Four separate species of rats evolved to mooch off humans
Rat are notorious pests, with populations throughout the world living off the scraps and garbage left behind by humans. Rats, it seems, are just born to mooch off humans, since they’ve gone down this same evolutionary path four different times.
Smithsonian Institution researcher Ken Aplin, along with an international team of collaborators, recently undertook the first comprehensive study of rat genetic diversity throughout the world. Examining rat genes from 32 countries, Aplin determined that there are six distinct groups that diverged about a million years ago. That’s long before modern humans emerged, and yet four of these six groups all developed the exact same parasitic relationship with humans.
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Shrimp-like species can create ultra-sticky silk that’s as strong as steel
The marine animal Crassicorophium bonellii looks like a shrimp, but it acts more like a spider. The creature uses its legs to spin silk that’s both incredibly hard and super sticky… and could be of great medical use to humans.
Researchers from the Oxford Silk Group have studied the creature’s silk-making, which it uses to construct the muddy tubes in which it lives. The silk shares some adhesive properties with the stuff barnacles use to stick to things. The fact that it can cement underwater already gives it some pretty impressive - and potentially useful - properties, but that isn’t the end of it. The silk has the same strength and flexibility seen in spider silk, which is as strong as steel.
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Human skin yields stem cell-like cells
Researchers from the UCLA School of Dentistry investigating how stem cells can be used to regenerate dental tissue have discovered a way to produce cells with stem cell-like characteristics from the most common type of human skin cell in the epidermis.
Scalable amounts of liver and pancreas precursor cells created using new stem cell production method
Scientists in Canada have overcome a key research hurdle to developing regenerative treatments for diabetes and liver disease with a technique to produce medically useful amounts of endoderm cells from human pluripotent stem cells. The research, published in Biotechnology and Bioengineering, can be transferred to other areas of stem cell research helping scientists to navigate the route to clinical use known as the ‘valley of death’.
“One million people suffer from type 1 diabetes in the United States, while liver disease accounts for 45,000 deaths a year,” said Dr Mark Ungrin from the University of Toronto. “This makes stem cells, and the potential for regenerative treatments, hugely interesting to scientists. Laboratory techniques can produce thousands, or even millions, of these cells, but generating them in the numbers and quality needed for medicine has long been a challenge.”
The research focused on the process of using pluripotent stem cells (PSC) to generate endoderm cells, one of the three primary germ layers which form internal organs including the lungs, pancreas, and liver. The ability to differentiate, or transform, PSCs into endoderm cells is a vital step to developing regenerative treatments for these organs.
More Evidence Found for Quantum Physics in Photosynthesis
Physicists have found the strongest evidence yet of quantum effects fueling photosynthesis.
Multiple experiments in recent years have suggested as much, but it’s been hard to be sure. Quantum effects were clearly present in the light-harvesting antenna proteins of plant cells, but their precise role in processing incoming photons remained unclear.
In an experiment published Dec. 6 in Proceedings of the National Academy of Sciences, a connection between coherence — far-flung molecules interacting as one, separated by space but not time — and energy flow is established.
“There was a smoking gun before,” said study co-author Greg Engel of the University of Chicago. “Here we can watch the relationship between coherence and energy transfer. This is the first paper showing that coherence affects the probability of transport. It really does change the chemical dynamics.”
How fruit flies can teach us about curing chronic pain and halting mosquito-borne diseases
Studies of a protein that fruit flies use to sense heat and chemicals may someday provide solutions to human pain and the control of disease-spreading mosquitoes.
In the current issue of Nature, biologist Paul Garrity of the National Center for Behavioral Genomics at Brandeis University and his team, spearheaded by KyeongJin Kang and Vince Panzano in the Garrity lab, discover how fruit flies distinguish the warmth of a summer day from the pungency of wasabi by using TRPA1, a protein whose human relative is critical for pain and inflammation.
In earlier research Garrity’s team showed that flies, like humans, sense chemical irritants with TRPA1, indicating an ancient origin for harmful chemical sensing. In 2008, the team demonstrated that this protein serves a second function in flies: sensing warmth.
Gentle warmth and nasty chemicals trigger distinct responses. How can both responses rely on the same sensor? The team has now discovered that there is an easy answer. Insects actually make two forms of TRPA1, one specialized for each task.
Such TRPA1 specialization has implications for devising bug sprays and traps to combat the transmission of diseases like malaria, dengue and West Nile virus. “This work on TRPA1 can explain how blood-sucking insects like mosquitoes discriminate noxious chemicals, which repel them, from the warmth of a human, which attracts them,” says Garrity. “By activating one kind of TRPA1 you might be able to deter mosquitoes from biting you, while activating the other kind of TRPA1 might lure mosquitoes to a trap.”
