Archive for the ‘Biology’ Category

Mystery solved: How bleach kills germs

Saturday, November 15th, 2008

Molecular, Cellular, and Developmental Biology Associate Professor Ursula Jakob Reuters – Molecular, Cellular, and Developmental Biology Associate Professor Ursula Jakob (L) and Jeannette Winter, …

CHICAGO (Reuters) – Bleach has been killing germs for more than 200 years but U.S. scientists have just figured out how the cleaner does its dirty work.

It seems that hypochlorous acid, the active ingredient in bleach, attacks proteins in bacteria, causing them to clump up much like an egg that has been boiled, a team at the University of Michigan reported in the journal Cell on Thursday.

The discovery, which may better explain how humans fight off infections, came quite by accident.

“As so often happens in science, we did not set out to address this question,” Ursula Jakob, who led the team, said in a statement.

The researchers had been studying a bacterial protein called heat shock protein 33, which is a kind of molecular chaperon that becomes active when cells are in distress, for example from the high temperature of a fever.

In this case, the source of the distress was hypochlorous acid or hypochlorite.

Jakob’s team figured out that bleach and high temperatures have very similar effects on proteins.

When they exposed the bacteria to bleach, the heat shock protein became active in an attempt to protect other proteins in the bacteria from losing their chemical structure, forming clumps that would eventually die off.

“Many of the proteins that hypochlorite attacks are essential for bacterial growth, so inactivating those proteins likely kills the bacteria,” Marianne Ilbert, a postdoctoral fellow in Jakob’s lab, said in a statement.

The researchers said the human immune system produces hypochlorous acid in response to infection but the substance does not kill only the bacterial invaders. It kills human cells too, which may explain how tissue is destroyed in chronic inflammation.

Hypochlorous acid is an important part of host defense,” Jakob said. “It’s not just something we use on our countertops.”

Fish Tale Has A DNA Hook - Students Find Bad Labels

Friday, August 22nd, 2008

From the New York Times - August 22, 2008

Many New York sushi restaurants and seafood markets are playing a game of bait and switch, say two high school students turned high-tech sleuths.

In a tale of teenagers, sushi and science, Kate Stoeckle and Louisa Strauss, who graduated this year from the Trinity School in Manhattan, took on a freelance science project in which they checked 60 samples of seafood using a simplified genetic fingerprinting technique to see whether the fish New Yorkers buy is what they think they are getting.

They found that one-fourth of the fish samples with identifiable DNA were mislabeled. A piece of sushi sold as the luxury treat white tuna turned out to be Mozambique tilapia, a much cheaper fish that is often raised by farming. Roe supposedly from flying fish was actually from smelt. Seven of nine samples that were called red snapper were mislabeled, and they turned out to be anything from Atlantic cod to Acadian redfish, an endangered species.

What may be most impressive about the experiment is the ease with which the students accomplished it. Although the testing technique is at the forefront of research, the fact that anyone can take advantage of it by sending samples off to a laboratory meant the kind of investigative tools once restricted to Ph.D.’s and crime labs can move into the hands of curious diners and amateur scientists everywhere.

The project began, appropriately, over dinner about a year ago. Ms. Stoeckle’s father, Mark, is a scientist and early proponent of the use of DNA bar coding, a technique that greatly simplifies the process of identifying species. Instead of sequencing the entire genome, bar coders — who have been developing their field only since 2003 — examine a single gene. Dr. Stoeckle’s specialty is birds, and he admits that he tends to talk shop at the dinner table.

One evening at a sushi restaurant, Ms. Stoeckle recalled asking her father, “Could you bar code sushi?”

Dr. Stoeckle replied, “Yeah, I think you could — and if you did that, I think you’d be the first ones.”

Ms. Stoeckle, who is now 19, was intrigued. She enlisted Ms. Strauss, who is now 18.

Their field technique was simple, Ms. Stoeckle said. “We ate a lot of sushi.”

Or, as Dr. Stoeckle put it, “It involved shopping and eating, in which they were already fluent.”

They hit 4 restaurants and 10 grocery stores in Manhattan. Once the samples were home, whether in doggie bags or shopping bags, they cut away a small piece and preserved it in alcohol. They sent those off to the University of Guelph in Ontario, where the Barcode of Life Database project began. A graduate student there, Eugene Wong, works on the Fish Barcode of Life (dubbed, inevitably, Fish-BOL) and agreed to do the genetic analysis. He compared the teenagers’ samples with the global library of 30,562 bar codes representing nearly 5,500 fish species. (Commercial labs will also perform the analysis for a fee.)

Three hundred dollars’ worth of meals later, the young researchers had their data back from Guelph: 2 of the 4 restaurants and 6 of the 10 grocery stores had sold mislabeled fish.

Dr. Stoeckle said he was excited to see a technology used in a new way. “The smaller and cheaper you make something,” he said, “the more uses it has.” He compared bar coding to another high-tech wonder turned everyday gadget, GPS.

Eventually, he predicted, the process will become more automatic, cheaper and smaller so that a handheld device could perform a quick analysis and connect to the database remotely. What his daughter did, he said, is like dropping film off at the supermarket for developing. The next generation could be more like a digital camera that displays the results on the spot.

