At the beginning, I really did not pay much attention to him. He was very small, almost invisible and harmless-looking. However, he started to reproduce all of a sudden. Now, there were billions of his copies on one of my leaves. Everything was happening so quickly. They were taking me over. Something had to be done urgently.

As plants, we cope with such environmental stresses everyday. If the stress factors affecting us are living organisms, such as bacteria, harmful insects, and weeds, we call those as biotic stresses (1). On the other hand, if we are exposed to drought, salinity, heat, cold, and deficiency or excess of a chemical in soil, those are abiotic stresses for us. Both biotic and abiotic stresses impair our growth and even lead to our death sometimes. Therefore, stress response mechanisms are very important for us. Unfortunately in the United States alone, crop losses due to plant pathogens amount to billions of dollars (2). As we are the main food resource for the humans and assigned for so many other important functions on earth by God, our health and productivity is taken very seriously by scientists. So, it is of great interest to them to find out how our defense responses against microbes work. If scientists learn what is going on when a plant is infected by pathogens thoroughly, they can introduce better resistance mechanisms into economically important crop plants via genetic engineering.

Oh “NO,” I am stressed!

Unlike animals, we are firmly attached to the ground so we can not escape from stress factors. However, thanks to God, we have fascinating defense mechanisms against environmental challenges. First of all, I need to know who this infectious agent (pathogen) is so that I can trigger a stress response mechanism against it. The interactions between me and these microbes are controlled by my receptor proteins and Pathogen-associated molecular patterns, or PAMPs, delivered by the pathogen. PAMPs help pathogen growth by suppressing my defenses and manipulating my metabolism (3).When I recognize a PAMP by my receptors, I activate a set of defense mechanisms known as the hypersensitive response (HR) to arrest and terminate pathogen growth before it terminates me (4). Just before or in conjunction with HR, I increase synthesis of several families of pathogenesis-related (PR) proteins in my infected part (5).

Do you want to know what I do after I identify a pathogen? I bet you do, so I am going to tell you about the other components of my signal transduction cascade that is activated upon brutal attack of microbes (Fig. 1). One of the early steps in this signaling cascade is the elevation of cellular calcium (Ca (2+)) levels mediated by my plasma membrane and channels such as cyclic nucleotide gated channels (CNGCs). After the initial Ca(2+) increase, I activate some of my calcium-binding proteins (calmodulin or CaM) and protein kinases, which modify other proteins by chemically adding phosphate groups to them, and ultimately I generate nitric oxide (NO) and reactive oxygen species (ROS) (6). ROS function as signaling molecules that coordinate a wide range of diverse plant processes, such as growth, development, stress adaptation, and cell self-destruction (programmed cell death) (7). However, the real reason I produce ROS under attack is to use them as local toxins to form unfavorable conditions for pathogen growth and reproduction. NO plays a key role in our immunity in synergy with ROS regulating responses that include defense gene expression and programmed cell death (8). As a result, I utilize both ROS and NO to say “NO” to the pathogens. Other important signaling molecules I utilize are salicylic acid and jasmonic acid. These essential plant hormones are chemical messengers that enable me to respond to my environment. Salicylic acid, SA, which is chemically similar to but not identical to the active component of aspirin (acetylsalicylic acid), is involved in the defense against pathogens that feed and reproduce on live host cells and activates signaling processes providing systemic acquired resistance, protecting the plant from further infection after an initial pathogen attack (9) (Fig. 2). On the other hand, jasmonic acid (JA) induces defense against pathogens that kill host cells for nutrition and reproduction (10). Another hormone in the complex cross talk of signaling pathways regulating my defense responses to microbial attack is ethylene, ET (11).

Although, I have not even told you all the details, I bet you have started to think that all these signaling cascades, regulators, hormones, molecular patterns, and receptors are highly complicated. Do not worry; I am not planning to tell you all the molecular mechanism(s) and relevant pathways I execute during biotic stress responses. If I do, then what will the plant scientists who are interested in plant pathogen interactions do for the rest of their lives? Instead I am going to briefly describe to you what strategies I use to prevent the spread of infection that the small microbe started.

