Global Climate Report. NOAA National Centers for Environmental Information (http://www.ncdc.noaa.gov). July 2019.

It’s summer, and it is hot out there; but if it feels like record-breaking temperatures are becoming more common globally, they are. The National Oceanic and Atmospheric Administration and European Copernicus Climate Change Service announced that July 2019 was the hottest month across the globe ever measured since measurements began, in 1880. Global temperatures averaged 16.73°C in July, which is 0.95 °C higher than the 20th-century average of 15.78°C . Average Antarctic sea-ice coverage was 8.5% below the 1981-2010 average. And sea ice coverage was 10.5% below the overall average, which is based on records beginning in 1979. The scientists also released geographical data, showing that the regions where temperatures varied furthest from averages, were Alaska, Central Europe, Northern and Southwestern parts of Asia, and certain regions in Africa and Australia. These findings corroborate scientific predictions regarding the effects of man-made climate change. Human activities, primarily from burning fossil fuels, emit carbon dioxide and other greenhouse gases that trap heat in the atmosphere. Increasing greenhouse gas emissions are associated with warmer global surface temperatures. The planet’s 10 hottest years on record have all fallen in the past two decades. Scientists and policymakers around the globe are also feeling this heat.

Unless significant measures to curb greenhouse gas emissions are adopted, scientists expect temperature records to keep falling. Scientists say global temperatures could increase by at least 3°C this century, which will create conditions on Earth that have not been seen in more than 2 million years. Given the notable trends in higher temperatures and natural disasters, we might be pushing the climate system toward states that we haven’t seen in our societal experience – and even in our species’ experience.

Manipulation of brain circuits using smartphone-controlled device

Qazi R et al. Wireless optofluidic brain probes for chronic neuropharmacology and photostimulation. Nature Biomedical Engineering, August 2019.

Scientists recently designed a device that can regulate brain circuits using a tiny brain implant controlled by a smartphone. This bluetooth-enabled device utilizes replaceable lego-like drug cartridges to target neurons with drugs and light. Existing methods to deliver drugs and light to the brain typically involve metal tubes and optical fibers. These tools are rigid and can substantially damage the brain’s soft tissue over time. Moreover, this bulky equipment often limits the patient’s movement because of the wired connections, making them unfit for long-term use. To achieve chronic remote-controlled drug delivery without exhaustion and evaporation of drugs, scientists invented a neural device with a replaceable drug cartridge, which could allow neuroscientists to study the same brain networks for several months without depleting the drug supply. These “plug-n-play” drug cartridges were integrated into a brain implant for mice with a soft and ultrathin probe (about the thickness of a human hair), which consisted of microfluidic channels and tiny LEDs (smaller than a grain of salt), for unlimited drug doses and light delivery. The implant is regulated via a smartphone, allowing researchers to trigger precise combinations and sequences of drug and light delivery. In animal models, these stimuli can be triggered with the target outside of the laboratory, allowing researchers to wirelessly instill changes in the animal’s brain while in its natural habitat. Using these neural devices, researchers are now able to perform fully automated animal studies where the behavior of one animal could positively or negatively affect behavior in other animals by conditional triggering of light and/or drug delivery. This device will allow researchers to better dissect the neural circuit basis of behavior and how specific neuromodulators in the brain tune behavior in various ways. In addition, the device can be utilized in complex pharmacological studies to develop potentially new therapeutics for pain, addiction, and emotional disorders.

The secret weapon of E.Coli 

Melson E. at al. The sRNA DicF integrates oxygen sensing to enhance enterohemorrhagic Escherichia colivirulence via distinctive RNA control mechanisms. Proceedings of the National Academy of Sciences, June 2019.

