Friday, December 24, 2010

CHAMPION HYDROGEN-PRODUCING MICROBE

0 comentarios
Inside a small cabinet the size of a dorm refrigerator in one of Himadri B. Pakrasi's labs, a blue-green soup percolates in thick glass bottles under the cool light of red, blue and green LEDS.

This isn't just any soup, however. It is a soup of champions.


The soup is colored by a strain of blue-green bacteria that bubble off roughly 10 times the hydrogen gas produced by their nearest competitors—in part because of their unique genetic endowment but also in part because of tricks the scientists have played on their metabolism.


Hydrogen gas can be produced by microbes that have enzymes called hydrogenases that take two hydrogen ions and bind them together. Although the soup microbes have hydrogenases, most of the hydrogen they evolve is a byproduct instead of an exceptionally efficient nitrogenase, an enzyme that converts the nitrogen in air to a nitrogen-containing molecule the microbes can use.


The microbe's gas-producing feat is described in December 14,2010 issue of the online journal Nature Communications.


Biohydrogen, like that bubbling up from the microbial soup, is one of the most appealing renewable energy fuels. Produced by splitting water with energy from the sun, it releases mostly water when it burns. It's hard to get any cleaner than that.


The strain growing in the Roux bottles in the cabinet, called Cyanothece 51142 was originally found in the Gulf of Mexico by Louis A. Sherman of Purdue University, one of the article's authors. Its genes were sequenced in 2008 at the Genome Sequencing Center at the School of Medicine.


Cyanothece 51142 may be new to science, but cyanobacteria, the group of organisms to which it belongs, have existed for at least 2.5 billion years, says Pakrasi, PhD, the George William and Irene Koechig Freiberg professor of biology in Arts & Sciences, and professor of energy in the School of Engineering. These ancient organisms have had to survive a wide variety of chemical environments and have the metabolic tricks to show for it.


All cyanobacteria have the ability to fix carbon from the atmosphere, stuffing it away in starch or glycogen, but Cyanothece is among the rarer strains that can also fix nitrogen, converting atmospheric nitrogen to ammonia and eventually to larger nitrogen-rich molecules.


Because it can fix both carbon and nitrogen, when conditions warrant Cyanothece can survive on air, water and sunlight alone. It is about as self-reliant an organism as it is possible to be.


There is one catch. Nitrogenase is very sensitive to oxygen and so carbon fixing (photosynthesis), which produces oxygen as a byproduct, has to separated from nitrogen-fixing in some way.


Cyanothece accomplishes this by time division; it has an internal biological clock that establishes a circadian rhythm. (Cyanobacteria are the only prokaryotes (organisms without nuclei) that have a clock.)


So Cyanothece fixes carbon glycogen molecules during the day, producing oxygen as a byproduct, and it fixes nitrogen in ammonia during the night, producing hydrogen as a byproduct. For every nitrogen molecule that's fixed, says Pakrasi, one hydrogen molecule is produced.


Each half of the cycle powers the other. The glycogen produced in the day is consumed in the energy intensive process of fixing nitrogen at night. The fixed nitrogen produced at night is used to make nitrogen-containing proteins during the day.


Pakrasi, who is also the director of I-CARES, the International Center for Advanced Renewable Energy and Sustainability, calls the microbes biobatteries because they store daytime energy for use at night and nighttime energy for use in the day.


The separation in time prevents the two metabolic processes from competing with one another. At night the bacteria begin to metabolize the glycogen (or respire). Quickly consuming intracellular oxygen, respiration creates the oxygen-free or anoxic conditions inside the bacteria the nitrogenase needs to do its work.


Cyanothece's clock is set by the environmental cue of changing light levels. But once entrained by the day/night cycle, the clock continues to run even in the absence of the cues. Just as a prisoner kept in solitary confinement will maintain a roughly 24-hour sleep/wake cycle, Cyanothece will continue to fix nitrogen even if it is incubated under continuous light.


As Pakrasi puts it, the entrained microbes are still experiencing "subjective dark" for 12 hours of the day.


More strangely, entrained Cyanothece incubated under continuous light evolve more hydrogen than those cycling between light and dark. This is probably because the energy in light somehow fuels the energy-intensive nitrogenase reaction, says Anindita Bandyopadhyay, PhD, a postdoctoral fellow in Pakrasi's lab. The scientists are still trying to understand exactly why this happens.


In addition to keeping the microbes awake all night, the scientists have another trick up their lab coat sleeves. Cyanothece can survive on the starvation diet of sunlight and air but adaptable microbe that it is, it can also live on carbon-containing molecules or on a mix of sunlight and carbon-containing molecules.