The results of Ms. Strauss and Ms. Stoeckle’s research are being published in Pacific Fishing magazine, a publication for commercial fishermen. The sample size is too small to serve as an indictment of all New York fishmongers and restaurateurs, but the results are unlikely to be a mere statistical fluke.

The experiment does serve as a general caveat emptor for fish lovers, particularly because the students, their parents and their academic mentor all declined to give the names of the vendors, citing fear of lawsuits. Besides, they noted, mislabeling could occur at any stage of the process.

Dr. Stoeckle was willing to divulge the name of one fish market whose products were accurately labeled in the test: Leonards’ Seafood and Prime Meats on Third Avenue. John Leonard, the owner, said he was not surprised to find that his products passed the bar code test. “We go down and pick the fish out ourselves,” he said. “We know what we’re doing.” As for the technology, Mr. Leonard said, “it’s good for the public,” since “it would probably keep restaurateurs and owners of markets more on their toes.”

Ms. Stoeckle said the underlying message of the research was simple: “If you’re paying for white tuna and you’re eating tilapia, I think you’d want to know that.”

Although the students did not present the project for a grade at school, they made sure to mention it on their college applications. Both will enroll at Johns Hopkins University this fall.

Neither, however, expects to major in the sciences. “I’ve always been into art history,” Ms. Strauss said, “which is really different from this.” Ms. Stoeckle, who is the granddaughter of the entertainer and arts patron Kitty Carlisle Hart, is thinking about studying writing or psychology. But that, they said, is the point. “If we found it interesting — which we did — I think lots of people like us can do it, too,” Ms. Stoeckle said.

Peter B. Marko, a professor at Clemson University who used a more detailed genetic technique in a 2004 paper to show that red snapper was commonly mislabeled, called their project “quite remarkable,” though he added that genetic analysis had been simplified to the point that high school students could now perform the task without sending samples off.

Mr. Marko prefers to work with whole genomes — “more information is better,” he explained — which can be sequenced now with lightning speed. He plans to perform a broad genetic comparison of fishes that were separated millions of years ago by the rise of the Isthmus of Panama. “The technology is allowing us to ask questions that really would not have been possible in the past.”

The students worked under the tutelage of Jesse H. Ausubel of Rockefeller University, a champion of the DNA bar coding technique. As for Ms. Strauss and Ms. Stoeckle, Dr. Ausubel said they “have contributed to global science” by adding to the database, built on a model similar to that of Wikipedia, in which people around the world can contribute.

In a way, Dr. Ausubel said, their experiment is a return to an earlier era of scientific inquiry. “Three hundred years ago, science was less professionalized,” he said, and contributions were made by interested amateurs. “Perhaps the wheel is turning again where more people can participate

 

Shark-Inspired Boat Surface

Sunday, August 10th, 2008

Materials Engineers Turn to Ferocious Fish for Nonstick Ship Coating

May 1, 2005 — Researchers are using shark skin as a model for creating new coatings that prevent adhesion of algae and barnacles to boats. The new coating is modeled after sharks’ placoid scales, which have a rectangular base embedded in the skin with tiny spines or bristles that poke up from the surface that prevent things from attaching to the shark’s skin.

GAINESVILLE, Fla.–In the boating industry, a huge problem exists that can be summed up in three words — algae, barnacles and slime. Until now, the only way to prevent these organisms from growing was toxic paint. But researchers are studying a more natural approach that’s inspired by the ocean’s fiercest predator.

In movies, they’re the enemy, but in the world of science, sharks are allies.

Materials engineer Tony Brennan, of University of Florida in Gainesville, uses shark skin as a model for creating new surfaces. “The shark scales have a roughness that approximates the roughness that we had predicted would be a good roughness to stop adhesion,” he says.

Brennan designed the surfaces to prevent algae and barnacles from growing on boats. He says, “We started making surfaces that are mimicking the shark’s skin.”

A computer program helped researchers create the pattern and structure…

“Whatever we can draw, we can make into a surface,” says UF graduate student, Jim Schumacher.

And just like shark skin, spores can’t fit in the ridges and don’t want to balance on top of the surface Brennan and his team designed in the lab. “That’s a tremendous benefit to energy consumption, dollars and maintenance,” Brennan says.

Getting rid of those barnacles and other organisms would mean less cleaning and not having to drag around the extra weight would lower fuel costs.

“If it’s effective, it would tremendously affect the industry,” Emerson says.

When the surface hits the market in the next year, it could impact private boaters and Navy vessels, too. Researchers are also studying the shark-coated surface for medical applications.

Exploring Energy Conservation Through Shark Research

Sunday, August 10th, 2008

Web address:
     http://www.sciencedaily.com/releases/2007/11/
     071130155548.htm 

Dr. Amy Lang and a graduate student work in UA’s water tunnel lab researching skin friction over solid surfaces. (Credit: University of Alabama Photography)ScienceDaily (Dec. 1, 2007) — The stars of the “Jaws” films–sharks–have recently become the subject of a University of Alabama engineering research project. Conducted by Dr. Amy Lang, assistant professor of aerospace engineering and mechanics, the project explores energy conservation and boundary layer control in regard to a shark’s surface.