Scientists have revealed how E. coli (Escherichia coli) bacteria seeks out the most oxygen-free parts of your colon to cause the worst infection possible. E. coli normally live in the intestines of healthy people and animals. Most varieties of E. coli are harmless or cause relatively brief diarrhea. But a few particularly nasty strains can cause cramps, diarrhea, vomiting – even kidney failure and death. Children are particularly at risk. A new study uncovers how this foodborne pathogen knows where and when to begin colonizing the colon on its way to making you sick. Bacterial pathogens typically colonize a specific tissue or organ in the host. Therefore, as part of their infection strategies, bacterial pathogens precisely time deployment of proteins and toxins to these specific colonization niches in the human host. This allows the pathogens to save energy and avoid detection by our immune systems and ultimately cause disease. The researchers in this study identified how E.Coli detects low oxygen levels in the large intestine and then produces proteins that allow it to attach to host cells and establish infection. Oxygen actually diffuses from the intestinal tissue into the gut, and there are comparably higher levels in the small intestine than the large. Remarkably, E. coli specifically waits until it has reached the-low oxygen large intestine before striking. E. coli controls this process via a small form of RNA that activates particular genes when oxygen levels are low. This is the point when the infection really gets established and the bacteria are able to begin to manufacture harmful Shiga toxins. The researchers predict that other bacterial pathogens, such as Shigella and Salmonella, likely utilize a similar control mechanism. Researchers suggest that if we can find a way to block oxygen sensing, we may be able to prevent the infection by allowing E. coli to pass harmlessly through the body.

Our immune system handles our body’s security. It’s equipped with the resources necessary to deal with different levels of security threats. This system walls off the body, but also has the equipment to hunt down any intruders. We can think of our immune system as a game of strategy, where defensive and offensive maneuvers are equally important. This game is not a simple, single-session one. It involves constant information gathering, weapon developing, and soldier training. In short, it involves constant change.

The body’s general defense mechanisms, called the innate immune system, can be considered the first line of defense, aimed at preventing bacteria or other pathogens (sickness-inducing factors) from entering the body in the first place. These include the skin (the walls of the castle), as well as mucus, tears, saliva, and acids (the boiling oils of the castle). Vulnerable entry points such as the respiratory system are covered with thick, sticky mucus, which traps pathogens and then disposes of them by way of sneezing or coughing. Other sensitive spots such as the eyes are constantly washed with tears. Tears are produced on top of the eye and drain into the bottom, near the nose, ensuring sterility.

The innate system also uses a mechanism called inflammation to handle pathogens that manage to breach the outer defenses. The main goal of inflammation is to prevent the pathogens that enter through the skin from reaching the blood. Inflammation is initiated by immune cells that are found within the injured tissue. These immune cells can be considered “patrol cells” and are found everywhere in the body, not just the blood. The moment these cells come across a foreign antigen (the molecular fingerprint of a cell or virus), they sound the alarm, triggering inflammation. Inflammatory precautions include blood clotting, macrophage migration, and increased blood flow to the area. Blood clotting occurs relatively quickly, since inactive clotting factors are already present and only need to be activated. This seals off the security breach, preventing more pathogens from entering. Macrophages are very large immune cells that migrate to the scene and capture any bacteria they encounter. Increased blood flow to the area both eases and accelerates the entrance of reinforcements, such as antibacterial proteins and other white blood cells. This is the reason for the swelling we see.

If all fails and the pathogens manage to enter the bloodstream, the body has no choice but to pull out the big guns: the adaptive immune system. The adaptive immune system is unique in that it knows its enemy and adapts accordingly, hence the name. Each type of pathogen has strong and weak spots. Some are resistant to antibacterial proteins, while others are resistant to being phagocytosed (being eaten alive!) by macrophages. During the first encounter, the adaptive immune system tries different methods of destroying the pathogen, and “records” the most effective method. It then stores the antigen of that specific pathogen. So, during the second encounter, the adaptive immune system already “knows” what to do and eliminates the pathogen almost immediately.

Now, let’s get into some detail.

There are many types of cells in the adaptive immune system. Each has a very specific role to play. Cytotoxic T cells are the ones responsible for destroying bacteria. One feature that distinguishes these cells from macrophages is the method of activation. Unlike macrophages, cytotoxic T cells only kill after being activated by another type of cell, the helper T cell. The helper T cells’ main purpose is to activate or suppress the immune response, like an on-off switch. They are so effective that without the secretions of these helper T cells, the adaptive immune system literally shuts down. The cytotoxic T cells also need a means of recognition. This role is fulfilled by antigen-presenting cells (APCs). When APCs find foreign antigens left behind in the blood by bacteria, they stick them on their own membranes. Then, they start handing them around to cytotoxic T cells, like police identifying bandits from WANTED posters. After obtaining these outlaws, cytotoxic T cells kill any of those bacteria they encounter.