Initially, I build physical barriers around the infection by increasing my cuticle, a protective waxy covering, and cell wall thickness, and then I release antimicrobial compounds, such as phenolics and phytoalexins to the sites of invasion (11). However, this effort is usually not enough to stop the microbes. Therefore, most of the time, the cells in the local region surrounding the infection decide to commit suicide to limit the growth of the pathogen through programmed cell death, which is a highly coordinated and sophisticated phenomenon. This resembles to the firefighters’ strategy to put down a forest fire. Firefighters control flames by cutting down trees, clearing brush away from the existing edge of the fire. This way they can form borders to mitigate the forest fire.

While I am fighting the infection, I also try to confer a long-lasting protection against this pathogen. I send mobile signals like salicylic acid to activate defense responses in distal tissues in case a secondary pathogen attack might occur there (12). Salicylic acid also induces numerous genes that encode PR proteins with antimicrobial properties (13).

I have done all those things I have told you here and a lot more that are still undisclosed to humans in a really short time because it was a matter of “to be, or not to be.” After all that stress, I have won the battle against the microbe at least for now. I have gained a life experience and will defend myself better in the future. I am recovering, but unfortunately my leaf, where all that fighting happened, has a big lesion, an abnormal tissue, which was formed when my poor cells died during the attack (Figure3).

As you can tell from my story, plants get stressed out too. However, we are not stressed due to problems at home, school, or work or spending time stuck in traffic. We deal with salinity, heavy metals, temperature, drought, lack of nutrition, herbivores (insects, mammals, etc.), and pathogens. Thanks to God that He gave us astonishingly complicated response mechanisms to resist all sorts of stresses to some extent, especially biotic stress. Otherwise, we might have become extinct. Can you imagine a world without us? You would have no more oxygen in the air, no more food for animals and humans, no more papers or books, no more clothes, no more furniture, no more blooming beautiful gardens, no more roses for your loved ones, and no more trees, which hold the soil in place so that wind and rain don’t cause severe erosion and destruction of homes for so many species. In addition, there will be fewer resources for drugs and dyes. Oh my God, you are the Most Gracious and the Most Merciful. Thank you that You created us, shaped us and gave us smell, taste, color, and resistance to stresses.

Safiye Arslan is a research fellow in the area of biological chemistry and lives in Nevada.

References

1. Holopainen JK, Gershenzon J. 2010. “Multiple stress factors and the emission of plant VOCs.” Trends Plant Sci. 15,176–184.

2. http://www.apsnet.org/online/feature/biotechnology/

3. Wulff BB, Chakrabarti A, Jones DA. 2009. “Recognitional specificity and evolution in the tomato-Cladosporium fulvum pathosystem.” Mol Plant Microbe Interact. 22, 1191–202.

4. Genger RK, Jurkowski GI, McDowell JM, Lu H, Jung HW, Greenberg JT, Bent AF. 2008. “Signaling pathways that regulate the enhanced disease resistance of Arabidopsis ‘defense, no death’ mutants.” Mol Plant Microbe Interact. 21, 1285–96.

5. Klessig DF, Durner J, Noad R, Navarre DA, Wendehenne D, Kumar D, Zhou JM, Shah J, Zhang S, Kachroo P, Trifa Y, Pontier D, Lam E, Silva H. 2000. “Nitric oxide and salicylic acid signaling in plant defense.” Proc Natl Acad Sci USA. 97, 8849–8855.

6. Ma W, Berkowitz GA. 2007. “The grateful dead: calcium and cell death in plant innate immunity.” Cell Microbiol. 9, 2571–85.

7. Gechev TS, Van Breusegem F, Stone JM, Denev I, Laloi C. 2006. “Reactive oxygen species as signals that modulate plant stress responses and programmed cell death.” Bioessays. 28, 1091–101.

8. Asai S, Yoshioka H. 2009. “Nitric oxide as a partner of reactive oxygen species participates in disease resistance to nectrotophic pathogen Botryis cinerea in Nicotiana benthamiana.” Mol Plant Microbe Interact. 22, 619–29.