The project findings will allow researchers to explore natural solutions for the reduction of skin friction over solid surfaces, which could result in new innovations and applications concerning energy conservation. This research will not only provide a greater understanding of the evolutionary development of sharks, but it will also investigate methods of flow control and drag reduction that can be easily applied to mobile vehicles.

Research has shown the issue of reducing drag over solid surfaces can save thousands of dollars. For example, it is estimated that even a 1 percent reduction in drag can save an airline company up to $200,000 and at least 25,000 gallons of fuel per year per aircraft. The resulting reduction in emissions into the air is equally impressive.

Funded through a National Science Foundation Small Grant, the project is investigating the boundary layer flow over a surface that mimics the skin of a fast-swimming shark. The boundary layer is the area closest to the surface where viscous conditions cause drag–in this instance a shark’s skin.

Lang hopes to explain why fast sharks that swim upwards of 60 mph have smaller denticles, or scales, than slower shark species. Evidence suggests that sharks with smaller denticles have the ability to stick out their scales when they swim, allowing them to swim faster and creating a unique surface pattern on the skin that results in various mechanisms of boundary layer control.

“We hope to explain how a shark’s skin controls the boundary layer to decrease drag and swim faster,” said Lang. “If we can successfully show there is a significant effect, future applications to reduce drag of aircraft and underwater vehicles could be possible.”

Lang’s research is being conducted using a water tunnel facility in Hardaway Hall. The water tunnel lab can increase the shark skin geometry by 100 times with a corresponding decrease in flow over the model. This makes the flow over the skin observable, and it allows for the visualization and measurement of flow using modern experimental techniques.

In addition to the National Science Foundation Small Grant, Lang recently received a Lindbergh Grant for this research project. Lindbergh Grants are made in amounts up to $10,580, a symbolic amount representing the cost of building Charles Lindbergh’s plane, the Spirit of St. Louis.
University of Alabama (2007, December 1). Exploring Energy Conservation Through Shark Research. ScienceDaily. Retrieved August 10, 2008, from http://www.sciencedaily.com­ /releases/2007/11/071130155548.htm

Herpes Research Uncovers Possible Clue To Alzheimer’s Disease

Sunday, August 10th, 2008

ScienceDaily (Nov. 7, 2003) — Providence, R.I. — Researchers at Brown University and the Marine Biological Laboratory at Woods Hole, Mass., have found a physical connection between the herpes simplex virus and amyloid precursor protein, a protein that breaks down to form a major component of the amyloid plaques that are consistently present in the brains of persons with Alzheimer’s disease.

Amyloid precursor protein – or APP – breaks down to form beta-amyloid. There is strong evidence, according to the researchers, that beta-amyloid is the underlying cause of Alzheimer’s.

While the scientists caution that no conclusions about Alzheimer’s can be drawn from their findings, Dr. Elaine Bearer, senior research scientist and associate professor in Brown’s Department of Pathology and Laboratory Medicine, believes the work does in fact link the common herpes virus of cold sores with the neurodegenerative disorder. Bearer isalso a summer investigator at the Marine Biological Laboratory at Woods Hole, Mass.

Past studies have implicated the herpes virus in the onset of Alzheimer’s disease, but agreement within the scientific community on the value of that research is far from universal. Bearer expects that the discovery of a physical interaction between APP and the herpes virus will trigger further investigations into the role the virus may play in the disease, and even into possible uses of the virus in therapy.

The scientists stress that none of what they found should cause alarm among those who have at one time had a cold sore. According to Bearer, nearly 85 percent of us harbor the herpes simplex virus and most of us never develop Alzheimer’s.

The researchers discovered the interaction between the herpes simplex virus (HSV) and APP while conducting experiments in the giant axon of squid at the Marine Biological Laboratory. Prasanna Satpute-Krishnan and Joseph A. DeGiorgis, both doctoral candidates in Brown’s graduate program at the time of the research, were seeking to learn how viruses are carried around the body – within cells and from one cell to another. Specifically, they were examining how the herpes simplex virus travels back to the lip area to form a recurring blister after remaining latent for some time in the trigeminal ganglion, a collection of nerve cells next to the brain.

What they found was that the herpes virus was interacting with APP, a putative motor receptor that recruits a microtubular motor, kinesin, for transport through neurons. This was the first time scientists had observed any physical interaction between the herpes virus and APP.

Without the APP, the virus moves backward up an axon (a long extension of a neuron) from the area of the lip towards the trigeminal ganglion. But the Brown researchers discovered that once it interacts with the APP, the virus travels in the opposite direction – what scientists describe as anterograde transport – back down to the lip. The researchers also found that once coupled with the APP, the virus moves remarkably fast.

“It’s as if the virus hijacks a car – which in this case would be the kinesin – and the APP is the driver,” explains Bearer. “The virus takes the APP where it wants to be, not where the APP wants to be.”

The build-up of beta-amyloid (formed in the breakdown of APP) is found consistently in the brains of Alzheimer’s patients, and many scientists are now convinced it is involved in the disease, according to Satpute-Krishnan. Questions persist, however, as to what that involvement is, and why, when APP is found in all of us, it causes problems only in a few.

