Source: Purdue University
Published on 3rd July 2011
Source: Purdue University
Published on 3rd July 2011
Scientists could take greater strides toward crop improvement if there were wider adoption of advanced techniques used to understand the mechanisms that allow plants to adapt to their environments, current and former Purdue University researchers say.
In a perspective for the journal Science, Brian Dilkes, a Purdue assistant professor of genetics, and Ivan Baxter, a research computational biologist for the U.S. Department of Agriculture’s Agricultural Research Service, argue that today’s technology could allow scientists to match physiological and genetic characteristics of plants with the soil characteristics that promote or inhibit their growth. Making those connections could reduce the time necessary to improve plants that are coping with changing environmental and climatic conditions.
“Evolution has solved the problems that we face in terms of adapting plants to grow in a multitude of environments,” Dilkes said. “If we understand these processes, we’ll be able to apply that knowledge to maintaining diversity in natural systems and improving and maintaining crop yield.”
The majority of a plant’s makeup, besides carbon dioxide, comes from elements and minerals absorbed from the soil as the plant grows. The physiological and genetic mechanisms that allow plants to obtain iron from the soil, for instance, can also cause the plant to accumulate other elements. Understanding how those changes interact is an important piece of improving plants, Baxter said.
“This is just a hint of the complexity that’s out there,” said Baxter, a former post-doctoral researcher at Purdue who works for the USDA at the Donald Danforth Plant Science Center in St. Louis. “If we’re going to make the necessary improvements in agricultural productivity, we will have to move forward with these techniques.”
Much of the work done to understand how plants have adapted to their environments focuses on one gene and one element it controls at a time. Pinpointing one or more genes responsible for a particular trait can take years, even decades.
Dilkes and Baxter believe a wider adoption of molecular phenotyping techniques, such as ionomics and genome-wide association mapping, could allow scientists to work with multiple elements and genes at once.
“By focusing on one gene or one element at a time, you miss out on the other physiological mechanisms occurring in the plant,” Dilkes said. “The potential to broaden our understanding of these complex interactions and have a dramatic effect on agriculture is there.”
Genome-wide association mapping allows scientists to find genetic associations among multiple phenotypes, or physical traits. The process quickly shows which genes may be responsible for the physical characteristics.
Ionomics studies the elemental composition of plants and how those compositions change in response to environmental or genetic changes.
“Experiments with thousands of samples are now possible,” Baxter said. “We’ve just started to put these things together.”
Research in Baxter’s lab is supported by the National Science Foundation, the U.S. Department of Energy and the U.S. Department of Agriculture’s Agricultural Research Service.
Source: Purdue University
Published on 3rd July 2011
Compared to normal cells, cancer cells have a prodigious appetite for glucose, the result of a shift in cell metabolism known as aerobic glycolysis or the “Warburg effect.” Researchers focusing on this effect as a possible target for cancer therapies have examined how biochemical signals present in cancer cells regulate the altered metabolic state.
Now, in a unique study, a UCLA research team led by Thomas Graeber, a professor of molecular and medical pharmacology, has investigated the reverse aspect: how the metabolism of glucose affects the biochemical signals present in cancer cells.
In research published June 26 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation — that is, depriving cancer cells of glucose —activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species, the cell-damaging molecules and ions targeted by antioxidants like vitamin C.
The research, which involved UCLA scientists from the Crump Institute for Molecular Imaging, the Institute for Molecular Medicine, the California NanoSystems Institute, the Jonsson Comprehensive Cancer Center, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, and the Department of Pathology and Laboratory Medicine, demonstrates the power of systems biology in uncovering relationships between metabolism and signaling at the network level.
“Most strikingly, our discovery that glucose withdrawal causes both cell death and increased tyrosine phosphorylation is intriguing because increased tyrosine kinase signaling is normally associated with cell growth,” said Nicholas A. Graham, a senior postdoctoral scholar in Graeber’s lab who helped design the project.