9. Beckers GJ, Spoel SH. 2006. “Fine-Tuning Plant Defence Signalling: Salicylate versus Jasmonate.” Plant Biol (Stuttg). 8, 1–10.

10. Spoel SH, Johnson JS, Dong X. 2007. “Regulation of tradeoffs between plant defenses against pathogens with different lifestyles.” Proc Natl Acad Sci USA. 104, 18842–7.

11. Bouchez O, Huard C, Lorrain S, Roby D, Balagué C. 2007. “Ethylene is one of the key elements for cell death and defense response control in the Arabidopsis lesion mimic mutant vad1.” Plant Physiol. 145, 465–77.

12. Ficke A, Gadoury DM, Seem RC, Godfrey D, Dry IB. 2004. “Host Barriers and Responses to Uncinula necator in Developing Grape Berries.” Phytopathology. 94, 438–45.

13. Liu PP, Bhattacharjee S, Klessig DF, Moffett P. 2010. “Systemic acquired resistance is induced by R gene-mediated responses independent of cell death.” Mol Plant Pathol. 11, 155–60.

14. Durrant WE, Dong X. 2004. “Systemic acquired resistance.” Annu Rev Phytopathol. 42, 185–209.

When Alexander Fleming first discovered penicillin in 1929, it was touted as a miracle drug, and at the time it was. After antibiotics became common, once-fatal infections became only minor inconveniences. But now it appears that bacteria, the target of antibiotics, are fighting back by developing resistance to the drugs that once killed them. In order to grasp how this has occurred, we need to understand a little more about both antibiotics and bacteria.

Antibiotics and Bacteria

Antibiotic literally means against life. Antibiotics are natural substances, compounds made by living organisms, which either kill or inhibit the growth or production of bacteria. The antibiotics we take when we are ill are manufactured. They have been altered or synthesized in order to enhance their potency or increase the range of the species they affect. Some antibiotics, such as tetracycline, interfere with the production of new bacteria by binding to ribosomes and thereby preventing them from manufacturing proteins. Others, among them penicillin, obstruct the synthesis of cell walls. Whatever their mode of operation, antibiotics hinder the proliferation of bacteria and allow the human immune system to overcome any remaining organisms.

Bacteria are complex one-celled organisms. Contrary to popular belief, most bacteria are necessary and beneficial. Beneficial bacteria aid digestion, decompose dead organisms, and often protect us from an invasion of harmful bacteria.

Genomic or chromosomal DNA in bacteria is in the form of a continuous strand. This circular DNA is located in a nucleoid.¹ A plasmid, another form of DNA, is an extra-chromosomal self-replicating structure found in bacteria cells. Plasmids, which carry genes for a variety of functions not essential for cell growth and normal survival, can be thought of as mini-chromosomes.

Compared with genomic DNA, which may contain 4 million base pairs, plasmids are small -they contain only 1,000 to 25,000 base pairs. A bacterial cell may contain one plasmid, many copies of the same plasmid, several different kinds of plasmids, or no plasmids. It is generally believed that DNA in plasmids helps bacterial cells to overcome the various stresses in their environment. One such survival mechanism is a gene or several genes for antibiotic resistance. Plasmids also may carry genes for virulence. For example, the severe food-borne disease caused by a strain of E. coli is a plasmid-based illness.

Reproducing and Exchanging Genetic Material

As bacteria usually reproduce through binary fission, or splitting to form two identical daughter cells, there is no recombination of DNA. However, many bacteria do exchange and then recombine genetic information through transformation, transduction, or conjugation. All three techniques have been exploited by specialists involved in the genetic engineering revolution.

When a bacterium (donor) dies, the cell ruptures (lyses) and thereby sets the cellular material free in the environment. Fragments of this naked DNA are then absorbed by recipient (host) bacteria, which incorporate and recombine it with their own. This process, known as transformation, has been exploited to produce such transgenic organisms as cows or plants that contain functional human genes.

