One gene mutation can change entire biological communities

New research have found that one gene mutation in a single species can trigger great changes in whole biological communities.
Scientists from Trinity College Dublin use bacteria to replicate ecological systems in the lab and found that mutations of a single gene that change how one bacterial species interacts with others had huge structural impacts across their multi-species microbial communities. These mutants produce biofilms according to their ability and many of which cause great health problems in body. It had chain effect on other species and completely change the structure of the communities.
"We know that predators are hugely important in influencing how ecosystems are structured, as they control the numbers and diversity of other species in the food web. It is incredible that such a small genetic change can cause these mutants to completely alter communities as much as the extinction of something as important as a predator," said Assistant Professor in Zoology at Trinity, Dr Ian Donohue.
The study shows wide scope for fine-scale genetic differences within populations to change entire ecosystems including microbial ones to lakes, forests and marine system.
"It's amazing to know that just one change in a single gene has the potential to have such a huge effect that it can change whole ecosystems," said Deirdre McClean, lead author of the study and PhD Researcher in Zoology at Trinity.
The results will be helpful to disease researchers, drug developers, ecologists and even geneticists. Besides, better understanding of the effect will be critical to develop treatments aimed at manipulating our gut microbiota specifically.
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New technology developed to unlock DNA secrets of elusive vaquita

The vaquita is one of the most endangered marine mammals on Earth. Protecting these enigmatic animals is extremely urgent. Surprisingly, a new method of teasing information from scarce and highly degraded samples is helping NOAA Fisheries and Mexican scientists unlock the genetic heritage of the endangered Mexican based animal.

Genetic studies can help scientists unlock the DNA secrets of the vaquita. For example, through the study we can get to know the story of how and how long ago the animals evolved into a unique species adapted to warm desert environment when most porpoises live in cool waters. All these information can do great help.

The scientists are faced with a great problem. Fewer than 100 vaquita remain living in the murky waters of the northern Gulf of California. It's hard to find them and collecting samples of their DNA since they are so wary and skittish. Most of the available genetic samples of vaquita come from animals inadvertently killed in fishing nets, which is a chief cause of mortality. They usually have been deteriorated by the time they reach a laboratory.

A small biotechnology company based in Ann Arbor, Michigan, called Enter Swift Biosciences, has developed new methods for dealing with damaged and highly degraded DNA. Traditional methods require sizeable samples of intact DNA in its double-stranded form. The Swife's "next-generation" DNA sample preparation approach can extract genetic material even from bits and pieces of single-stranded DNA which have severely degraded for a long time.

You can obtain useful information though they're not that much. But it is a valuable tools to protect our wildlife resources.

Morin's team then applied the technology to 12 samples of vaquita DNA - including some that were even more degraded and of poorer quality than the harbor porpoise samples. The Swift sample preparation system produced useful data from all of the vaquita samples.

"It was a pleasant surprise to find that we had been able to generate genetic information that had seemed beyond reach without the Swift technologies," said Barbara Taylor, the SWFSC's leading vaquita biologist.

There is not much of a fossil record for porpoises, so genetics also provides the only real way to understand the animal's evolutionary history. Initial findings from the new research now confirm that vaquita apparently split from another species of porpoise from the Southern Hemisphere about 2 to 3 million years ago and have since survived on their own, in relatively small numbers.

The lab plans to apply the technology to other degraded DNA samples to find more evolutionary clues of other animals. The data will be a precious part for preserving endangered animals.

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Gene is found in fruit flies to affect fertility of rival males

Pheromones are chemicals cues used for communication for many animals. They are a kind of chemical language guiding important information decisions between animals. Now scientists at the University of Hawai'i - Mānoa's (UHM) Pacific Biosciences Research Center (PBRC) have done a new research identifying a single gene in fruit flies that controls male pheromone production, male fertility and fertility of rival males unexpectedly.

Insects use a wide diversity of pheromone chemical signals to guide their behaviors. But we know little about how the diversity evolves.

"Our work reveals that one way new pheromones are produced is by hijacking genes which are used for other biological processes - in this case, male fertility," said Joanne Yew, assistant professor at PBRC and lead author of the study published today in Nature Communications. "The findings reveal a molecular mechanism by which novel traits evolve, a long-standing problem in evolutionary biology."

