Lifeboat Foundation

The Tasmanian devil (Sarcophilus harrisii), the largest marsupial carnivore, is endangered due to a transmissible facial cancer spread by direct transfer of living cancer cells through biting. Here we describe the sequencing, assembly, and annotation of the Tasmanian devil genome and whole-genome sequences for two geographically distant subclones of the cancer. Genomic analysis suggests that the cancer first arose from a female Tasmanian devil and that the clone has subsequently genetically diverged during its spread across Tasmania. The devil cancer genome contains more than 17,000 somatic base substitution mutations and bears the imprint of a distinct mutational process. Genotyping of somatic mutations in 104 geographically and temporally distributed Tasmanian devil tumors reveals the pattern of evolution and spread of this parasitic clonal lineage, with evidence of a selective sweep in one geographical area and persistence of parallel lineages in other populations.

Circa 2013

In a feat of “molecular time travel,” the researchers resurrected and analyzed the functions of the ancestors of genes that play key roles in modern human reproduction, development, immunity and cancer. By re-creating the same DNA changes that occurred during those genes’ ancient history, the team showed that two mutations set the stage for hormones like estrogen, testosterone and cortisol to take on their crucial present-day roles.

“Changes in just two letters of the genetic code in our deep evolutionary past caused a massive shift in the function of one protein and set in motion the evolution of our present-day hormonal and reproductive systems,” said Joe Thornton, PhD, professor of human genetics and ecology & evolution at the University of Chicago, who led the study.

“If those two mutations had not happened, our bodies today would have to use different mechanisms to regulate pregnancy, libido, the response to stress, kidney function, inflammation, and the development of male and female characteristics at puberty,” Thornton said.

Continue reading “Two mutations triggered an evolutionary leap 500 million years ago” »

Circa 2011 essentially cancer could help with evolution as it can challenge the immune system to be more strong. Essentially a symbiotic relationship to evolve with it and grow stronger with it then like it can be used as a good thing to make sure that evolution has stronger genetic code.

Evolutionary theories are critical for understanding cancer development at the level of species as well as at the level of cells and tissues, and for developing effective therapies. Animals have evolved potent tumor suppressive mechanisms to prevent cancer development. These mechanisms were initially necessary for the evolution of multi-cellular organisms, and became even more important as animals evolved large bodies and long lives. Indeed, the development and architecture of our tissues were evolutionarily constrained by the need to limit cancer. Cancer development within an individual is also an evolutionary process, which in many respects mirrors species evolution. Species evolve by mutation and selection acting on individuals in a population; tumors evolve by mutation and selection acting on cells in a tissue. The processes of mutation and selection are integral to the evolution of cancer at every step of multistage carcinogenesis, from tumor genesis to metastasis. Factors associated with cancer development, such as aging and carcinogens, have been shown to promote cancer evolution by impacting both mutation and selection processes. While there are therapies that can decimate a cancer cell population, unfortunately, cancers can also evolve resistance to these therapies, leading to the resurgence of treatment-refractory disease. Understanding cancer from an evolutionary perspective can allow us to appreciate better why cancers predominantly occur in the elderly, and why other conditions, from radiation exposure to smoking, are associated with increased cancers. Importantly, the application of evolutionary theory to cancer should engender new treatment strategies that could better control this dreaded disease.

We expect that the public generally views evolutionary biology as a science about the past, with stodgy old professors examining dusty fossils in poorly lit museum basements. Evolution must certainly be a field well-separated from modern medicine and biomedical research, right? If the public makes a connection between evolution and medicine, it is typically in the example of bacteria acquiring antibiotic resistance. But what does evolution have to do with afflictions like heart disease, obesity, and cancer? As it turns out, these diseases are intricately tied to our evolutionary histories, and understanding evolution is essential for preventing, managing and treating these diseases (1, 2). This review will focus on cancer: how evolutionary theories can be used to understand cancer development at the level of species as well as at the level of cells and tissues. We will also discuss the implications and benefits of an evolutionary perspective towards cancer prevention and therapies.

Continue reading “How cancer shapes evolution, and how evolution shapes cancer” »

https://news.wisc.edu/study-reveals-interplay-of-an-african-…d-a-virus/

Since the emergence of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrom Coronavirus (MERS-CoV) it has become increasingly clear that bats are important reservoirs of CoVs. Despite this, only 6% of all CoV sequences in GenBank are from bats. The remaining 94% largely consist of known pathogens of public health or agricultural significance, indicating that current research effort is heavily biased towards describing known diseases rather than the ‘pre-emergent’ diversity in bats. Our study addresses this critical gap, and focuses on resource poor countries where the risk of zoonotic emergence is believed to be highest. We surveyed the diversity of CoVs in multiple host taxa from twenty countries to explore the factors driving viral diversity at a global scale. We identified sequences representing 100 discrete phylogenetic clusters, ninety-one of which were found in bats, and used ecological and epidemiologic analyses to show that patterns of CoV diversity correlate with those of bat diversity. This cements bats as the major evolutionary reservoirs and ecological drivers of CoV diversity. Co-phylogenetic reconciliation analysis was also used to show that host switching has contributed to CoV evolution, and a preliminary analysis suggests that regional variation exists in the dynamics of this process. Overall our study represents a model for exploring global viral diversity and advances our fundamental understanding of CoV biodiversity and the potential risk factors associated with zoonotic emergence.

