes may affect the state of the environment now. This is what's called eco-evolutionary feedback.
"Cities are not simply affecting biodiversity by reducing the number and variety of species that live in urban habitats," Alberti said. Humans in cities are causing organisms to undergo accelerated evolutionary changes "that have effects on ecosystem functions such as biodiversity, nutrient cycling, seed dispersal, detoxification, food production and ultimately on human health and well-being."
How a brilliant-green sea slug manages to live for months at a time "feeding" on sunlight, like a plant, is clarified in a recent study published in The Biological Bulletin.
The authors present the first direct evidence that the emerald green sea slug's chromosomes have some genes that come from the algae it eats.
These genes help sustain photosynthetic processes inside the slug that provide it with all the food it needs.
Importantly, this is one of the only known examples of functional gene transfer from one multicellular species to another, which is the goal of gene therapy to correct genetically based diseases in humans.
"Is a sea slug a good [biological model] for a human therapy? Probably not. But figuring out the mechanism of this naturally occurring gene transfer could be extremely instructive for future medical applications," says study co-author Sidney K. Pierce, an emeritus professor at University of South Florida and at University of Maryland, College Park.
The team used an advanced imaging technique to confirm that a gene from the alga V. litorea is present on the E. chlorotica slug's chromosome. This gene makes an enzyme that is critical to the function of photosynthetic "machines" called chloroplasts, which are typically found in plants and algae.
It has been known since the 1970s that E. chloritica "steals" chloroplasts from V. litorea (called "kleptoplasty") and embeds them into its own digestive cells. Once inside the slug cells, the chloroplasts continue to photosynthesize for up to nine months--much longer than they would perform in the algae. The photosynthesis process produces carbohydrates and lipids, which nourish the slug.
How the slug manages to maintain these photosynthesizing organelles for so long has been the topic of intensive study and a good deal of controversy. "This paper confirms that one of several algal genes needed to repair damage to chloroplasts, and keep them functioning, is present on the slug chromosome," Pierce says. "The gene is incorporated into the slug chromosome and transmitted to the next generation of slugs." While the next generation must take up chloroplasts anew from algae, the genes to maintain the chloroplasts are already present in the slug genome, Pierce says.
Researchers at the Stanford University School of Medicine have developed a new procedure to increase the length of human telomeres. This increases the number of times cells are able to divide, essentially making the cells many years younger. This not only has useful applications for laboratory work, but may point the way to treating various age-related disorders – or even muscular dystrophy.
Telomeres are the caps at the ends of our chromosomes that protect the DNA code of the genome. Linked to aging and disease, they are 8,000 to 10,000 nucleotides long in young people, but this decreases as we age (a nucleotide is an organic molecule that is a subunit of nucleic acids DNA and RNA). The researchers have found a way to lengthen a telomere by 1,000 nucleotides, which Dr. Helen Brau, professor of microbiology and immunology at Stanford, says is the equivalent of "many years of human life."
Telomeres shorten each time a cell divides and at a certain point, when they reach a critical length, the cell can no longer divide and will die. Their limited lifespan means that growing cells in laboratories can be tricky, given there can only be so many cell doublings before they give up the ghost. Telomere function in humans has been linked to many diseases and they have been studied for decades, often in the hope of better understanding or delaying the aging process.
Cells treated with Stanford’s procedure multiply in a similar way to much younger cells, compared with untreated cells of the same age. According to the researchers, skin cells with telomeres lengthened by the procedure were able to divide around 28 more times than untreated cells, while muscle cells divided about three more times. With this new procedure, which uses modified RNA, many more cells can be easily generated for study and drug development or disease modeling.
Human infrared vision is triggered by two-photon chromophore isomerization
Authors:
Palczewska et al
Abstract:
Vision relies on photoactivation of visual pigments in rod and cone photoreceptor cells of the retina. The human eye structure and the absorption spectra of pigments limit our visual perception of light. Our visual perception is most responsive to stimulating light in the 400- to 720-nm (visible) range. First, we demonstrate by psychophysical experiments that humans can perceive infrared laser emission as visible light. Moreover, we show that mammalian photoreceptors can be directly activated by near infrared light with a sensitivity that paradoxically increases at wavelengths above 900 nm, and display quadratic dependence on laser power, indicating a nonlinear optical process. Biochemical experiments with rhodopsin, cone visual pigments, and a chromophore model compound 11-cis-retinyl-propylamine Schiff base demonstrate the direct isomerization of visual chromophore by a two-photon chromophore isomerization. Indeed, quantum mechanics modeling indicates the feasibility of this mechanism. Together, these findings clearly show that human visual perception of near infrared light occurs by two-photon isomerization of visual pigments.