The gene is named bond. It uses genetic screening which identified genes in fruit flies that are involved in pheromone synthesis. Researchers used the technique to eliminate the function of other genes within the male reproductive organs one by one. Finally the scientists noted that the male flies in which bond expression was silenced were missing one of the major sex pheromones. The bone they discovered is a powerful gene that encodes an enzyme to make certain pheromones and components of sperm cell membranes, thus affecting behavior and fertility.

The mutant males produced very few offspring compared to normal flies.
One normal male was placed in the company of either mutant males or normal males to determine the influence of bond on social behaviors. A few days later the results showed that, in the absence of the normal chemical signals that signify potential rivals, males lower their sperm investment, which implies that males need a sense of competition to ensure reproductive success.

From the research we can know that fertility is a dynamic trait which can be influenced by social conditions and the perception of sensory signals. What's more, the perception of tastes and smells, that is, the sense that are used to detect pheromones, have great relevance with reproductive physiology and reproductive disorders.

These scientists will research further in this field in the future.

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A large genome is a good genome

Recently a study shows variation in genome size may be much more important than we throught before. It is obvious that sometimes, a large genome is a good genome. The study was led by researchers at Uppsala University.

"Our study shows that females with larger genome lay more eggs and males with larger genome fertilize more eggs", says research leader G?ran Arnqvist, Professor of Animal Ecology at Uppsala University.

The amount of nuclear DNA per cell, or the size of the genome, varies by orders of magnitude across organisms. We know not too much about the evolutionary forces that are responsible for this variation. the evolutionary forces that are responsible for this variation. For unknown reasons, there are simple plants with a genome almost 50 times as large and grasshoppers with a genome 5 times as large as our own! In fact, the insects with the smallest and largest genomes differ by a factor of 200, yet they all look and act like typical insects.

There are two viewpoints about dramatic differences in biology.

The first suggests that variation in genome size is made up by "junk" DNA that has little bearing on organismal function and that random processes determine genome size.

While the second suggests that the amount of DNA matters and that natural selection shapes genome size. The study of seed beetles now present evidence suggesting that natural selection may be more important.

The study of seed beetles was published in the scientific journal Proceedings of the Royal Society of London. Welcome to read more about the interesting study.

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How do blood cancers develop?

Our immune system always do strange things out of control. For example, when it makes small mistakes, the body amplifies its response to a large extent. It will edit errors in the DNA of developing T and B cells can cause blood cancers.

Recently, researchers from the Perelman School of Medicine, University of Pennsylvania have shown that when the enzyme key to cutting and pasting segments of DNA hits so-called "off-target" spots on a chromosome, the development of immune cells can lead to cancer in animal models. Learning about the nature of these editing errors is quite helpful in designing therapeutic enzymes based on these molecular scissors.

V(D)J recombinase, the editing enzyme that generates specific receptors on the surface of immune cells that match foreign invaders, collectively called antigens, can miss its target from time to time. V(D)J recombinase works only in the early stage of immune cell maturation. In this stage, the diverse array of antibodies and cell-surface receptors found on immune B cells and T cells are respectively made to counteract all the foreign invaders the human body encounters.

Breaks in DNA strands associated with V(D)J cutting are normally repaired with high fidelity by finely tuned molecular machinery. Previous studies from the Roth lab showed that V(D)J recombinase (consisting of the RAG1 and RAG2 proteins) normally sends a break in DNA down the correct repair path by preventing access to other, inappropriate repair mechanisms. This shepherding process can be disabled if the "C" terminus of the RAG2 protein subunit is removed. This causes genomic instability in developing immune cells and, in the absence of a working tumor suppressor protein such as p53, an aggressive form of lymphoma develops in mice.

According to David Roth, the lab of senior author, MD, PhD, chair of the Department of Pathology and Laboratory Medicine, genome wide analysis of lymphomas of the thymus in these mice with the truncated Rag2 protein revealed a surprise: numerous off-target DNA rearrangements, causing deletions. And these rearrangements affected several known and suspected oncogenes and tumor suppressor genes, such as Notch1, Pten, Ikzf1, Jak1, Phlda1, Trat1, and Agpat9.
We can learn more from the genomewide analysis of chromatin marks that normal interactions between the C-terminus of the Rag2 protein subunit and a specific chromatin modification helps maintain the fidelity of DNA target recognition by the enzyme.