To explain the seemingly contradictory result that glucose deprivation reduced viability and at the same time increased signaling, the authors used an unbiased systems-biology approach that included phospho-tyrosine mass spectrometry and other biochemical profiling techniques.
Assessing the “crosstalk” between metabolism and signaling, they discovered that the glucose deprivation activates a positive feedback loop whereby the withdrawal of glucose induces increased levels of reactive oxygen species, which in turn inhibit negative regulators of tyrosine signaling. The resulting supra-physiological levels of tyrosine phosphorylation then generate additional reactive oxygen species.
“Because cancer cells live on the edge of what is metabolically feasible, this amplifying cycle of oxidative stress ultimately overwhelms and kills the cancer cell,” Graeber explained. “These findings illustrate the delicate balance that exists between metabolism and signaling in the maintenance of cancer cell homeostasis.”
In addition, the authors showed the possibility of exploiting this positive feedback loop for therapeutic intervention. Combining short-term glucose deprivation with an inhibitor of tyrosine phosphatases, they demonstrated synergistic cell death in a cancer cell line.
“Understanding the links between metabolism and signaling will empower new therapeutic approaches toward inducing this metabolic catastrophe,” Graham said. “This study provides a framework for rational design of combinatorial therapeutics targeting both metabolism and signaling in cancer.”
The findings by Graeber and his colleagues add to the emerging concept of systems integration between oncogenic signaling networks and the metabolism of malignant tumors. The work lays a foundation for future studies delineating how signaling and metabolism are linked, with the ultimate goal of refining therapeutic strategies targeting cancer metabolism.
The research team also included collaborators from the department of neurology and the human oncology and pathogenesis program at Memorial Sloan–Kettering Cancer Center and the department of pharmacology at Weill–Cornell Medical College.
The research was funded by the National Institutes of Health, UCLA’s Jonsson Comprehensive Cancer Center, and the California Institute of Technology–University of California, Los Angeles, Joint Center for Translational Medicine.
Source: University of California, Los Angeles
Published on 28th June 2012
Scientists at UCLA have identified a new compound that could treat certain types of genetic disorders in muscles. It is a big first step in what they hope will lead to human clinical trials for Duchenne muscular dystrophy.
Duchenne muscular dystrophy, or DMD, is a degenerative muscle disease that affects boys almost exclusively. It involves the progressive degeneration of voluntary and cardiac muscles, severely limiting the life span of sufferers.
In a new study, senior author Carmen Bertoni, an assistant professor in the UCLA Department of Neurology, first author Refik Kayali, a postgraduate fellow in Bertoni’s lab, and their colleagues demonstrate the efficacy of a new compound known as RTC13, which suppresses so-called “nonsense” mutations in a mouse model of DMD.
The findings appear in the current online edition of the journal Human Molecular Genetics.
“We are excited about these new findings because they represent a major step toward the development of a drug that could potentially treat this devastating disease in humans,” Bertoni said. “We knew that the compounds were effective in cells isolated from the mouse model for DMD, but we did not know how they would behave when administered in a living organism.”
Nonsense mutations are generally caused by a single change in DNA that disrupts the normal cascade of events that changes a gene into messenger RNA, then into a protein. The result is a non-functioning protein. Approximately 13 percent of genetic defects known to cause diseases are due to such mutations. In the case of DMD, the “missing” protein is called dystrophin.
For the study, Bertoni and Kayali collaborated with the laboratory of Dr. Richard Gatti, a professor of pathology and laboratory medicine and of human genetics at UCLA. Working with the UCLA Molecular Shared Screening Resource facility at the campus’s California NanoSystems Institute, the Gatti lab screened some 35,000 small molecules in the search for new compounds that could ignore nonsense mutations. Two were identified as promising candidates: RTC13 and RTC14.