The second method of recombination is transduction, or the exchange of genetic material by a viral carrier. Viruses that invade bacteria are called bacteriophages, or just phages by most scientists. When a phage infects a bacterium, it injects its own DNA, which then takes over the host’s metabolism and turns it into a small factory capable of assembling more phages. After it has produced a sufficient number of viruses, the cell lyses and the new phages are released and begin to infect more bacteria. If some of the host DNA is incorporated into a phage during the assembly process, an extremely rare occurrence, the defective phage still can bind to and inject its DNA into a host cell. However, it does not carry the virus’ genetic material and so cannot infect the cell. Thus it is no more than a mode of transport for DNA from one bacterium into another. As in transformation, the new DNA can be recombined with that of the host.

In the 1950s, scientists observed a third form of recombination: conjugation. This form of exchange features bacteria that are connected to each other through a tube or bridge. Donor cells carry fertility (or sex) plasmids, which allow the cell to synthesize long, thin hollow tubes called pili. The “sticky” pili bond to the cell walls of the recipient cell, and the two cells become united. A special enzyme then cuts a strand of the donor DNA, which is then transferred. Sometimes an entire chromosome is transferred and then recombined in the recipient cell. Bacteria also exchange plasmids through the conjugation bridge. This exchange is rapid and efficient. Not only do exchanges take place among bacteria of the same species, but they also cross species lines and even occur between bacteria and eukaryotic (plant and animal) cells.

Resistant Genes and Antibiotic Abuse

Resistant genes work in several ways. Certain genes prevent destruction by producing enzymes that either degrade antibiotics or alter them chemically so that they become ineffective. Another gene helps the bacteria replace the receptor site for the antibiotic, thereby preventing it from binding to the bacteria. And yet a third gene can be used to manufacture a pump that removes the antibiotic from the cell.

When antibiotics are taken, the bacterial cells that are susceptible to the drug die. But some cells may survive. Those cells then reproduce and pass on that resistance to the daughter cells. This often happens when too little of a drug is used or if it is not taken over a long-enough period. If patients do not take enough of their prescribed medication or stop taking it after a few days, they are promoting resistance. Another problem is that non-life-threatening illnesses, such as acne and chronic ear infections, often are treated with low doses of antibiotics over a long period of time. This practice also aids the development of resistant genes.

Many patients view antibiotics as a quick cure, and unfortunately doctors succumb to demands to prescribe them even if they are not necessary. Although antibiotics do not kill viruses, they are prescribed for patients who do not want to be told just to go home, rest, and drink plenty of fluid. Unless a culture is done to identify the infection, a doctor can only guess which anti-biotic to use. Increasingly stronger or broader-spectrum antibiotics are employed in cases involving unidentified infections, which can be analogous to killing a fly with a machine gun. Most minor illnesses will succumb to the body’s immune system. Furthermore, we need to remember that the symptoms being treated are the body’s reaction to invasions by pathogens.

In many developing countries, antibiotics are available without prescription and are taken inappropriately. Some pharmaceutical companies offer doctors bonuses and gifts for every prescription they write, and so antibiotics are overprescribed.

The United States Food and Drug Administration (USFDA) reports that over 40 percent of all antibiotics produced in the U.S. are given to animals. Low doses of antibiotics are routinely fed over the lifetime of meat-producing animals to promote growth and improve feed conversion. This practice creates a perfect environment for the development of resistant genes. One example, which already has produced dire consequences, is the emergence of a strain of salmonella that is resistant to several antibiotics commonly used to treat it.

Antibiotics are routinely sprayed on crops to treat and prevent disease. Although bacteria that invade plants are not harmful to people, many are related to those which cause such food-borne illnesses as E. coli, salmonella, and shigella.² If plant bacteria develop resistance, they could pass it on to bacteria that infect humans. There also appears to be evidence that we acquire resistant bacteria from our food. One researcher, Denis E. Corpet of the National Institute of Agricultural Research, has discovered that the amount of resistant bacteria humans obtain from food is quite significant. When his volunteers went on a diet of bacteria-free food, the quantity of resistant bacteria in their feces diminished by 1,000-fold.