The scientists found that the microbes produced more hydrogen if they were grown in cultures that contained glycerol, a colorless, sweet-tasting molecule that is frequently used as a food additive.


The additional carbon in the glycerol revs up the nitrogenase to meet the increased demand for nitrogen in the cells, Pakrasi says. And the more active the nitrogenase, the more hydrogen is produced.


Despite journalistic hype, Pakrasi warns, hydrogen is not the fuel of tomorrow. It's hard to transport and its energy density is too low. The fuel tank for a semi-trailer powered by hydrogen would take up half the trailer, he says.


What intrigues him about the microbes is not their utility but rather their ingenuity. Their unique metabolism gives them the ability to produce hydrogen, a clean fuel, while disposing of two wasteproducts: glycerol, a copious byproduct of biodiesel production, and carbon dioxide, a waste product from coal-fired power plants. "They give you a lot of bang for your buck," he says.


Cyanothece may soon be moving house—from cramped flasks in Pakrasi's lab to the giant bioreactors in Washington University's Advanced Coal and Energy Facility. There scientists will be able to monitor their every metabolic move as they feast on carbon-dioxide-rich flue gas from the site's combuster and bubble up hydrogen.


(Photo: Whitney Curtis)


Washington University in St. Louis

WE SPEND MORE TIME SICK NOW THAN A DECADE AGO

0 comentarios
Increased life expectancy in the United States has not been accompanied by more years of perfect health, reveals new research published in the December issue of the Journal of Gerontology.

Indeed, a 20-year-old today can expect to live one less healthy year over his or her lifespan than a 20-year-old a decade ago, even though life expectancy has grown.

From 1970 to 2005, the probability of a 65-year-old surviving to age 85 doubled, from about a 20 percent chance to a 40 percent chance. Many researchers presumed that the same forces allowing people to live longer, including better health behaviors and medical advances, would also delay the onset of disease and allow people to spend fewer years of their lives with debilitating illness.

But new research from Eileen Crimmins, AARP Chair in Gerontology at the University of Southern California, and Hiram Beltrán-Sánchez, a postdoctoral fellow at the Andrus Gerontology Center at USC, shows that average "morbidity," or, the period of life spend with serious disease or loss of functional mobility, has actually increased in the last few decades.

"We have always assumed that each generation will be healthier and longer lived than the prior one," Crimmins explained. "However, the compression of morbidity may be as illusory as immortality."

While people might be expected to live more years with disease simply as a function of living longer in general, the researchers show that the average number of healthy years has decreased since 1998. We spend fewer years of our lives without disease, even though we live longer.

A male 20-year-old in 1998 could expect to live another 45 years without at least one of the leading causes of death: cardiovascular disease, cancer or diabetes. That number fell to 43.8 years in 2006, the loss of more than a year. For young women, expected years of life without serious disease fell from 49.2 years to 48 years over the last decade.

At the same time, the number of people who report lack of mobility has grown, starting with young adults. Functional mobility was defined as the ability to walk up ten steps, walk a quarter mile, stand or sit for 2 hours, and stand, bend or kneel without using special equipment.

A male 20-year-old today can expect to spend 5.8 years over the rest of his life without basic mobility, compared to 3.8 years a decade ago — an additional two years unable to walk up ten steps or sit for two hours. A female 20-year-old can expect 9.8 years without mobility, compared to 7.3 years a decade ago.

"There is substantial evidence that we have done little to date to eliminate or delay disease while we have prevented death from diseases," Crimmins explained. "At the same time, there have been substantial increases in the incidences of certain chronic diseases, specifically, diabetes."

From 1998 to 2006, the prevalence of cardiovascular disease increased among older men, the researchers found. Both older men and women showed an increased prevalence of cancer. Diabetes increased significantly among all adult age groups over age 30.

The proportion of the population with multiple diseases also increased.

"The increasing prevalence of disease may to some extent reflect better diagnostics, but what it most clearly reflects is increasing survival of people with disease," Crimmins said. "The cost of maintaining and providing care for people with chronic conditions is an important part of determining the economic well-being of countries with established social security and government-provided health services."

Crimmins and Beltrán-Sánchez note that only delaying the onset of disease through preventive care will clearly lead to longer disease-free lives.

"The growing problem of lifelong obesity and increases in hypertension and high cholesterol are a sign that health may not be improving with each generation," Crimmins said. "We do not appear to be moving to a world where we die without experiencing significant periods of disease, functioning loss, and disability."