The Bertoni lab tested RTC13 and RTC14 in a mouse model of DMD carrying a nonsense mutation in the dystrophin gene. While RTC14 was not found to be effective, RTC13 was able to restore significant amounts of dystrophin protein, making the compound a promising drug candidate for DMD. When RTC13 was administered to mice for five weeks, the investigators found that the compound partially restored full-length dystrophin, which resulted in a significant improvement in muscle strength. The loss of muscle strength is a hallmark of DMD.
The researchers also compared the level of dystrophin achieved to the levels seen with another experimental compound, PTC124, which has proved disappointing in clinical trials; RTC13 was found to be more effective in promoting dystrophin expression. Just as important, Bertoni noted, the study found that RTC13 was well tolerated in animals, which suggests it may also be safe to use in humans.
The next step in the research is to test whether an oral formulation of the compound would be effective in achieving therapeutically relevant amounts of dystrophin protein. If so, planning can then begin for clinical testing in patients and for expanding these studies to other diseases that may benefit from this new drug.
Other study authors included Jin-Mo Ku, Gregory Khitrov, Michael E. Jung and Olga Prikhodko, all from UCLA. The researchers report no conflicts of interest. The work has been supported in large part by the Muscular Dystrophy Association (MDA) and, more recently, by the National Institutes of Health.
Source: University of California, Los Angeles
Published on 28th June 2012
UCLA researchers have discovered that a diet enriched with a popular omega-3 fatty acid and an ingredient in curry spice helps to preserve walking ability in rats that have experienced damage to their spinal cords.
The findings, published June 26 in the Journal of Neurosurgery: Spine, suggest that these dietary supplements help repair nerve cells and maintain neurological function after degenerative damage to the neck.
“Normal aging often narrows the spinal canal, putting pressure on the spinal cord and injuring tissue,” said principal investigator Dr. Langston Holly, associate professor of neurosurgery at the David Geffen School of Medicine at UCLA. “While surgery can relieve the pressure and prevent further injury, it can’t repair damage to the cells and nerve fibers. We wanted to explore whether dietary supplementation could help the spinal cord heal itself.”
The UCLA team studied two groups of rats with a condition that simulated cervical myelopathy — a progressive disorder that often occurs in people with spine-weakening conditions like rheumatoid arthritis and osteoporosis. Cervical myelopathy can lead to disabling neurological symptoms, such as difficulty walking, neck and arm pain, hand numbness, and weakness of the limbs. It’s the most common cause of spine-related walking problems in people over 55.
The first group of animals was fed rat chow that replicated a Western diet high in saturated fats and sugar. The second group consumed a standard diet supplemented with docosahexaenoic acid (DHA) and curcumin, a compound in the Indian curry spice turmeric. A third set of rats received a standard rat diet and served as a control group.
Why these supplements? DHA is an omega-3 fatty acid shown to repair damage to cell membranes. Curcumin is a strong antioxidant that previous studies have linked to tissue repair. Both reduce inflammation.
“The brain and spinal cord work together, and years of research demonstrate that supplements like DHA and curcumin can positively influence the brain,” said study co-author Fernando Gomez-Pinilla, a professor of neurosurgery at UCLA. “We suspected that what works in the brain may also work in the spinal cord. When we were unable to find good data to support our hypothesis, we decided to study it ourselves.”
The researchers recorded a baseline of the rats walking and re-examined the animals’ gait on a weekly basis. As early as three weeks, the rats eating the Western diet demonstrated measurable walking problems that worsened as the study progressed. Rats fed a diet enriched with DHA and curcumin walked significantly better than the first group even six weeks after the study’s start.
Next, the scientists examined the rats’ spinal cords to evaluate how diet affected their injury on a molecular level. They measured levels of three markers respectively linked to cell-membrane damage, neural repair and cellular communication.
The rats that ate the Western diet showed higher levels of the marker linked to cell-membrane damage. In contrast, the DHA and curcumin appeared to offset the injury’s effect in the second group, which displayed marker levels that were equivalent to the control group.
