Key genes in the root development of poplar trees in low-nitrogen soil

Poplar tree is commonly known as aspen and cottonwood. It can grow anywhere between 15 to 50 meters tall with trunks up to 2.5 meters in diameter. It grow well in low-nitrogen soil. It is used as an energy crop for biomass or bio-fuel, in energy forestry systems.

Nitrogen is considered the most important component for supporting plant growth. Nitrogen is widely used as an agricultural fertilizer which affects root growth in plants. The scientists always wanted to grow more nitrogen-efficient plants, so less nitrogen could be used as fertilizer. But first they had to unlock the secret to the genetic mechanisms underlying plant root growth.

Three scientists from Michigan Technological University have identified a network of genes that cause poplar roots to grow well in low-nitrogen soil. This makes them ideal candidates for biofuel tree plantations on marginal lands.

The research was conducted by Hairong Wei, Yordan Yordanov and Victor Busov, and was published by the international journal New Phytologist.

The first species of poplar tree to have its full DNA code in the year of 2006.There are tens of thousands of genes in the poplar genome. It was a big task for them to determine which genes are doing what, how they affect each other and how they work together to regulate root growth under low nitrogen conditions.

In their laboratory they planted poplar seedlings under normal nitrogen levels. Then they transplanted them to a medium that contained almost no nitrogen. they find that the roots got larger and longer. The scientists did a series of experiments over time under the same experimental conditions, to identify the genes involved in the changes they observed. They found 9.198 genes that produced significantly different amounts or kinds of proteins at six different times. Further analysis closed in on a gene called PtaNAC1.

when they tweak PtaNAC1 the entire network responds, and the roots grow 58 percent more than controls.        They compared the functioning of genes together with a functioning of a machine in which, there is a master switch that turns on the engine and the engine activates other switches that make all the little cogs and gears in the machine do what they are supposed to do.

Now that the scientists understand the poplar's genetic "engine," they can work to develop new varieties of plants that can thrive on marginal lands.

Green tea extract plus polyethylene glycol helps in reducing weight

Green tea is good for health. Evidences has shown its several health benefits - helps in loosing weight, boosts exercise endurance, reduces the risk of heart attack, fights against various cancers, hydration benefits, protection from harmful ultraviolet rays, keeps Diabetes in check, prevention and treatment of neurological diseases, anti- Ageing benefits, boosts immunity.

In order to ascertain whether green tea truly has the potential to control weight and helps in regulating glucose in type 2 diabetes, Jae-Hyung Park and his colleagues from the Keimyung University School of Medicine in the Republic of Korea conducted a study, now published in the Springer journal Naunyn-Schmedeberg's Archives of Pharmacology.

The active constituents of green tea, which have been shown to inhibit intestinal glucose and lipid uptake, are a certain type of flavonoid called gallated catechins. Previously it was suggested that the amount of gallated catechins necessary to reduce blood glucose concentrations can be achieved from a daily dose of green tea. However, the amount of green tea needed to decrease lipid uptake from the gut is higher and has been shown to have adverse effects in humans. Once in the bloodstream, gallated catechins can actually increase insulin resistance, which is a negative consequence especially in obese and diabetic patients.

To prevent a high dose of gallated catechins from reaching the bloodstream, researchers used a non-toxic resin, polyethylene glycol, to bind the gallated catechins in the gut to prevent their absorption.

For their study they tested the effects of green tea extract on body weight and glucose intolerance in both diabetic mice and normal mice fed a high-fat diet. they fed mice one mice with green tea extract only and another with green tea extract and polyethylene glycol. They compared these against the effects of two other therapeutic drugs routinely prescribed for type 2 diabetes.

Results showed that green tea extract alone did not give any improvements in body weight and glucose intolerance but with addition of polyethylene glycol, there was a significant reduction in body weight gain, insulin resistance and glucose intolerance in both normal mice on a high fat diet and diabetic mice. 

Interestingly, the effects of the green tea extract in both the intestines and in the circulation were measurable at doses which could be achieved by drinking green tea on a daily basis. In addition, the effects of green tea extract were comparable to those found when taking two of the drugs which are currently recommended for non-insulin dependent diabetes.

CETSA - technology to measure the extent to which drugs reach their targets in the cell.