It is noteworthy that the cancer-causing effects of off-target deletions mistakenly created by the V(D)J enzyme need to be considered in designing site-specific enzymes for genome modification such as zinc-finger nucleases, TALENS, or CRISPRs.

The Penn team's findings appear online this week in Cell Reports ahead of the print issue. All these foundings contribute much to treatment of blood cancers.

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Human relative been found in cave

A new species of human relative was discovered and the big news was announced on 10 September 2015, by the University of the Witwatersrand (Wits University), the National Geographic Society and the Department of Science and Technology (DST) and the National Research Foundation of South Africa (NRF).

The new species is called Homo naledi, which sheds light on the origins and diversity of our genus. Besides, it seems to have intentionally deposited bodies of its dead in a remote cave chamber, a behaviour previously thought limited to humans. It consists of more than 1 550 numbered fossil elements, making the discovery be the largest fossil hominin find yet made on the continent of Africa.

Let's introduce something about h.naledi. It was first found in a cave known as Rising Star in the Cradle of Humankind World Heritage Site, 30 miles) northwest of Johannesburg, South Africa, by Wits University scientists and volunteer cavers. The fossils have yet to be dated. A special team of very slender individuals were set to retrieve them, for those fossils laid about 90 meters from the cave entrance and they can only be accessible through a chute. The team has recovered parts of at least 15 individuals of the same species and a small fraction of the fossils believed to remain in the chamber. Homo naledi is already practically the best-known fossil member of our lineage.

In general, Homo naledi looks like one of the most primitive members of our genus, but it also has some surprisingly human-like features, enough to warrant placing it in the genus Homo, According to John Hawks of the University of Wisconsin-Madison, US, a senior author on the paper describing the new species. H. naledi had a tiny brain, about the size of an average orange (about 500 cubic centimeters), perched atop a very slender body. From the research we can know that on average H. naledi stood approximately 1.5 meters  tall and weighed about 45 kilograms.

The findings are published in the scientific journal eLife and reported in the cover story of the October issue of National Geographic magazine and a NOVA/National Geographic Special. If you're interested in the new species of human relative, you can refer to them.

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A new technology is developed to help scientists understand the work process of proteins and fix the broken proteins. The user-friendly technology is believed to lend a hand to finding new drugs for many diseases, including cancer.
As we know that the human body has a coordinating way of turning its proteins on and off to alter their function and activity in cells. It is phosphorylation, which is the reversible attachment of phosphate groups to proteins. They provide an enormous variety of function and are essential to all forms of life. However, we know little about the detail of this dynamic process.
Researchers have built a cell-free protein synthesis platform technology that can manufacture large quantities of these human phosphoproteins for scientific study using a special strain of E. coli bacteria. The technology can enable scientists to learn more about the function and structure of phosphoproteins and identify the one which are involved in disease. The study was published Sept. 9 by the journal Nature Communications.
Trouble in the phosphorylation process is a trait of disease like cancer, inflammation and Alzheimer's disease. The human proteome is estimated to be phosphorylated at more than 100,000 unique sites. It makes study of phosphorylated proteins and their role in disease be a tough task.
The new technology just developed begins to make the job a tractable problem. It can make these special proteins at unprecedented yields, with a freedom of design that is not possible in living organisms. The consequence of this innovative strategy is enormous in the long run.
Michael C. Jewett is a biochemical engineer who led the Northwestern team. He uses cell-free systems to create new therapies, chemicals and novel materials to impact public health and the environment. Jewett and his colleagues combined state-of-the-art genome engineering tools and engineered biological "parts" into a "plug-and-play" protein expression platform that is cell-free. Cell-free systems activate complex biological systems without using living intact cells. Crude cell lysates, or extracts, are employed instead.
To be specific, the researchers prepared cell lysates of genomically recoded bacteria that incorporate amino acids not found in nature. This allowed them to harness the cell's engineered machinery and turn it into a factory, capable of on-demand biomanufacturing new classes of proteins.
The manufacturing technology will help scientists to unclock the phosphorylation 'code' that exists in the human proteome. The study was published on Sept. 9 by the journal Nature Communications.
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