Merri Moken, a student in Morristown, NJ, found that bacteria quickly developed resistance to common household disinfectants. The consequences of the proliferation of new anti-bacterial soaps, steering wheels, sponges, toys, and toothbrushes that we have seen in the past few years could be quite serious if it is causing an increase in resistance.

Solutions and Conclusions

The first step in combating resistance should be to reduce the number of antibiotics used for treating illness. When possible, doctors should identify the pathogen before prescribing antibiotics. Patients should complete the full course of antibiotic treatment by taking all of their medication instead of saving some for later. They also should not demand these drugs for colds or minor infections. Second, developing countries should enact legislation to control sales of antibiotics without prescriptions.

Another important step is a drastic reduction in the use of antibiotics in agriculture. Routine feeding of antibiotics to meat-producing animals needs to be prohibited. Some European countries, Sweden for example, have banned the use of these drugs for growth promotion. Consumers should demand antibiotic-free meat. The practice of spraying fruit and vegetable crops, even though they are not infected, also needs to stop, and consumers should be encouraged to wash all produce thoroughly in order to remove bacteria and antibiotic residues.

Consumers need to consider the consequences of overusing disinfectants and anti-bacterial products. Generally, washing your hands with ordinary soap is all that is necessary if we have been exposed bacteria in public places. Perhaps more education on the necessity of bacteria is another solution.

Finally, new antibiotic drugs need to be developed so that we will continue to have a last line of defense against resistance genes. Other research designed to improve our understanding of all of the mechanisms of resistance could perhaps result in a new family of drugs. In our ever-shrinking world, it has become essential for us to consider the significance of our impact on other organisms, including bacteria. Bacteria were created with a purpose and are indispensable. So let’s stop waging war on all of them. We need the susceptible bacteria as our allies against those which are resistant

Footnotes

1. Plasmoid: The part of a bacterium or virus that contains nucleic acid and is analogous in function to the nucleus of a eukaryotic cell.
2. E. coli: A bacillus (Escherichia coli) normally found in the human gastrointestinal tract and existing as numerous strains, some of which are responsible for diarrheal diseases; Salmonella: Any of various rod-shaped bacteria of the genus salmonella, many of which are pathogenic, causing food poisoning, typhoid, and paratyphoid fever in humans and other infectious diseases in domestic animals; Shigella: Any of various nonmotile, rod-shaped bacteria of the genus shigella, which includes some species that cause dysentery.

References

• Ambile-Cuevas, et.al. “Antibiotic Resistance.” American Scientist 83, no. 4 (Jul.-Aug. 1995).
• “Antimicrobial Resistance: An Ecological Perspective.” American Society for Microbiology. (1999). Online at: www.asmusa.org/acasrc/pdfs/Antimicrobial rpt.pdf.
• Center for Disease Control Antibiotic Resistance Page. Online at: www.cdc.gov/ncidod/dbmd/antibioticresistance/default.htm
• Center for Science in the Public Interest Antibiotic Resistance Project. Online at: www.cspinet.org/ar/index.html
• “Chemotherapy of Bacterial Infections.” Online at: www.life.umd.edu/classroom/bsci424/Chemotherapy/Chemotherapy.htm
• Copet, D. E. “Antibiotic Resistance from Food.” New England Journal of Medicine, 318 (1988): 1206-7.
• Davies, Julian. “Bacteria on the Rampage.” Nature (Sept. 1996): 219-20.
• Levy, Stuart. “The Challenge of Antibiotic Resistance.” Scientific American (Mar. 1998): 46-54.
• “The Microbial World.” Univ. of Edinburgh. Online at: http://helios.bto.ed.ac.uk/bto/microbes/penicill.htm
• European Commission Directorate B-Science and Health Opinions. “Opinion of the Scientific Steering Committee on Antimicrobial Resistance.” (1999). Online at: http://europa.eu.int/comm/food/fs/sc/ssc/out50_en.pdf
• Seachrist, L. “Infections Making a Deadly Comeback.” Science News (20 Jan. 1996): 38. “Types of Antibiotics and Related Resistance Genes.” Online at: http://biosafety.ihe.be/AR/ ARmenu.html
• Washington State University Microbiology. Online at: www.wsu.edu:8080/~hurlbert/pages/Chap9.html

The Process of Discovery

Kamerlingh Omnes, a Dutch physicist dedicated to achieving ultracold refrigeration, opened this field in 1908 by liquefying helium at -452 F (4 K or -269 C).(1) This achievement enabled scientists to cool materials to very low temperatures and study their properties.