Perhaps, Bearer speculates, when the APP is co-opted by the herpes virus, the APP breaks down at a location where it would not normally appear – and at a very different rate. “When APP piles up around neurons, the neurons die,” she explains. “But we don’t yet know if this is a secondary or a primary cause of Alzheimer’s.”

“At this point, of course, we don’t yet know whether herpes plays a causal role in Alzheimer’s disease,” DeGiorgis notes. “But our research does provide some interesting new insight into both diseases.”

A paper outlining the findings of the Brown/MBL researchers – titled “Fast Anterograde Transport of Herpes Simplex Virus: Role of Amyloid Precursor Protein” – will appear in the December issue of Aging Cell, published by Blackwell Publishing in England and at the publisher’s “OnlineEarly” site [http://www.blackwell-synergy.com/links/toc/ace].

Satpute-Krishnan, the first author of the paper, is a graduate student in Brown’s Molecular Biology, Cell Biology and Biochemistry Graduate Program. Bearer, who holds both an M.D. and a Ph.D., is an experimental pathologist. DeGiorgis, who earned his Ph.D. in Bearer’s lab last year, is now with the National Institutes of Health.

Experiments in this study were conducted in the giant axon of squid, a model widely used in research because with a diameter of nearly a millimeter it is 1,000 times thicker than a human axon. Researchers are able to inject substances into the giant axon and then observe the behavior of those substances through high-powered microscopes.

“It is pretty extraordinary that breakthroughs in Alzheimer’s disease and in the pathogenesis of herpes virus should be made using the squid of the North Atlantic sea,” notes Bearer.

Last summer Brown University and the Marine Biological Laboratory formalized their alliance for teaching and research. The affiliation between the two institutions established the Brown-MBL Graduate Program in Biological and Environmental Sciences. In addition, it will promote faculty exchanges and research collaborations, such as the one conducted by Satpute-Krishnan, DeGiorgis and Bearer.

### The affiliation between MBL and Brown takes advantage of the geographic proximity of the two institutions, uniting their faculty expertise in biology and medicine, particularly for molecular biology, genomics, ecosystems studies, environmental science, global infectious diseases, neuroscience and public health. Student recruitment for the Brown-MBL Graduate Program got under way this fall, with the first students expected to begin their studies next year.

MBL is an internationally known, independent, nonprofit institution dedicated to improving the human condition through creative research and education in the biological, biomedical and environmental sciences. Founded in 1888, the MBL is the oldest private marine laboratory in the Western Hemisphere.


Adapted from materials provided by Brown University.
Brown University (2003, November 7). Herpes Research Uncovers Possible Clue To Alzheimer’s Disease. ScienceDaily. Retrieved August 10, 2008, from http://www.sciencedaily.com­ /releases/2003/11/031107055048.htm

Scientists aim camera at fossilized dino tracks

Tuesday, July 29th, 2008

KANAB, Utah -Call them the paleo-paparazzi. Scientists trying to learn more about dinosaurs are snapping aerial photos of tracks left behind millions of years ago near southern Utah’s Coral Pink Sand Dunes.
Researchers in a specially equipped helicopter crisscrossed an area called the Moccasin Mountain track site, shooting photos of fossilized footprints scattered across the red sandstone.
Alan Titus, a Bureau of Land Management paleontologist, said it’s the first time a helicopter has been used to take detailed images of a track site.
The tracks were left by at least six species of dinosaurs _ some with three toes, others with five _ that roamed the landscape about 180 million years ago.
The camera, able to pick up tracks as small as a centimeter, will give scientists a bird’s-eye view of footprints dotting the 3-acre site.
The photos will be used to help create maps of the tracks and three-dimensional images so scientists can better understand dinosaur behavior. They’ll also be used on interpretive displays for visitors.
“We will be able to make a precise map of the location of the tracks, their spatial patterns and possibly determine what the (dinosaurs) were doing,” said Neffra Matthews, the geographer from the BLM’s National Operations Center in Colorado who conducted the imaging work.
The fossilized tracks have been known locally for years at Moccasin Mountain, a popular spot for ATV riders.
BLM scientists investigated last fall and found tens of thousands of tracks, ranging from bird-size footprints to others left by animals that were probably 20 feet long.
“The site is outstanding for the quality and size of the tracks, the diversity of animals represented and the range of time they were created,” Titus said.
The tracks have been linked to three-toed species similar to the horned Dilophosaurus and five-toed animals similar to crocodiles.
The site, which is now closed to motorized traffic, was probably an oasis where early Jurassic dinosaurs found water and relief from desert-like temperatures, Titus said.
Matthews has taken similar photographs at a track site near Grand Staircase-Escalante National Monument. Those were taken with the help of a blimp.
___

“Dinosaur eel” points to body armour of the future

Monday, July 28th, 2008

So say Pentagon-backed scientists who have pored over the scales of Polypterus senegalus, also called the Senegal bichir or the dinosaur eel.