These findings also have implications for understanding the way that human damage-sensing neurons work, explains Garrity. Since human TRPA1 is a drug target aimed at treating diseases such as asthma, migraines, and chronic pain, Garrity says it’s important to understand how TRPA1 proteins operate.
Researchers design Alzheimer’s antibodies
Researchers at Rensselaer Polytechnic Institute have developed a new method to design antibodies aimed at combating disease. The surprisingly simple process was used to make antibodies that neutralize the harmful protein particles that lead to Alzheimer’s disease.
The process is reported in the Dec. 5 Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS). The process, outlined in the paper, titled “Structure-based design of conformation- and sequence-specific antibodies against amyloid β,” could be used as a tool to understand complex disease pathology and develop new antibody-based drugs in the future.
Antibodies are large proteins produced by the immune system to combat infection and disease. They are comprised of a large Y-shaped protein topped with small peptide loops. These loops bind to harmful invaders in the body, such as a viruses or bacteria. Once an antibody is bound to its target, the immune system sends cells to destroy the invader. Finding the right antibody can determine the difference between death and recovery.
Scientists have long sought methods for designing antibodies to combat specific ailments. However, the incredible complexity of designing antibodies that only attached to a target molecule of interest has prevented scientists from realizing this ambitious goal.
When trying to design an antibody, the arrangement and sequence of the antibody loops is of utmost importance. Only a very specific combination of antibody loops will bind to and neutralize each target. And with billions of different possible loop arrangements and sequences, it is seemingly impossible to predict which antibody loops will bind to a specific target molecule.
The new antibody design process was used to create antibodies that target a devastating molecule in the body: the Alzheimer’s protein. The research, which was led by Assistant Professor of Chemical and Biological Engineering Peter Tessier, uses the same molecular interactions that cause the Alzheimer’s proteins to stick together and form the toxic particles that are a hallmark of the disease.
Discovery On How Sugars Are Moved Throughout a Plant
Food prices are soaring at the same time as Earth’s population is nearing 9 billion. As a result the need for increased crop yields is extremely important. New research led by Carnegie’s Wolf Frommer into the system by which sugars are moved throughout a plant — from the leaves to the harvested portions and elsewhere — could be crucial for addressing this problem. Their work is published December 8 by Science Express.
Just as it’s necessary for the human body to move nutrients to all of the organs, it is vital for green plants to transport sugars to supply its various parts. In humans, this is the circulatory system’s job. But plants do not have a heart-like pump to move these vital energy sources. Instead, plants use a molecular pump.
Twenty years ago, the Frommer team identified one of the key components of this molecular pump, which actively loads a sugar called sucrose into the plant’s veins, a tissue called phloem. But how the sucrose produced in the leaves via photosynthesis is delivered to the transporters that move it into the phloem has remained a mystery. Thus, a critical piece of the molecular pump was unknown—the protein that moves the sucrose to the inside of the plant’s leaf cell walls.
Frommer’s team included Carnegie’s Li-Qing Chen, the paper’s lead author, Xiao-Quing Qu, Bi-Huei Hou and Davide Sosso, as well as Sonia Osorio and Alisdair Fernie of the Max Planck Institute of Molecular Plant Physiology. In this new research they have identified the missing piece of the molecular pump system.
16,000 Eyes: The Vision of a Cambrian Superpredator.
→ By John Timmer, Ars Technica
Those of you who get a bit weirded out by spiders and other arthropods would probably have a coronary if an Anomalocaris were to swim in your direction. The animals were about a meter long, and shaped as a flattened oval, a bit like a modern flounder. That’s about the only similarity with a fish, though. Instead of fins, the Anomalocarids propelled themselves through the water using a series of elongated paddle-like structures running down both edges of the body. In front, a pair of appendages could shovel prey into a circular mouth located on its underside.
And then there were the large, bulging eyes, springing from each side of the animal’s head. Until now, we could only guess at what the eyes looked like, but some spectacular, 515-million-year-old fossils from Australia have now shown that they had a huge number of small lenses, arranged much like those in modern insects and other arthropods. The finding suggests that the compound eyes evolved right at the origin of this branch of the evolutionary tree, long before the sorts of hard exoskeletons we now consider typical of arthropods.