Scientists knew that a metal’s resistance fell as the temperature was lowered, but did not know what the limiting value would be when 0 K (the absolute minimum temperature) was approached. In 1911, Omnes began investigating the electrical properties of metals at very low temperatures. Many contemporaries, including Lord Kelvin, believed that resistance eventually would level off to a nonzero value. While passing a current through a very pure mercury wire whose temperature was being steadily lowered, Omnes noticed that its resistance vanished at 4.2K. He remarked: “Mercury passed into a new state, which on account of its extraordinary electrical properties may be called the superconducting state.” This marks the birth of superconductivity.

Scientific and commercial potentials were obvious. A resistance-free metal wire could carry current for a long time without any loss. Omnes tried to determine the amount of such a loss. After letting a superconducting loop run for a year, he determined that there was no significant current loss. He was awarded the Nobel Prize in 1913 for his discovery.

In 1933, Walter Meissner and Robert Ochsenfeld discovered that superconductors are both perfect conductors and perfect diamagnets, for magnetic fields cannot penetrate a superconductor’s interior. When a material is superconducting and a field is applied, the current flowing on the superconductor’s surface generates a magnetic field that cancels the applied field inside the superconductor (the Meissner effect). Since the magnetic field generated inside the superconductor opposes the applied field, superconductors are diamagnetic. This shielding of an applied magnetic field occurs only if the applied field is not very large. Superconductivity is destroyed at a certain point.

Theoretical Progress and Surprises

Theoretical progress was much slower, however, almost as if superconductivity had been discovered too early. The scientific community’s incomplete understanding of quantum mechanics made it impossible to understand the mechanism behind superconductivity. Some phenomenological theories were developed during the 1930s and 1940s, but a clearer picture only began to emerge in 1957.

Three American physicists, John Bardeen, Leon Cooper, and Robert Schriffer, used quantum field theory and many-body physics to develop the BCS theory, which explains superconductivity for elements and some alloys.(2) In essence, the theory states that a superconductor’s electrons condense into a quantum ground state and move together coherently. Pairs of electrons (Cooper pairs)-not single electrons-achieve current transfer. These physicists received the Noble Prize in 1972.

Another milestone came in 1962. Brian Josephson, a Cambridge University graduate student, predicted that an electrical current could flow between two superconductors separated by thin insulating barrier. He made a suitable device (the Josephson Junction) by inserting an insulating material between two superconductors. Sending current through one superconductor, he saw it pass through to the other one. Known as the Josephson effect, it is one of the most important components in superconducting electronics. Josephson was awarded a share of the Nobel Prize in 1973.

In 1986, Alex Miiller and Georg Bednorz of IBM Research Lab (Switzerland) synthesized a ceramic compound that superconducted at 30K (-243C), the highest superconductor temperature ever reached. This compound contained lanthanum, barium, copper, and oxygen. Scientists do not know why it super-conducts, for it insulates at high temperatures and conducts electricity very poorly before it superconducts. Bednorz and Miiller received the Noble Prize in 1987.

This discovery inspired many researchers to combine elements to achieve superconductivity at higher temperatures. In January 1987, researchers at the University of Alabama replaced the lanthanum in the Bednorz-Miiller compound with yttrium and reached a transition temperature (Tc) of 92K. As a result, the much cheaper liquid nitrogen could replace liquid helium as a coolant. By trial-and-error experimentation, a Tc of 138K was reached in a compound consisting of mercury, thallium, barium, calcium, copper, and oxygen.

These new materials all contain layered copper and oxygen planes with other elements in between the crystal structure. Superconductivity occurs on the planes, and the rest of the crystal serves as a charge reservoir. The magnetic field gradually penetrates these new materials (called High Tc superconductors), causing a mixed state between the normal state and the superconducting state.