Levels of the markers linked to neural repair and cellular communication were significantly lower in the rats raised on the Western diet. Again, levels in the animals fed the supplemented diet appeared similar to those of the control group.
“DHA and curcumin appear to invoke several molecular mechanisms that preserved neurological function in the rats,” said Gomez-Pinilla. “This is an exciting first step toward understanding the role that diet plays in protecting the body from degenerative disease.”
“Our findings suggest that diet can help minimize disease-related changes and repair damage to the spinal cord,” Holly said. “We next want to look at other mechanisms involved in the cascade of events leading up to chronic spinal-cord injury. Our goal is to identify which stages will respond best to medical intervention and identify effective steps for slowing the disease process.”
Other co-authors included Dr. Donald Blaskiewicz, Aiguo Wu, Cameron Feng and Zhe Ying, all of UCLA. Their research was supported by grants from the National Institutes of Health (RO1 NS056413) and the Craig H. Neilsen Foundation.
Source: University of California, Los Angeles
Published on 28th June 2012
Psoriasis is an autoimmune disorder in which skin cells proliferate out of control. For some hard-to-heal wounds, the problem is just the opposite: Restorative skin cells don’t grow well or fast enough. In a paper published in the June 21, 2012 issue of Immunity, researchers at the University of California, San Diego School of Medicine describe a molecule that may lead to new treatments for both problems.
An international team of scientists led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego’s Division of Dermatology, and first author Yuping Lai, PhD, professor of microbiology and immunity at East China Normal University in Shanghai, analyzed skin biopsies of patients with and without psoriasis, as well as the skin of mice with psoriasis and with wounds on their backs. They discovered that a molecule called regenerating islet-derived protein 3-alpha (REG3A) is highly expressed in skin cells during psoriasis and wound-healing, but not under normal skin conditions.
In tests on mice, researchers found that inhibiting REG3A slowed wound-healing but cleared up psoriasis, which is commonly characterized by patches of inflammation and white, scaly skin.
The scientists also noted that REG3A acts in concert with interleukin-17 (IL-17), an immune system protein involved in the signaling cascade which prompts skin cells to multiply in excess numbers. “IL-17 binds to receptors on skin cells and causes REG3A to be expressed, which then binds to another protein inside the cells that promotes cell growth,” said Lai.
Gallo said the discovery of REG3A’s dual roles provides a new target for different therapies.
“A drug that inhibits the expression of REG3A could represent a more targeted way to treat psoriasis without the systemic immunosuppression problems of current treatments,” Lai. “Conversely, a drug that stimulates or mimics REG3A could boost cell growth and improve wound healing.”
Co-authors are Dongqing Li, Changwei Li, Ziwei Jiang, Zhiheng Li, Hu Lei, Yanchun Quan and Tian Zhang, all at the Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University; Beda Muhleisen, Paul Kotol and Tissa R. Hata, Division of Dermatology, Departments of Medicine and Pediatrics, UC San Diego; Katherine A. Radek, Department of Surgery, Burn and Shock Trauma Institute, Loyola University, Chicago; Hyun Jeong Park, Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul; Shin Morizane and Keiji Iwatsuki, Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Japan; Ge Tang, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo.
Funding for this research came, in part, from the National Institutes of Health (grants AR052728, AI052453, AI083358), the National Natural Science Foundation of China and the Science and Technology Commission of Shanghai Municipality.
Published on 26th June 2012
Hemimegalencephaly is a rare but dramatic condition in which the brain grows asymmetrically, with one hemisphere becoming massively enlarged. Though frequently diagnosed in children with severe epilepsy, the cause of hemimegalencephaly is unknown and current treatment is radical: surgical removal of some or all of the diseased half of the brain.
In a paper published in the June 24, 2012 online issue of Nature Genetics, a team of doctors and scientists, led by researchers at the University of California, San Diego School of Medicine and the Howard Hughes Medical Institute, say de novo somatic mutations in a trio of genes that help regulate cell size and proliferation are likely culprits for causing hemimegalencephaly, though perhaps not the only ones.