Most drugs work by binding to the target receptor site on the surface of cells or enzymes (which regulate the rate of chemical reactions) within cells, they can either block the physiological function of the protein, or mimics it's effect. Till date drugs are designed by following this phenomenon. Optimization of target engagement by drugs in cells is often challenging, because drug binding cannot be monitored inside cells.

Researchers at Karolinska Institute in Sweden have developed the first method for directly measuring the extent to which drugs reach their targets in the cell - Cellular thermal shift assay (CETSA). 

It is based on the biophysical principle (target proteins usually get stabilized when drug molecules bind). Using this assay, researchers validated drug binding for a set of important clinical targets and monitored processes of drug transport and activation, off-target effects and drug resistance in cancer cell lines, as well as drug distribution in tissues. 

The lack of methods to directly measure the binding of a drug to its target protein has caused a degree of uncertainty in many phases of drug development. In some cases, where drug candidates have not lived up to expectations in clinical trials on humans, it has transpired that the drug molecules have failed to bind to the right protein

The group behind the study believes that CETSA will be an important control stage and a complement to other methods. The team believes that by virtue of its ability to determine whether existing drugs are suitable for individual patients, the method is of potential value to the practice of individualized treatment.

The study was published in the journal Science. 

"We believe that the method can provide an important diagnostic tool in the treatment of cancer, for example, as CETSA can, in principle, enable us to determine which drug is most effective at targeting the proteins in the tumour," says Daniel Martinez, who leads a team in the project.

Image: - http://images.sciencedaily.com/2013/07/130705101541-large.jpg

Genetic editing shows promise in Duchenne Muscular Dystrophy

Duchenne muscular dystrophy (DMD) is a recessive X-linked form of muscular dystrophy. It affects around 1 in 3,600 boys. In this disease there is a progressive loss of muscle function and weakness, which begins in the lower limbs. Over time, patients with the disorder suffer gradual muscle deterioration, which leads to paralysis and eventual death, usually by age 25.

The disorder is caused by a mutation in the dystrophin gene, the largest gene located on the human X chromosome, which codes for the protein dystrophin, an important structural component within muscle tissue that provides structural stability to the dystroglycan complex (DGC) of the cell membrane.

Bio-medical engineers of Duke University by using genetic editing technique, have been able to repair a defect responsible for Duchenne muscular dystrophy, in cell samples from the patients.

The bio-medical engineers have developed a way to change the existing mutated gene responsible for the disorder into a normally functioning gene instead of, gene therapy approach of adding new genetic material to "override" the faulty gene. They believe that their approach could be safer and more stable than current methods of gene therapy.

The researchers are now conducting further tests of this new approach in animal models of the disease.

The results of the Duke study were published online in Molecular Therapy, the journal of the American Society for Gene and Cell Therapy.

For their experiment they used synthetic proteins known as transcription activator-like effector nucleases (TALENs), which are artificial enzymes that can be engineered to bind to and modify almost any gene sequence.The TALEN finds its target site in the human genome by binding to DNAwith an engineered DNA-recognition protein. Once the protein finds its target site, the DNA is modified by the enzyme domain of the protein

Duchenne muscular dystrophy has been extensively studied by scientists, and it is believed that more than 60 percent of patients with this type of mutation can be treated with this novel genetic approach. The approach could be helpful in treating other genetic diseases where a few gene mutations.

New research shows that bacteria communicate to help each other to resist antibiotics

It is already known that bacteria communicate with one another using chemical signal molecules. Chemical signalling involves producing, releasing, detecting, and responding to small hormone-like molecules termed autoinducers. The process of communication in bacteria is known as quorum sensing. 

New research from Western University unravels a novel means of communication that allows bacteria such as Burkholderia cenocepacia (B. cenocepacia) to resist antibiotic treatment. The bacteria is everywhere but infection hasn't been a problem because our immune system can fight it off but it causes devastating infections in patients with cystic fibrosis (CF) or with compromised immune systems.

Researchers, Dr. Miguel Valvano and Omar El-Halfawy, PhD candidate, found that within a bacterial population, the more antibiotic resistant cells produces and shares small molecules with less resistant cells, which makes bacteria with more resistant to antibiotic killing. They also find that small molecules protect not only the more sensitive cells of B. cenocepacia but also other bacteria including a highly prevalent CF pathogen, Pseudomonas aeruginosa, and E. coli. The research is published in PLOS ONE.