In 1997, existing theories were shattered when an alloy of gold and indium was used as a superconductor and a magnet. This is expected to have an important effect on magnetic data storage.

The most recent surprise came in November 2000. About 10 years ago, scientists learned that carbon-60 could superconduct at near absolute zero. By expanding the lattice structure, a Tc of 52K was reached. About a month later, the same group reached a Tc of 90K. Many believe that this temperature could reach well over 100K. Carbon-60 is the only material that has reached such high Tcs without having copper and oxygen planes in its structure.

Applications

Superconductors do more than just conduct electricity. Other important functions are as follows:

• The Korean-developed SQUID (Superconducting QUantum Interference Device) can detect magnetic field changes that are 100 billion times smaller than Earth’s minute magnetic field, and uses the most fundamental properties of superconductors and quantum mechanics. Medical researchers use SQUIDs to study the human brain. Systems in which hundreds of SQUIDs are arranged in a helmet-like configuration containing liquid helium are commercially available. These systems detect the magnetic field produced by thousands of neurons. Although neurons produce huge fields when compared to the SQUID’s sensitivity, a magnetically shielded room is required to filter out fields produced by TVs, computers, cars, and so on. In these rooms, external stimulation applied to the patient’s brain enables specialists to locate tumors or other ill-functioning areas by mapping the brain’s functions. The human brain has two types of responses: stimulated and self-generated (spontaneous). By using the SQUID’s fast temporal response, one can locate non-invasively the epileptic loci, which causes some diseases. Alzheimer’s and Parkinson’s research also use SQUIDs at the detection level.

• Magnetic levitation became possible after scientists built superconducting magnets. Since superconductors have no resistance, a small voltage can generate huge currents and, therefore, magnetic fields large enough to float vehicles on these superconducting magnets with almost no friction. In 1999, a train in Japan reached a speed of 343 miles per hour. Japanese researchers are studying the possibility of a mag-lev linear motor car.

• Superconducting magnets have been used extensively in particle accelerators since 1987. Particle physics requires the acceleration of subatomic particles to speeds very close to the speed of light. This necessitates high magnetic fields that, in turn, need high currents-something for which superconductors are ideal. One event that made superconducting better known is probably the American Congress’ cancellation of the multi-billion Superconducting Super Collider (SSC) project in 1993. A European consortium is now pursuing this research field.

•Superconducting wires improve an electric generator’s efficiency by more than 99 percent. In addition, such generators are about half the size of conventional ones. General Electric estimates that there is a potential $20-30 billion global market for superconducting generators. Unfortunately, the high costs of cooling systems rules out using this technology to supply cities with electricity. But the moment sufficiently high Tcs are reached, superconductivity’s impact in this area will be immeasurable.

•Other applications are high-performance and high-capacity electronic filters (currently used in some cellular phone systems); a petaflop-computer (1,000 trillion floating point operations per second-1,000 times faster than today’s computers); mine and submarine detection (the U.S. Navy); and storing energy to enhance power stability (American Superconductor Corp.); satellites; telescopes and other light detection instruments; and Internet routers.

Footnotes

1. F (Fahrenheit): A temperature scale registering water’s freezing point as 32F and boiling point as 212 F at one atmosphere of pressure. K (Kelvin): A unit of absolute temperature equal to 1/273.16 of the absolute temperature of the water’s triple point; equal to one Celsius degree. C (Celsius): A temperature scale registering water’s freezing point as 0 C and boiling point as 100 C under normal atmospheric pressure.
2. Quantum field theory: A body of physical principles that accounts for subatomic phenomena. Quantum many-body physics: The branch of theoretical physics that studies the new collective phenomena or “elementary” constituents of a many-particle system and the underlying quantum mechanics that determines their behavior.