De novo somatic mutations are genetic changes in non-sex cells that are neither possessed nor transmitted by either parent. The scientists’ findings – a collaboration between Joseph G. Gleeson, MD, professor of neurosciences and pediatrics at UC San Diego School of Medicine and Rady Children’s Hospital-San Diego; Gary W. Mathern, MD, a neurosurgeon at UC Los Angeles’ Mattel Children’s Hospital; and colleagues – suggest it may be possible to design drugs that inhibit or turn down signals from these mutated genes, reducing or even preventing the need for surgery.
Gleeson’s lab studied a group of 20 patients with hemimegalencephaly upon whom Mathern had operated, analyzing and comparing DNA sequences from removed brain tissue with DNA from the patients’ blood and saliva.
“Mathern had reported a family with identical twins, in which one had hemimegalencephaly and one did not. Since such twins share all inherited DNA, we got to thinking that there may be a new mutation that arose in the diseased brain that causes the condition,” said Gleeson. Realizing they shared the same ideas about potential causes, the physicians set out to tackle this question using new exome sequencing technology, which allows sequencing of all of the protein-coding exons of the genome at the same time.
The researchers ultimately identified three gene mutations found only in the diseased brain samples. All three mutated genes had previously been linked to cancers.
“We found mutations in a high percentage of the cells in genes regulating the cellular growth pathways in hemimegalencephaly,” said Gleeson. “These same mutations have been found in various solid malignancies, including breast and pancreatic cancer. For reasons we do not yet understand, our patients do not develop cancer, but rather this unusual brain condition. Either there are other mutations required for cancer propagation that are missing in these patients, or neurons are not capable of forming these types of cancers.”
The mutations were found in 30 percent of the patients studied, indicating other factors are involved. Nonetheless, the researchers have begun investigating potential treatments that address the known gene mutations, with the clear goal of finding a way to avoid the need for surgery.
“Although counterintuitive, hemimegalencephaly patients are far better off following the functional removal or disconnection of the enlarged hemisphere,” said Mathern. “Prior to the surgery, most patients have devastating epilepsy, with hundreds of seizures per day, completely resistant to even our most powerful anti-seizure medications. The surgery disconnects the affected hemisphere from the rest of the brain, causing the seizures to stop. If performed at a young age and with appropriate rehabilitation, most children suffer less language or cognitive delay due to neural plasticity of the remaining hemisphere.”
But a less-invasive drug therapy would still be more appealing.
“We know that certain already-approved medications can turn down the signaling pathway used by the mutated genes in hemimegalencephaly,” said lead author and former UC San Diego post-doctoral researcher Jeong Ho Lee, now at the Korea Advanced Institute of Science and Technology. “We would like to know if future patients might benefit from such a treatment. Wouldn’t it be wonderful if our results could prevent the need for such radical procedures in these children?”
Co-authors are My Huynh, department of Neurosurgery and Psychiatry and Biobehavioral Sciences, Mattel Children’s Hospital, Geffen School of Medicine, UCLA; Jennifer L. Silhavy, Tracy Dixon-Salazar, Andrew Heiberg, Eric Scott, Kiley J. Hill and Adrienne Collazo, Institute for Genomic Medicine, Rady Children’s Hospital, UC San Diego and Howard Hughes Medical Institute; Sangwoo Kim and Vineet Bafna, Department of Computer Sciences, Jacobs School of Engineering, UC San Diego; Vincent Furnari and Carsten Russ, Institute for Medical Genetics, Cedars-Sinai Medical Center, Los Angeles and Department of Pediatrics, Geffen School of Medicine, UCLA; and Stacey B. Gabriel, The Broad Institute of MIT and Harvard, Cambridge.
Funding for this research came, in part, from the Daland Fellowship from the American Philosophical Society, the National Institutes of Health (grants R01 NS038992, R01 NS048453, R01 NS052455, R01 NS41537 and P01 HD070494), the Simons Foundation Autism Research Initiative and the Howard Hughes Medical Institute.