"These findings reveal a new mechanism of antimicrobial resistance based on chemical communication among bacterial cells by small molecules that protect against the effect of antibiotics," says Dr. Valvano

The hope is that with greater understanding of how the bacteria work, researchers can stop the way it interferes with life-saving drugs like antibiotics.

Greenhouse gas altering biodiversity of the oceanic ecosystem

Level of carbon dioxide in earth’s atmosphere is increasing, leading to rise in temperature of earth. Omg, can you imagine a time machine blender?!This increase is always a big question for scientists. Scientists are continuously trying to find, “how to minimize this effect?” They also want to know which organisms will thrive and which will perish in the environment of tomorrow.

Climate change is already having noticeable impacts on biodiversity. According to the research published in Nature Geoscience on June 30, increasing levels of carbon dioxide appear to be changing the biodiversity of the oceanic ecosystem, most notably the keystone bacterial organisms that form the foundation of the ocean's food-chain. 

The finding warns about the changes to populations of nitrogen-fixing cyanobacteria (also known as blue-green algae) will have implications for every living thing in the ocean. These bacteria obtain energy through photosynthesis. They convert nitrogen (which is inert) into usable form, that most other organisms need to survive. . Nitrogen-fixing not only allows some plants to continue growing even when nitrate and ammonium have run out, but also that it replenishes those other forms of nitrogen, fertilising the ocean. Any change in the population of these organisms can alter food chain.

Researcher David Hutchins, from the University of Southern California, and his team studied two major groups of nitrogen-fixing cyanobacteria: Trichodesmium and Crocosphaera. Trichodesmium forms large floating colonies big enough to see with the naked eye and makes vast "blooms" in the open ocean. Crocosphaera is also very abundant but is a single-celled, microscopic organism.

Previous research showed that these two types of cyanobacteria should be some of the biggest "winners" of climate change, thriving in high CO₂ levels and warmer oceans. However, those previous studies only examined one or two strains of the organisms.

The University of Southern California has a massive culture library of strains and species of the organisms assembled by its Associate Professor Eric Webb. Hutchins and his team by using the culture library was able to show that some strains grow better at CO2 levels not seen since the start of the Industrial Revolution, while others will thrive in the future "greenhouse" Earth.

"It's not that climate change will wipe out all nitrogen fixers; we've shown that there's redundancy in nature's system. Rather, increasing atmospheric carbon dioxide changes specifically which nitrogen fixers are likely to thrive," Hutchins explained. "And we're not entirely certain how that will change the ocean of tomorrow."

Father's lifestyle could affect DNA of multiple generations

Mutations are changes in the genetic sequence, and they are a main cause of diversity among organisms. These changes occur at many different levels, and they can have widely differing consequences. For mutations to affect an organism's descendants, they must: 1) occur in cells that produce the next generation, and 2) affect the hereditary material.

A new research has suggesed that paternal exposures to smoking can raise the number of mutations, that can be passed to the coming generations. These mutations can be inherited, even if those mutations occurred before conception. These findings were published in the July 2013 issue of The FASEB Journal.

These findings also show that mutations in the germ-line are present in all cells of the children, including their own germ cells. This means that a father's lifestyle has the potential to affect the DNA of multiple generations and not just his immediate offspring.

Roger Godschalk, Ph.D., a researcher involved in the work from the Department of Toxicology and the School for Nutrition, Toxicology and Metabolism at Maastricht University in the Netherlands looked to two groups of families (father, mother and child) from the Norwegian Mother and Child Cohort Study for their findings. They choose income as a criterion because it generally correlates to lifestyle choices of the parents. One group had a low yearly income, whereas the other had a relatively high yearly income.

For instance, fathers in the low income group were more often cigarette smokers than fathers in the high income group. Researchers looked for DNA mutations in the children and found that they were more frequent in the group with low income fathers than in the group of high income fathers.

"We've known for a very long time that preventive care among expectant mothers is critical to the health and well-being of their children," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. These results suggest that the parents living conditions before conception may directly impact the health of their children.