First, the fossils themselves, which are absolutely spectacular. We’ve discovered a number of different Anomalocarid species in fossil deposits around the globe but, at best, these simply left behind an impression of the eyes. So, we knew they were roughly pear-shaped and where they appeared on the animal, but nothing about their internal structure. The eyes found in the new fossils clearly show details of the internal structure. They aren’t actually attached to an Anomalocaris, but they match the impressions previously found with them, and we’ve not found anything else in these fossil beds big enough to support an eye of this size.
It takes a microscope to see them, but individual lenses were preserved in each eye. For someone who has seen countless images of the compound eyes of Drosophila, they are startling in how modern they look. Based on their density, the authors estimate that each eye housed 16,000 individual lenses, the most that have ever been seen on any animal we know about. Based on the curve of the eye and what we know about modern compound eyes, they suggest that the animal had very good visual acuity.
(Above) The fossilized remains of 515 million year old eyes. (John Paterson)
Anatomy of a worker ant (Pachycondyla verenae)
(image: Mariana Ruiz)
A ‘wild card’ in your genes
The human genome and the endowments of genes in other animals and plants are like a deck of poker cards containing a “wild card” that in a genetic sense introduces an element of variety and surprise that has a key role in life. That’s what scientists are describing in a review of more than 100 studies on the topic that appears in ACS Chemical Biology.
Rahul Kohli and colleagues focus on cytosine, one of the four chemical “bases” that comprise the alphabet that the genetic material DNA uses to spell out everything from hair and eye color to risk of certain diseases. But far from just storing information, cytosine has acquired a number of other functions that give it a claim to being the genome’s wild card. “In poker, the rules of the game can occasionally change,” they note in the article. “Adding a ‘wild card’ to the mix introduces a new degree of variety and presents opportunities for a skilled player to steal the pot. Given that evolution is governed by the same principles of risk and reward that are common to a poker game, it is perhaps not surprising that a genomic ‘wild card’ has an integral role in biology.”
They discuss the many faces of cytosine that make it such a game-changer and the biological processes that help to change its identity. Removing something called an amine group from cytosine, for instance, allows the immune system to recognize and destroy foreign invaders such as viruses. Adding so-called “methyl groups” on cytosines acts as on/off switches for genes. The authors say that these many faces of cytosine allow it to play various roles and give it true “wild card” status.
More information: The Curious Chemical Biology of Cytosine: Deamination, Methylation,and Oxidation as Modulators of Genomic Potential, ACS Chem. Biol., Article ASAP. DOI: 10.1021/cb2002895
Abstract
A multitude of functions have evolved around cytosine within DNA, endowing the base with physiological significance beyond simple information storage. This versatility arises from enzymes that chemically modify cytosine to expand the potential of the genome. Some modifications alter coding sequences, such as deamination of cytosine by AID/APOBEC enzymes to generate immunologic or virologic diversity. Other modifications are critical to epigenetic control, altering gene expression or cellular identity. Of these, cytosine methylation is well understood, in contrast to recently discovered modifications, such as oxidation by TET enzymes to 5-hydroxymethylcytosine. Further complexity results from cytosine demethylation, an enigmatic process that impacts cellular pluripotency. Recent insights help us to propose an integrated DNA demethylation model, accounting for contributions from cytosine oxidation, deamination, and base excision repair. Taken together, this rich medley of alterations renders cytosine a genomic “wild card”, whose context-dependent functions make the base far more than a static letter in the code of life.
Midichloria mitochondrii inside the mitochondria of the tick Ixodes ricinus (A), and structure of the M. mitochondrii genome (B). Of relevance here is the fifth circle from the outside, which shows the position of flagellar genes.
Star Wars-inspired bacterium provides glimpse into life
A bacterium whose name was inspired by the Star Wars films has provided new clues into the evolution of our own cells and how they came to possess the vital energy-producing units called mitochondria.
The University of Sydney research investigated the bacterium Midichloria mitochondrii- named after helpful Star Wars microbes, called Midi-chlorians, that live inside cells and grant the mystical power known as The Force. It has revealed that mitochondria may have entered our cells though a parasitic bacterium that used a tail to swim and could survive with almost no oxygen.
The work, published in this month’s issue of Molecular Biology and Evolution, challenges traditional explanations of how the ancestors of mitochondria first entered our cells between one and a half and two billion years ago. It also sheds new light on a process recognized as one of the major transitions in the history of life on earth.
“Our results challenge the paradigm - shown in every biology textbook - that mitochondria were passive bacteria gobbled up by a primordial cell,” says co-author Dr. Nathan Lo from the University of Sydney’s School of Biological Sciences.
“We have found instead that the mitochondrial ancestor most likely had a flagellum, so was able to move, and possibly acted as a parasite, rather than prey, on early eukaryotic cells,” added Dr. Lo, who collaborated with scientists from Italy and Spain on the research.