Published on 26th June 2012
Human Papilloma Virus (HPV), once almost exclusively associated with cancer of the cervix, is now linked to head and neck cancer. According to a new University at Buffalo study just published in the Archives of Otolaryngology — Head & Neck Surgery, a JAMA publication, gum disease is associated with increased odds of tumors being HPV-positive.
Mine Tezal, DDS, PhD, assistant professor of oral biology in the UB School of Dental Medicine who is the primary investigator on the study, and a team of scientists from UB evaluated data from 124 patients diagnosed with primary head and neck squamous cell carcinoma (HNSCC) between 1999 and 2007.
“The aim of the study was to test the presence of periodontitis, a persistent inflammatory process and HPV-status of HNSCC,” she said.
Of the 124 tumor samples Tezal and her team studied, 50 were positive for HPV-16 DNA and that subjects with HPV-positive tumors had a significantly higher severity of periodontitis when compared to subjects with HPV-negative tumors.
According to the National Cancer Institute, there has been a steady increase in the prevalence of oropharyngeal cancers in the U.S. since 1973 despite the significant decline in tobacco use since 1965.
Tezal notes that this increase has mainly been attributed to oral HPV infection.
Understanding the natural history of the oral HPV infection and targeting factors associated not only with its acquisition but also with its persistence, says Tezal, will lead to more effective strategies, not only for prevention, but also for treatment.
“While there is an effective vaccine for cervical HPV infection if given prior to the exposure of the virus (females 9-26; males 9-21), oral HPV infection can be transmitted at or any time after birth, and the target population for a vaccine to prevent oral HPV infection has not yet been defined,” said Tezal.
Tezal pointed out that though many previous studies combined periodontitis and dental decay as indicators of poor oral health, dental decay was not significantly linked to tumor-HPV status in the present study.
“The fact that only periodontitis was associated with tumor HPV status points to the potential association of inflammation with tumor HPV status,” she says.
When Tezal and colleagues started their research about eight years ago they were looking at the potential association between chronic inflammation and head and neck cancers because the importance of the local oral environment for malignant tumor growth was widely accepted. However there wasn’t research evaluating the role of local oral factors in the natural history of HNSCC, Tezal said.
“The next step in this research will be intervention studies to test whether treating the sources of inflammation, like gum disease, can reduce the acquisition and/or persistence of oral HPV infection and improve the prognosis of HPV-related diseases,” she said.
Source:- University at Buffalo
Published on 22nd June 2012
Researchers at the University of California, San Diego Jacobs School of Engineering have developed a technique that enables metallic nanocrystals to self-assemble into larger, complex materials for next-generation antennas and lenses. The metal nanocrystals are cube-shaped and, like bricks or Tetris blocks, spontaneously organize themselves into larger-scale structures with precise orientations relative to one another. Their findings were published online June 10 in the journal Nature Nanotechnology.
This research is in the new field of nanoplasmonics, where researchers are developing materials that can manipulate light using structures that are smaller than the wavelength of light itself. The nanocubes used in this study were less than 0.1 microns; by comparison, the breadth of a human hair is 100 microns. Precise orientation is necessary so that the cubes can confine light (for a nanoscale antenna) or focus light (for a nanoscale lens) at different wavelengths.
“Our findings could have important implications in developing new optical chemical and biological sensors, where light interacts with molecules, and in optical circuitry, where light can be used to deliver information,” said Andrea Tao, a professor in the Department of NanoEngineering at the Jacobs School. Tao collaborated with nanoengineering professor Gaurav Arya and post-doctoral researcher Bo Gao.
To construct objects like antennas and lenses, Tao’s team is using chemically synthesized metal nanocrystals. The nanocrystals can be synthesized into different shapes to build these structures; in this study, Tao’s team created tiny cubes composed of crystalline silver that can confine light when organized into multi-particle groupings. Confining light into ultra-small volumes could allow optical sensors that are extremely sensitive and that could allow researchers to monitor how a single molecule moves, reacts, and changes with time.