University of Southern California

UNLOCKING THE SECRETS OF A PLANT’S LIGHT SENSITIVITY

0 comentarios
Plants are very sensitive to light conditions because light is their source of energy and also a signal that activates the special photoreceptors that regulate growth, metabolism, and physiological development. Scientists believe that these light signals control plant growth and development by activating or inhibiting plant hormones. New research from Carnegie plant biologists has altered the prevailing theory on how light signals and hormones interact. Their findings could have implications for food crop production.

It was previously known that a plant hormone called brassinosteroid is essential for plant's responses to light signals. This crucial steroid-type hormone is found throughout the plant kingdom and regulates many aspects of growth and development. Surprising new research from a team led by Carnegie plant biologist Zhi-Yong Wang shows that light does not control the level of brassinosteroid found in plants as was expected. Instead brassinosteroid dictates the light-sensitivity of the plant. It does this by controlling the production of a key light-responsive protein.

The team's findings on interactions between brassinosteroid and light in sprouting seedlings have changed the prevailing model for understanding the relationship between light conditions and hormone signals in regulating photosynthesis and growth. Their results are published in Developmental Cell on December 14.

While under the soil's surface, in the dark, plant seedlings grow in a special way that speeds the process of pushing the budding stem out into the air, while simultaneously protecting it from damage. This type of growth is called skotomorphogenesis. Once exposed to light, seedlings switch to a different, more regular, type of growth, called photomorphogenesis, during which the lengthening of the stem is inhibited and the leaves expand and turn green.

Many components are involved in this developmental switch, including brassinosteroid. Previous studies showed that mutant plants created to be deficient in brassinosteroid grew as if they were in the light, even when in the dark. Research also showed that many genes responded to stimulation from light and brassinosteroid in opposite ways. But scientists were unsure how this antagonistic process worked, especially after they found the levels of brassinosteroid in plant cells were not significantly different between plants grown in the dark or in the light.

The Carnegie team's new research identifies a protein called GATA2 as a missing link in this communications system. This protein tells developing seedlings which type of growth to pursue.

GATA2 is part of the GATA factor class of proteins, which are found in plants, fungi and many animals. GATA factors promote the construction of a variety of new proteins, the recipes for which are encoded in DNA. It does this by switching on and off different genes. In Arabidopsis, the experimental mustard plant used in this study, there are 29 genes for different members of the GATA factor family. Some of these have been demonstrated to play a role in flower development, the metabolism of carbon and nitrogen, and the production of the green pigment chlorophyll.

Wang's team found that GATA2 switches on many genes that are turned on by light but turned off by brassinosteroid. It then showed that brassinosteroid inhibits the production of GATA2 and light stabilizes the presence of GATA2 protein in plant cells.

First, the team showed that GATA2 functions to turn on select plant growth genes in the presence of light. The scientists genetically manipulated Arabidopsis plants to cause the GATA2 protein to be overproduced. As a result, the plants started to show patterns of growing in light, even when they were in the dark. This manipulation demonstrates that GATA2 is a major promoter of light-type growth.

What's more, this is the same reaction that was produced when plants were genetically manipulated to be brassinosteroid-deficient. This means that the over abundance of GATA2 had the same result as the scarcity of brassinosteroids. These results show that GATA2 proteins and brassinosteroid hormones have antagonistic effects on developing plants.

Next, the Carnegie team showed that brassinosteroid is actually involved in inhibiting the actions of GATA2. Brassinosteroids turn on a protein that prevents GATA2 from working when the seedling is in the dark. This inhibition of GATA2 is stopped by exposure to light. This likely happens due to the involvement of yet another protein—one that is widely involved in light-signaling— although further study is needed to be sure.

Together all these results show that GATA2 is an important factor in signaling light-type growth. It also serves as a communications junction between internal plant systems that are turned on by light and those that are turned on by brassinosteroids.

"Brassinosteroids and light antagonistically regulate the level of GATA2 activity, and thus the creation of proteins stimulated by GATA2," says Wang. "As a result, GATA2 represents a key junction of crosstalk between brassinosteroid and light signaling pathways."

The framework created by this research leaves plenty of avenues for further study of the various components of light signaling in plants. Some other members of the GATA class of proteins may be involved, as well as other light-responsive compounds.

Carnegie Institution of Washington

Followers

Archive

 

Selected Science News. Copyright 2008 All Rights Reserved Revolution Two Church theme by Brian Gardner Converted into Blogger Template by Bloganol dot com