Eukaryotes include all forms of animal and plant life on earth that are more complex than bacteria. They differ from simpler life forms because their cells have both a nucleus and mitochondria, which are like little batteries that generate energy to power the cell.
“How eukaryotic cells evolved remains one of the most vexing problems in biology,” said Dr. Lo.
“Mitochondria are actually highly reduced bacteria, with their own set of DNA, that reside in our cells. It has long been thought that this relationship developed when an ancient eukaryotic cell engulfed the mitochondrial ancestor.
“But there is still mystery around the question of how exactly the mitochondrial ancestor was engulfed, and how it survived in the oxygen-poor atmosphere of early eukaryotic life.”
For clues Dr. Lo and collaborators studied Midichloria mitochondrii- a bacterium they discovered in 2004 and successfully obtained permission from director George Lucas to name after the Star Wars Midi-chlorians. M. mitochondrii is from the Rickettsiales family, considered to be the closest living relatives of the ancestor of mitochondria.
“We studied M. mitochondrii because its genome has never been analysed and because it is the only bacterium known to be able to enter into the mitochondria of living cells,” said Dr. Lo.
After determining the DNA sequence of M. mitochondrii’s entire genome, Dr. Lo and collaborators found the bacterium contained 26 genes coding for an entire flagellum - including all the key components such as hook, filament and basal body.
He also found a second set of genes which coded for enzymes that would allow the bacterium to survive in low-oxygen environments. These genes have never been seen before in bacterial relatives of mitochondria.
Dr. Lo says: “We found these two sets of genes were inherited from the common ancestor shared by M. mitochondrii and our own mitochondria. Mitochondria’s ancestor most likely possessed a flagellum, which is a key characteristic of many parasitic bacteria.
“Our results show the ancestor of mitochondria probably played a much more active, even parasitic, role in the early interactions with its eukaryotic host than previously thought. They also explain how the relationship could have evolved in the low-oxygen environments of two billion years ago.
“This should cause a rethink of how the symbiosis between mitochondria and eukaryotic cells originally developed - one of the most controversial topics in biology.”
A whole new meaning for thinking on your feet
Smithsonian researchers report that the brains of tiny spiders are so large that they fill their body cavities and overflow into their legs. As part of ongoing research to understand how miniaturization affects brain size and behavior, researchers measured the central nervous systems of nine species of spiders, from rainforest giants to spiders smaller than the head of a pin. As the spiders get smaller, their brains get proportionally bigger, filling up more and more of their body cavities.
“The smaller the animal, the more it has to invest in its brain, which means even very tiny spiders are able to weave a web and perform other fairly complex behaviors,” said William Wcislo, staff scientist at the Smithsonian Tropical Research Institute in Panama. “We discovered that the central nervous systems of the smallest spiders fill up almost 80 percent of their total body cavity, including about 25 percent of their legs.”
Some of the tiniest, immature spiderlings even have deformed, bulging bodies. The bulge contains excess brain. Adults of the same species do not bulge. Brain cells can only be so small because most cells have a nucleus that contains all of the spider’s genes, and that takes up space. The diameter of the nerve fibers or axons also cannot be made smaller because if they are too thin, the flow of ions that carry nerve signals is disrupted, and the signals are not transferred properly. One option is to devote more space to the nervous system.
The brains of smaller spiders, like nymphs in the genus Mysmena, extend out of their body cavity into their legs. Credit: Wcislo lab.
“We suspected that the spiderlings might be mostly brain because there is a general rule for all animals, called Haller’s rule, that says that as body size goes down, the proportion of the body taken up by the brain increases,” said Wcislo. “Human brains only represent about 2-3 percent of our body mass. Some of the tiniest ant brains that we’ve measured represent about 15 percent of their biomass, and some of these spiders are much smaller.”
Brain cells use a lot of energy, so these small spiders also probably convert much of the food they consume into brain power.
The enormous biodiversity of spiders in Panama and Costa Rica made it possible for researchers to measure brain extension in spiders with a huge range of body sizes. Nephila clavipes, a rainforest giant weighs 400,000 times more than the smallest spiders in the study, nymphs of spiders in the genus Mysmena.
More information: Quesada, Rosanette, Triana, Emilia, Vargas, Gloria, Douglass, John K., Seid, Marc A., Niven, Jeremy E., Eberhard, William G., Wcislo, William T. 2011. “The allometry of CNS size and consequences of miniaturization in orb-weaving and cleptoparasitic spiders.” Arthropod Structure and Development 521-529, doi10.1016/j.asd.2011.07.002