Long and skinny and of ancient heritage, the 40-centimetre (16-inch) predator has multiple layers of scales that first dissipate the energy of a strike, then protect against any penetration to the soft tissues below and finally limit any damage to the shield to the immediate area surrounding the assault.

Experts at the Massachusetts Institute of Technology (MIT) used nano-scale measurements to look at several scales that were harmlessly removed from a living fish.

They found the scales — about 500 millionths of a metre thick — have four layers. The tiny shield was then put to the test, in a simulation of a biting attack.

The team believe the scales’ protection is remarkably effective because of the different composite materials, the geometry and thickness of each of these layers.

The overlapping junctions between the layers themselves also play an important role.

The design is “fascinating, complex and multiscale,” say the scientists.

“Such fundamental knowledge holds great potential for the development of improved biologically-inspired structural materials,” said Christine Ortiz, an MIT associate professor in materials science and engineering.

“Many of the design principles we describe — durable interfaces and energy-dissipating mechanisms, for instance — may be translatable to human armour systems.”

The study appears on Sunday in a specialist journal, Nature Materials.

The Most Important Disease of a Most Important Fruit

Saturday, July 19th, 2008
Randy Ploetz
Tropical Research and Education Center,
University of Florida, IFAS, Homestead

Origins and importance of banana as a food crop
Banana is one of the most fascinating and important of all crops. It is a large monocotyledenous herb that originated in Southeast Asia. Virtually all of the cultivars that are grown are thought to have been selected as naturally occurring hybrids in this region by the earliest of farmers. In fact, Norman Simmonds proposed that banana was one of the first crops to be domesticated by man. In writing of the beginnings of agriculture in Southeast Asia, he concluded, “It seems a reasonable assumption that the bananas evolved along with the earliest settled agriculture of that area and may therefore be some tens of thousands of years old.”

Despite the current, clear understanding of its ancestry, the edible bananas’ origins are often confused in the literature. Almost all of the 300 or more cultivars that are known arose from two seeded, diploid species, Musa acuminata Colla and M. balbisiana Colla; they are diploid, triploid and tetraploid hybrids among subspecies of M. acuminata, and between M. acuminata and M. balbisiana.

Conventionally, the haploid contributions of the respective species to the cultivars are noted with an A and B. For example, the Cavendish cultivars that are the mainstays of the export trades are pure triploid acuminata and, thus, AAA. The Linnaean species M. paradisiaca (the AAB plantains) and M. sapientum (the sweet dessert bananas, of which Silk AAB is the type cultivar) are invalid and no longer used.

 

Women selling fruit of Dwarf Cavendish AAA  and Pisang awak ABB  in a market in Karonga, Malawi, East Africa. The lower photograph shows preparation of male buds of Pisang awak for cooking in a market in Sungai Kolok, Thailand. For many of the world’s poorest people, banana is a nutritious and important staple food. Click images for enlargement.

Banana is now one of the most popular of all fruits. Although it is viewed as only a dessert or an addition to breakfast cereal in most developed countries, it is actually a very important agricultural product. After rice, wheat and milk, it is the fourth most valuable food. In export, it ranks fourth among all agricultural commodities and is the most significant of all fruits, with world trade totaling $2.5 billion annually. Yet, only 10% of the annual global output of 86 million tons enters international commerce. Much of the remaining harvest is consumed by poor subsistence farmers in tropical Africa, America and Asia. For most of the latter producers, banana and plantain (which is a type of banana) are staple foods that represent major dietary sources of carbohydrates, fiber, vitamins A, B6 and C, and potassium, phosphorus and calcium.

This photograph shows seed-packed fruit of Musa balbisiana, one of the ancestors of the edible bananas. Since the edible cultivars are parthenocarpic and often female or male sterile, seeds are rarely found in their fruit. The latter factors, however, have made it difficult to improve this crop by breeding.

Impact of banana diseases
Diseases are among the most important factors in banana production worldwide. They are the reasons for which all of the world’s breeding programs were created and remain a primary focus of all current programs. Recently, diseases also became principal targets of biotechnological efforts to improve this crop and www-cgi.cnn.com/TECH/science/9807/24/t_t/banana.science/index.html ).

A leaf spot disease is the most important of these problems. Black Sigatoka, which is also known as black leaf streak, causes significant reductions in leaf area, yield losses of 50% or more, and premature ripening, a serious defect in exported fruit. It is more damaging and difficult to control than the related yellow Sigatoka disease, and has a wider host range that includes the plantains and dessert and ABB cooking bananas that are usually not affected by yellow Sigatoka.

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A close-up of the adaxial surface of a banana leaf that is affected by black Sigatoka. Under high rainfall and humidity, these lesions will coalesce and kill the entire leaf. Click image for enlargement.

Damage caused by black Sigatoka in a planting of Dwarf Cavendish AAA in Malawi, East Africa. Note the scarcity of healthy leaf tissue on plants that carry fruit. Yields from such plants are usually a half or less than that from healthy plants.
Click image for enlargement.