The second phase of an ambitious project to gather valuable information on ocean processes and marine life using a fleet of innovative marine robots has just reached its conclusion. Co-ordinated by the National Oceanography Centre (NOC), the Exploring Ocean Fronts project took place off southwest England and saw the largest deployment of robotic vehicles ever attempted in UK waters .
The marine robots, which are powered by a combination of wave, wind and solar power, are controlled by satellite communications and can cover hundreds of kilometres in a single mission.
In the latest phase of the project, three unmanned surface vehicles were used to track fish carrying acoustic ‘pingers’ off the Devon coast. About 85 fish, including rays, sole and plaice, were tagged and released by scientists from the Marine Biological Association (MBA), with the aim of understanding how these fish use Marine Protected Areas. The roaming robotic vehicles carried acoustic receivers and worked alongside a series of fixed receivers on the seabed in order to track fish movements inside and outside of the protected sites.
Commenting on the fish-tracking trial, Professor David Sims of the MBA said: “The patrolling robots successfully located tagged fish, and also tracked the movements of individual fish over several days by re-locating them. This demonstrates the potential of ocean robots for monitoring dynamic changes in distributions of commercially important fish, which will underpin effective management and understanding of climate change impacts”.
On the origin of sex chromosomes from meiotic drive
Authors:
Ubeda et al
Abstract:
Most animals and many plants make use of specialized chromosomes (sex chromosomes) to determine an individual's sex. Best known are the XY and ZW sex-determination systems. Despite having evolved numerous times, sex chromosomes present something of an evolutionary puzzle. At their origin, alleles that dictate development as one sex or the other (primitive sex chromosomes) face a selective penalty, as they will be found more often in the more abundant sex. How is it possible that primitive sex chromosomes overcome this disadvantage? Any theory for the origin of sex chromosomes must identify the benefit that outweighs this cost and enables a sex-determining mutation to establish in the population. Here we show that a new sex-determining allele succeeds when linked to a sex-specific meiotic driver. The new sex-determining allele benefits from confining the driving allele to the sex in which it gains the benefit of drive. Our model requires few special assumptions and is sufficiently general to apply to the evolution of sex chromosomes in outbreeding cosexual or dioecious species. We highlight predictions of the model that can discriminate between this and previous theories of sex-chromosome origins.
Through the careful study of modern and early fossil tortoise, researchers now have a better understanding of how tortoises breathe and the evolutionary processes that helped shape their unique breathing apparatus and tortoise shell. The findings published in a paper, titled: Origin of the unique ventilatory apparatus of turtles, in the scientific journal, Nature Communications, on Friday, 7 November 2014, help determine when and how the unique breathing apparatus of tortoises evolved.
Lead author Dr Tyler Lyson of Wits University's Evolutionary Studies Institute, the Smithsonian Institution and the Denver Museum of Nature and Science said: "Tortoises have a bizarre body plan and one of the more puzzling aspects to this body plan is the fact that tortoises have locked their ribs up into the iconic tortoise shell. No other animal does this and the likely reason is that ribs play such an important role in breathing in most animals including mammals, birds, crocodilians, and lizards."
Instead tortoises have developed a unique abdominal muscular sling that wraps around their lungs and organs to help them breathe. When and how this mechanism evolved has been unknown.
"It seemed pretty clear that the tortoise shell and breathing mechanism evolved in tandem, but which happened first? It's a bit of the chicken or the egg causality dilemma," Lyson said. By studying the anatomy and thin sections (also known as histology), Lyson and his colleagues have shown that the modern tortoise breathing apparatus was already in place in the earliest fossil tortoise, an animal known as Eunotosaurus africanus.
Whether birds are breathing in or out, air flows in a one-directional loop through their lungs. This pattern was unexpected and for decades, biologists assumed it was unique to birds, a special adaptation driven by the intense energy demands of flight.
But that view is wrong, according to University of Utah scientists who now have shown that bird-like breathing also developed in green iguanas - reptiles not known for high-capacity aerobic fitness. The finding bolsters the case that unidirectional bird-like flow evolved long before the first birds, arising nearly 300 million years ago in a common ancestor of lizards, snakes, crocodiles and dinosaurs including birds.
"We thought we understood how these lungs work, but in fact most of us were completely wrong," says Colleen Farmer, an associate professor of biology at the U and lead author of the new study published today in Proceedings of the National Academy of Sciences. "People have made a lot of assumptions about how lungs work in animals such as reptiles and crocodiles but they never actually measured flow," she says.
In humans and other mammals, lungs have airways with a tree-like branching structure. A main trunk in each lung splits into branches and twigs. Air flows in and out in a tidal fashion. Oxygen and carbon dioxide pass to and from blood in tiny air sacs, called alveoli, at the tips of the smallest airway branches.
In bird lungs, air loops in one direction through a series of tubes lined with blood vessels for gas exchange. Aerodynamic forces act like valves to sustain the one-way flow through cycles of inhalation and exhalation.