Scientists have discovered a form of natural selection that doesn’t rely on DNA.

Am Nat. 2017 Nov;190:694–706. doi: 10.1086÷693854. Epub 2017 Sep 5.

Biological invasions offer interesting situations for observing how novel interactions between closely related, formerly allopatric species may trigger phenotypic evolution in situ. Assuming that successful invaders are usually filtered to be competitively dominant, invasive and native species may follow different trajectories. Natives may evolve traits that minimize the negative impact of competition, while trait shifts in invasives should mostly reflect expansion dynamics, through selection for colonization ability and transiently enhanced mutation load at the colonization front. These ideas were tested through a large-scale common-garden experiment measuring life-history traits in two closely related snail species, one invasive and one native, co-occurring in a network of freshwater ponds in Guadeloupe. We looked for evidence of recent evolution by comparing uninvaded or recently invaded sites with long-invaded ones.

Astronomers have discovered a mysterious new class of objects at the heart of the Milky Way, unlike anything else found previously in our galaxy. The objects “look like gas but behave like stars,” according to senior researcher Andrea Ghez, as they start off small and compact but are stretched to a larger size when they approach the supermassive black hole in the center of the galaxy.

The researchers believe these objects could teach us about the evolution of stars and what happens to celestial bodies in environments of extreme gravity.

Continue reading “Astronomers Discover Stretchy Objects Unlike Anything Else in Our Galaxy” »

“Tim Crow must be proud to see his theory being tested at a complex level.” That’s how I tweeted the news on a recent Brain article by van den Heuvel et al (2019). Tim Crow’s theory on schizophrenia as a possible by-product of human brain evolution was quite inspiring and led to many fruitful discussions in our evolutionary psychiatry group when I was a junior trainee (which I wrote about a while ago: EPSIG Newsletter, June 2018). And here it was, the theory was tested by using novel methodology. Now I am pleased to say that the article did not disappoint, so I can enjoy the initial thrill and share my take with the Mental Elf World.

Tim Crow’s original question was intriguing: “Is schizophrenia the price that Homo sapiens pay for language?” (Crow, 1997). He argued that schizophrenia may be considered an extreme variation of brain systems which are relatively new in evolutionary timescale. Brain structures that are mostly implicated in schizophrenia were also unique to humans as mediators of language and higher cognitive functions. Those relatively new (in evolutionary timescale) brain systems may be more vulnerable to insults (e.g. stress, trauma, neurodevelopmental conditions) and manifest as dysfunctional brain circuits in schizophrenia.

The prevalence of schizophrenia is fairly constant across human populations (Jablensky et al. 1992), and the prevalence does not change despite low fecundity rates of people with schizophrenia. This can only be possible in the case of overall genetic predisposition across the population.

Continue reading “Is schizophrenia a by-product of human evolution?” »

The size of the human brain increased profoundly during evolution. A certain gene that is only found in humans triggers brain stem cells to form a larger pool of stem cells. As a consequence, more neurons can arise, which paves the way to a bigger brain. This brain size gene is called ARHGAP11B and so far, how it works was completely unknown. Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden now uncovered its mode of action. They show that the ARHGAP11B protein is located in the powerhouse of the cell—the mitochondria—and induces a metabolic pathway in the brain stem cells that is characteristic of cancer cells.

The research group of Wieland Huttner, a founding director of the Max Planck Institute of Molecular Cell Biology and Genetics, has been investigating the molecular mechanisms underlying the expansion of the brain during mammalian evolution for many years. In 2015, the group reported a key role for a gene that is only present in humans and in our closest extinct relatives, the Neanderthals and Denisovans. This gene, named ARHGAP11B, causes the so-called basal brain stem cells to expand in number and to eventually increase the production of neurons, leading to a bigger and more folded brain in the end. How the gene functions within the basal brain stem cells has been unknown so far.

Takashi Namba, a postdoctoral scientist in the research group of Wieland Huttner, wanted to find the answer to this question, together with colleagues from the Max Planck Institute, the University Hospital Carl Gustav Carus Dresden, and the Department of Medical Biochemistry at the Semmelweis University, Budapest. He found that the ARHGAP11B protein is located in mitochondria, the organelles that generate most of the cell’s source of chemical energy and hence are often referred to as the powerhouse of the cell. Takashi Namba explains the results: We found that ARHGAP11B interacts with a protein in the membrane of mitochondria that regulates a membrane pore. As a consequence of this interaction, the pores in the membrane are closing up, preventing calcium leakage from the mitochondria. The resulting higher calcium concentration causes the mitochondria to generate chemical energy by a metabolic pathway called glutaminolysis.