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In export plantations, Black Sigatoka is controlled with frequent applications of fungicides and cultural practices, such as the removal of affected leaves, and adequate spacing of plants and efficient drainage within plantation. In total, these are very expensive practices. For example, fungicide application includes the use of airplanes or helicopters, permanent landing strips and facilities for mixing and loading the fungicides, and the high recurring expense of the spray materials themselves. In total, it has been estimated that the costs of control are ultimately responsible for 15-20% of the final retail price of these fruit in the importing countries. Their great expense makes them essentially unavailable to small-holder farmers who grow this crop, it is these producers who are affected most by this important disease.

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Aerial application of fungicides to control black Sigatoka in Honduras. In the final analysis, the costs associated with these control measures are directly responsible for 15-20% of the purchase price of exported fruit in the importing countries. (Photo courtesy of R.H. Stover)
Click image for enlargement.

Distribution, etiology and epidemiology of black Sigatoka
Black Sigatoka was first recognized in the Sigatoka Valley of Fiji in 1963, but was probably widespread in Southeast Asia and the South Pacific by that time. In the Western Hemisphere, it first appeared in 1972 in Honduras and now occurs on the mainland from central Mexico south to Bolivia and northwestern Brazil, and in the Caribbean basin in Cuba, Jamaica, the Dominican Republic and southern Florida. In Africa, the disease was first recorded in Zambia in 1973 and has since spread throughout the sub-Saharan portions of that continent. In most areas, black Sigatoka has now replaced yellow Sigatoka to become the predominant leaf spot disease of banana.

Black Sigatoka is caused by the ascomycete, Mycosphaerella fijiensis Morelet [anamorph: Paracercospora fijiensis (Morelet) Deighton] (a variant of the pathogen, M. fijiensis var. difformis, that was previously reported in tropical America, is no longer recognized). The pathogen produces conidia and ascospores, both of which are infective. They are formed under high moisture conditions, and are disseminated by wind, and in the case of conidia, also by rain and irrigation water. Due to their greater abundance and small size, ascospores are more important than conidia in spreading the disease within plants and plantations. In contrast, infected planting material and leaves, which are used often in the developing world as packing materials, are usually responsible for the long-distance spread of the disease. The recent outbreak of black Sigatoka in South Florida almost certainly resulted from the importation of infected germplasm by local growers (see Plant Disease note D-1998-1217-03N).

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“Damn, how did this get here?” Dr. Jonathan Crane, Extension Tropical Fruit Crops Specialist for the University of Florida in Homestead, examines a leaf of the banana cultivar Rajapuri AAB that is affected by black Sigatoka. The importation of infected propagation material, which is a common and effective means for moving this disease long distances, was probably responsible for the recent outbreak of black Sigatoka in South Florida. Click image for enlargement.

Control
Chemical control of first yellow, and then black, Sigatoka has evolved considerably over the last 65 years. Bordeaux mixture, first used in the mid-1930s, has been replaced by several succeeding generations of protectant and, later, systemic fungicides. Presently, a sterol biosynthesis inhibitor, tridemorph, several different sterol demethylation inhibitors, most importantly propiconazole, and the methoxyacrylate, azoxystrobin, are the most commonly used systemics.

Since there is a tendency for resistance or tolerance to develop in M. fijiensis towards the systemic fungicides, they are usually applied in combination or alternation with broad-spectrum, protectant fungicides, such as the dithiocarbamates and chlorothalonil. With the exception of chlorothalonil, these fungicides are usually mixed with petroleum-based spray oils. The oils themselves are fungistatic and retard the development of the pathogen in the infected leaf. When they are mixed in water emulsions with fungicides, the resulting “cocktails” provide superior disease control.

The export plantations in the Philippines and Central and South America that produce fruit for the developed world are vast monocultures of Cavendish cultivars, usually of Grand Nain but also of Williams and Valery. In order to treat these large areas with fungicides, helicopters or fixed wing aircraft are used. Application schedules in the plantations are routinely determined with disease-forecast systems that incorporate data on disease severity within the plantation and environmental factors that are known to affect infection and disease development. These epidemiological tools enabled producers in Central America to substantially reduce the number of fungicide applications that were needed for control. However, increased tolerance in the pathogen to the DMI fungicides has made it necessary to increase applications in several countries in the region to previous frequencies of 25 - 40 per year.

Aerial view of an export plantation of the Cavendish cultivar Grand Nain in the Sula Valley of Honduras. Such vast monocultures allow fruit to be produced efficiently, but require that fungicides for black Sigatoka control be applied by aircraft. Click image for enlargement.

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The annual cost of fungicide applications in export plantations is about $1,000 per hectare. Although the international trades can add this expense to the price they charge for fruit, this is not an option for subsistence farmers. Thus, the latter producers must use different strategies to manage black Sigatoka. These include the removal of older leaves to reduce inoculum levels in a plantation, interplanting with other nonsusceptible crops, and planting in partial shade which results in less severe disease development.

The potential for bred bananas
Given the high expense of fungicides, their unavailability for subsistence farmers, and the recurring problem with fungicide resistance in the export plantations, it is clear that genetic resistance to black Sigatoka would be most useful. If resistant, agronomically acceptable cultivars were available, they would provide the best solution to this problem in export and subsistence situations alike.