To control how the cubes organize, Tao and her colleagues developed a method to graft polymer chains to the silver cube surfaces that modify how the cubes interact with each other. Normally when objects like cubes stack, they pack side-by-side like Tetris blocks. Using simulations, Tao’s team predicted that placing short polymer chains on the cube surface would cause them to stack normally, while placing long polymer chains would cause the cubes to stack edge-to-edge. The approach is simple, robust, and versatile.
In demonstrating their technique, the researchers created macroscopic films of nanocubes with these two different orientations and showed that the films reflected and transmitted different wavelengths of light.
The research was supported by the National Science Foundation, the Hellman Foundation, and Jacobs School of Engineering at UC San Diego.
Published on 18th June 2012
A grasshopper’s change in diet to high-energy carbohydrates while being hunted by spiders may affect the way soil releases carbon dioxide into the atmosphere, according to research results published this week in the journal Science.
Grasshoppers like to munch on nitrogen-rich grass because it stimulates their growth and reproduction.
But when spiders enter the picture, grasshoppers cope with the stress from fear of predation by shifting to carbohydrate-rich plants, setting in motion dynamic changes to the ecosystem they inhabit, scientists have found.
“Under stressful conditions they go to different parts of the ‘grocery store’ and choose different foods, changing the makeup of the plant community,” said Oswald Schmitz, a co-author of the paper and an ecologist at Yale University.
The high-energy, carbohydrate diet also tilts a grasshopper’s body chemistry toward carbon at the expense of nitrogen.
So when a grasshopper dies, its carcass breaks down more slowly, thus depriving the soil of high-quality fertilizer and slowing the decomposition of uneaten plants.
“This study casts a new light on the importance of predation in natural communities,” said Saran Twombly, program director in the National Science Foundation’s Division of Environmental Biology, which funded the research.
“A clever suite of experiments shows that the dark hand of predation extends all the way from altering what prey eat to the nutrients their decomposing bodies contribute to soil.”
Microbes in the soil require a lot of nitrogen to function and to produce the enzymes that break down organic matter.
“It only takes a slight change in the chemical composition of that animal biomass to fundamentally alter how much carbon dioxide the microbial pool is releasing to the atmosphere while it is decomposing plant organic matter,” said Schmitz.
“This shows that animals could potentially have huge effects on the global carbon balance because they’re changing the way microbes respire organic matter.”
The researchers found that the rate at which the organic matter of leaves decomposed increased between 60 percent and 200 percent in stress-free conditions relative to stressed conditions, which they consider “huge.”
“Climate and litter quality are considered the main controls on organic-matter decomposition, but we show that aboveground predators change how soil microbes break down organic matter,” said Mark Bradford, a co-author of the study and also an ecologist at Yale.
Schmitz added: “What it means is that we’re not paying enough attention to the control that animals have over what we view as a classically important process in ecosystem functioning.”
The researchers took soil from the field, put it in test tubes and ground up grasshopper carcasses obtained from environments either with or without grasshopper predators.
They then sprinkled the powder atop the soil, where the microbes digested it.
When the grasshopper carcasses were completely decomposed, the researchers added leaf litter and measured the rate of leaf-litter decomposition.
The experiment was then replicated in the field at the Yale Myers Forest in northeastern Connecticut.
“It was a two-stage process where the grasshoppers were used to prime the soil, then we measured the consequences of that priming,” said Schmitz.
The effect of animals on ecosystems is disproportionately larger than their biomass would suggest.
“Traditionally people thought that animals had no important role in recycling of organic matter, because their biomass is relatively small compared to the plant material that’s entering ecosystems,” Schmitz said.
“We need to pay more attention to the role of animals, however. In an era of biodiversity loss we’re losing many top predators and larger herbivores from ecosystems.”
Source: National Science Foundation
Published on 18th June 2012