References 

• Clarke, J. “Superconductivity: A Macroscopic Quantum Phenomenon.” Beam Line 30, no. 2 (summer/fall 2000): 41-48.
• Dull, R. W. and H. R. Kerchner. “Applications of Superconductors.” A Teacher’s Guide to Superconductivity for High School Students (1994). Online at:
• www.ornl.gov/reports/m/ornlm3063r1/pt4.html.
• Gunnarsson, O. “C60: The Hole Story.” Nature 1408 (30 Nov. 2000): 528-29.
• http ://superconductors .org
• Tinkham, M. Introduction to Superconductivity. 2d ed. McGraw-Hill Higher Education: 1995.

Plant breeding has several other serious limitations for use as a tool to increase disease resistance. There are only a limited number of plant species which are able to cross-fertilize, thus restricting the transfer of potentially useful traits. Moreover, having found useful traits, it is impossible to prevent the co-transfer of undesirable ones, which can take many years to breed out again by back-crossing.

How can genetic engineering be of use in the quest for new answers to the problems of providing plants with the ability to resist disease? The aim of crop plant genetic engineering is to insert a gene (or genes) which improve an existing plant variety whilst retaining the desirable genetic make up of the original plant.

The main tool at the disposal of the scientist is the use of nature’s own genetic engineer, Agro-bacterium tumefaciens. The manipulation of this bacterium’s natural functions has allowed the biologist to transfer many foreign genes into plants. The bacterium is soil-borne and infects plants at the crown, usually through a wound site, causing cancerous growths of proliferating plant cells known as crown gall tumors. This disease in itself is ergonomically important and effects most dicotyledonous plants causing millions of dollars’ worth of damage to plants. In the 1940s, from experimental observations, it was concluded that a factor is transmitted from the invading bacteria to the host plant cell. Further studies demonstrated that the disease is actually the direct result of the transfer of a particular DNA fragment (genes) from the bacterium to the plant cell. In addition to its chromosomal DNA, Agro-bacterium contains a much smaller circular DNA molecule called a Ti (tumor-inducing) plasmodia, of which a small piece, called the T-DNA (Transferred-DNA), is the factor transferred into plant cells (see Figure 1). The T-DNA becomes stably integrated into the plant’s chromosomes, from where it is able to perturb the natural functions of the plant. The T-DNA encodes genes, which, when expressed, bring about the production of new enzymes that are able to alter the hormone balance within the infected cell. This brings about de-differentiation and cell division, leading to proliferation of cells and the formation of tumors. This appears to be of little benefit to the bacterium. However, other genes are also present in the T-DNA which, when expressed, are able to synthesize novel compounds from naturally occurring plant precursors. These novel compounds cannot be metabolized by the plant but are a good source of nutrients for the bacterium.

Mutation analysis of the T-DNA revealed two regions, the left and right borders, which were essential for integration into the chromosome. It was also found that any piece of DNA inserted between these borders was stably inserted into the host chromosome on transformation. Deletion of the genes for tumor formation (Disarmed Ti-Plasmid) were found to have no effect on the transfer efficiency from bacterium to plants. Availability of disarmed Ti-plasmids, tissue culture methods for the regeneration of whole fertile plants from single cells, and marker genes (such as antibiotic resistance) for the selection of transformed cells, have allowed for the production of a whole new range of plants containing foreign genes. Several genes responsible for pathogen and herbicide resistance proteins have been isolated from the bacteria and viruses. These genes have then been inserted into the T-DNA region of Agro-bacterium and introduced into plants, giving rise to insect, virus or herbicide resistant plants.

By using Agro-bacterium as a plant genetic engineer, many crop plants such as the tomato, potato and cucumber have now been engineered for virus resistance. Field tests showed that these genetically modified plants appeared to be highly resistant to viral infections. Similarly genetically-engineered cotton plants have proved to be resistant to insect attack and many herbicides (weed killers).

Another powerful new genetic engineering technique is ‘antigens’ technology, whereby specific gene transcripts are prevented from being translated into proteins. By using antigens technology, it has been possible to produce genetically engineered tomato plants that have a much increased shelf-life. Although many aspects of gene transfer from Agro-bacterium to plants are not fully understood, the use of Agro-bacterium for gene transfer will continue to increase; and it is likely that genetically engineered crops carrying traits for resistance to herbicides, insects and viral diseases will soon reach the market-place.