Unfortunately, resistance to black Sigatoka among pre-existing banana genotypes is poor. The Cavendish cultivars that are used for export are so susceptible that nothing short of intensive fungicide application will control the disease in most areas. Resistant cultivars that could be used in subsistence situations are available, but they are usually less productive or desirable than those that are susceptible. This situation has begun to change as a result of new, resistant hybrids that are being developed by the banana breeding programs (http://www.promusa.org ).

The first program to make significant progress in improving this crop was that of the Fundación Hondureña de Investigación Agrícola (FHIA http://www.honduras.com/fhia/espamenu.htm) in La Lima, Honduras. It was begun by the United
Fruit Company (now Chiquita Brands http://www.chiquita.com) in 1959, but was donated to this private agricultural research foundation in 1984. FHIA has developed numerous dessert, plantain and cooking hybrids, several of which have been tested in the International Musa Testing Programme of the International Network for the Improvement of Banana and Plantain (http://bananas.bioversityinternational.org/). Results from these and other trials indicate that the FHIA clones are generally very vigorous and produce high yields under a wide range of environmental and edaphic conditions. Importantly, they resist pathogenically and geographically diverse populations of M. fijiensis, as well as two other major problems, Panama disease, (fusarium wilt) and nematodes.
Unfortunately, since they do not yet meet the high standards of the export trades, they have only been adopted for local consumption in East Africa, tropical America and the Caribbean.

In the future, products of the breeding programs will play increasingly important roles in subsistence agriculture. Whether new hybrids are used eventually to replace the Cavendish cultivars that are used by the export trades, however, remains to be seen. The very substantial infrastructure that characterizes export production is focussed on producing only these cultivars. Converting these operations to the production and handling of another type of banana would be an expensive proposition. Moreover, the currently available hybrids do not meet the very high standards for fruit quality and post-harvest shelflife that are demanded by the trades. Yet, as fungicides continue to lose their effectiveness against black Sigatoka, and as the practice of fungicidal disease control becomes more expensive and less appealing to consumers in the importing countries, the trades may eventually be forced into making the difficult transition away from the Cavendish clones.

References
Carlier, J., X. Mourichon,  D. Gonzâlez de León, M.F. Zapater, and M.H Lebrun. 1994. DNA restriction fragment length polymorphisms in Mycosphaerella species that cause banana leaf spot diseases. Phytopathology 84:751-756.

Carreel, F., S. Fauré, D. Gonzâlez de León, P.J.L. Lagoda, X. Perrier, F. Bakry, H. Tezenas du Montcel, C. Lanaud,  and J.P. Horry. 1994. Évaluation de la diversité génétique chez les bananiers diploïdes (Musa spp.). Genet. Sel. Evol. 26:125s-136s.

Fullerton, R.A., and  R.H. Stover (eds.). 1990. Sigatoka Leaf Spot Diseases of Banana: Proceedings of an International Workshop held at San José, Costa Rica, 28 March – 1 April, 1989. INIBAP. Montpellier, France. 374 pp.

Gauhl, F. 1994. Epidemiology and Ecology of Black Sigatoka (Mycosphaerella fijiensis Morlet) on Plantain and Banana (Musa spp.) in Costa Rica, Central America. Ph.D. dissertation, Universität Göttingen, 1989. (translated to English from German by INIBAP, Montpellier, France). 120 pp.

International Network for the Improvement of Banana and Plantain. 1994. Annual Report, 1993. Montpellier, France. 73 pp.

Kress, W.J. 1990. The phylogeny and classification of the Zingiberales. Annals of the Missouri Botanical Garden 77:698-721.

Mourichon, X., J. Carlier, and Fouré. 1997. Sigatoka leaf spot diseases. Musa Disease Fact Sheet No. 8. INIBAP, Montpellier, France. 4 pp.

Ortiz, R. 1995. Musa genetics. In: Gowen, S. (ed.) Bananas and Plantains. Chapman & Hall. London. pp. 84-109

Ploetz, R.C., and X. Mourichon. 1999. First report of black Sigatoka in Florida. (Disease Note) Plant Disease 83:300.

Rhodes, P.L. 1964. A new banana disease in Fiji. Commonwealth Phytopathological News 10:38-41.

Simmonds, N.W. and K. Shepherd. 1955. Taxonomy and origins of cultivated bananas. Journal of the Linneaen Society of Botany (London) 55:302-312.

Simmonds, N.W. 1966. Bananas. 2nd edition. Longmans. London. 512 pp.

Stover, R.H. 1980. Sigatoka leaf spot diseases of bananas and plantains. Plant Disease 64:750-756.

Detangling DNA

Saturday, June 7th, 2008
Web edition: www.sciencenews.org
Deep inside our cells, the DNA that encodes the mysteries of our individuality twines into tidy little spiral staircases neatly side by side — or so we might imagine.

Consider, though, that if you scale up the nucleus of a cell to the size of a basketball, each molecule of DNA inside it would resemble fishing line more than four miles long. And now consider what happens to your iPod headphones when you cram them into a pocket: Invariably, it seems, they tangle. And they’re only a foot long!

Now you have a picture of the gargantuan task your cells face in managing the snarls that form in DNA. Storing the DNA isn’t a problem because the cell can pack each strand systematically into a tidy, tight ball. And for some tasks, the cell can just unwind the ball a bit, keeping the unruly strands in check. But when the cell needs to snip the DNA and rearrange its genetic sequence, the strands almost unavoidably kink into a tangled mess.

Researchers have found that DNA can form incredibly complex knots, sometimes with dozens of crossings. But now a pair of mathematicians has shown that DNA can only form certain kinds of knots, not any knot at all. The discovery may help biologists understand site-specific recombination, the way that cells perform surgery on their DNA.

Although we tend to think of our genetic sequence as being fixed at conception, cells occasionally need to shuffle specific bits of their DNA around. Cells might reverse a small stretch of a sequence or move a section from one strand to another. Brewer’s yeast, for example, uses recombination just before cell division to prepare its DNA to divide rapidly. Viruses use recombination to insert their own DNA into the host cell, tricking the cell into producing thousands of copies of the virus. And recombination is our tool when we create genetically engineered cells.

But the process almost always causes some nasty knots. To alter the genetic sequence, specialized enzymes grab two pieces of DNA, snip them apart, bring the ends together, reshuffle the genetic sequence between them and rejoin the ends. Because the DNA is so tightly packed together, this process often ends with strands wound around themselves or one another, forming a knot or link. Another type of enzyme cleans up the mess afterward, snipping strands, passing them through others and reattaching them until the knot is unwound.

Biologists still don’t understand very well how recombination works. “What you really want is to see an enzyme attaching to the DNA and watch it dragging it around,” says Dorothy Buck, a mathematical biologist at Imperial College London. “You want a YouTube video of the whole process, but you can’t get it.” Current technology in microbiology only allows for still images. And even getting still images of knotted DNA is very tricky.

Biologists have managed to learn some things about how recombination works, though. Buck and her collaborator Erica Flapan of Pomona College in Claremont, Calif., found three rules governing the behavior of the enzymes that perform the recombination. The precise path the enzymes take and the way they perform their surgery determines the knot that is formed. Buck and Flapan realized that their rules meant that site-specific recombination could twist the DNA only into particular knots and links, and they applied knot theory to figure out which ones they were. Only a small proportion of the very complicated knots could occur in DNA, they found.

 

Narrowing down the possible knots could in turn shed light back on the activities of the enzymes. Ultimately, this could help researchers use site-specific recombination to repair the faulty DNA that causes genetic diseases.

Microbes Clean Up Mercury: Bacteria could detoxify Native American artifacts

Saturday, June 7th, 2008
Web edition: www.sciencenews.org

 

BOSTON — In a sequel to the smallpox-contaminated blankets hand out, museums inadvertently began another round of toxic giving to Native Americans in the 1990s — returning headdresses and other artifacts that were laced with mercury. Now scientists are looking to a microbe that converts mercury into a form that evaporates, with hopes of cleaning up the artifacts before giving back more of them to their rightful tribes.

“Do we give them something covered in mercury just to have given them their things back? No — it is not OK,” says Munira Albuthi, a microbiologist at the University of Colorado Denver who did the research to see if such a microbial method is possible. “Mercury is a potent neurotoxin.”

The neurotoxic effects of headgear laced with mercury had been recognized anecdotally for years. At Alice’s tea party, the Mad Hatter wasn’t angry — he was crazy from wearing and working with hats, which used to be cured with mercury.

The 1990 Native American Graves Protection and Repatriation Act required federal agencies and institutions to return Native American cultural items and remains to their respective peoples. But when museums began giving back ceremonial head gear and other artifacts, many of the recipients ended up ill. The specimens were laced with mercury, a component of the pesticides that museums had used for years for preservation.

Once the problem of the poisoned artifacts was recognized, scientists had to figure out a culturally sensitive means of getting rid of the toxin.

“A lot of tribes see these artifacts as live spirits — these are relatives to a lot of people,” says Albuthi, who presented the work in Boston at the 108th meeting of the American Society for Microbiology. “So we needed to use something you would be OK with using on yourself.”

Albuthi began working with Cupriavidus metallidurans, a microbe that flourishes on metal and is not dangerous to humans. It has a set of proteins that turns mercury into a form that evaporates into the air. After contaminating paper, a watery broth and auger plates with the neurotoxin, she used a pipette to put the bacterium onto the items. Seven days later, 40 percent of the mercury had been removed from the broth, 50 percent was removed from the auger plates and 60 percent was removed from the paper. Because paper is porous and organic, it is most like the specimens that museums are dealing with, she notes.

Albuthi also investigated whether different temperatures or humidities enhanced the microbes’ mercury-morphing powers. She found that the microbes worked best at room temperature and 60 percent humidity, with about 80 percent of the mercury evaporated from the items.

The experiments used mercury concentrations of 10 parts per million, which are much higher than the quantities on most museum specimens, says Albuthi. “So maybe we’ll be able to get 100 percent, if there isn’t as much to begin with,” she says.

“This is a very interesting and particularly challenging project. They were very constrained in terms of what they could treat things with,” comments Gregory Hecht, a microbiologist at Rowan University in Glassboro, N. J. “And microbes are probably the best way to get around the issue.”