A second difference between cytotoxic T cells and macrophages is how they kill. Rather than phagocytosing (eating alive) bacteria, they shove a tube-like protein into their membrane, allowing its insides to flow out and ultimately deflating and killing it.

After the body recovers from the sickness, most of the outlaws are destroyed. But a few are kept and stored in memory B cells. Memory B cells are like the immune system’s archives, in that they have long lifespans and are kept safe deep in the bone marrow. The file of each bacterium is kept in these cells, with its poster on the front for quick identification. Therefore, if the body encounters the bacteria again in the future, the immune system loses no time trying to identify them. The elimination process starts promptly, even before any signs of illness. This mechanism is, in fact, what makes vaccination possible. Dead or harmless pathogens are injected into the body so that their files can be created in our archives without the hassle of illness.

Unfortunately, bacteria also have a few tricks up their sleeves. Bacteria are single cells, and this enables them to change their genetic material without major consequences. These genetic changes also cause structural changes. Even though each bacterium is individual and independent, they get their strength from their large numbers. For example, imagine a population of 100 bacteria, all with different genetics. During an infection, our immune system uses a special tactic – for example, phagocytosis – to get rid of the bacteria. But one of these bacteria has a genetic feature – say, a strong cell wall – that gives it immunity from this tactic. So, while the other 99 bacteria get eradicated, this one bacterium survives. This bacterium then multiplies into 100 new bacteria with strong, phagocytosis-resistant cell walls. This forces our immune system to find new strategies to overcome the bacteria’s new defenses. Resistance in bacteria only gets stronger if provoked. This is the reason why excessive use of antibacterials is not recommended. While they may give temporary relief, they cause the bacterial population to grow more resistant.

Even though bacteria are skilled in the art of genetic mutation, there is another pathogen that is undoubtedly the master: The Virus.

Viruses are so tiny that it has been debated whether they should be considered living creatures or just molecular structures. They contain very little genetic material, which makes them extremely prone to mutation. They mutate so rapidly that it is impossible for our body to create files for them. Moreover, they do not need provocation to mutate, since mutation is a part of their life cycle. This is the reason why immunodeficiencies (weaknesses of the immune system) are one of the most notorious disease types. Most immunodeficiencies are genetic and/or viral. The immunodeficiency with probably the worst reputation is AIDS. AIDS stands for “acquired immune deficiency syndrome,” and is caused by the human immunodeficiency virus (HIV). The thing that makes this particular virus so notorious is the fact that it targets the very cells that allow the immune system to operate, the helper T cells. Without the secretions of the helper T cells, the entire adaptive immune system virtually shuts down. After that, even the simplest illness can lead to serious consequences.

The HIV virus is an external threat, whereas another immunodeficiency, multiple sclerosis (MS), is an internal one. MS is a disease where our immune system sees our own cells (especially nerve cells) as enemies. This results in the destruction of cells by none other than our very own immune system. Destruction of the nerve cells may cause various neurological symptoms such as weakness, visual problems, or even psychiatric issues. Although the exact mechanism causing this deficiency is unknown, genetics is thought to play a big role. As a result, there is currently no known cure for MS.

In sum, our immune system continuously plays an extremely sophisticated, microscopic strategy game, of which we are observers more than we are players. Even as observers, we cannot entirely understand the battle at center stage, let alone the struggle going on in the game’s dark corners. Our immune system develops new strategies to keep us safe from thousands of daily attacks on the body. We are not even aware of all these strategies and defenses, unless they fail and we fall sick. There is no apparent winner or loser of this ongoing game, which requires extensive knowledge, intelligence, and uninterrupted adaptability, alertness, and creativity. As fantastic as observing this collective performance is, one cannot also help but ask whether each and every one of these players (our immune system, bacteria, viruses, etc.) a master strategist, owning all of these wondrous attributes, or are they directed to make their moves by the same One Master Strategist, for us to watch in awe and reflect upon?

There are lots of interesting examples of how plants communicate with insects. For instance, in self-defense against insects eating its leaves, a plant emits a volatile chemical that signals other insects, who are predators of those insects eating the plant. A byproduct of such insect communication may allow plants to signal danger to other extremely close, downwind plants. Professor of Entomology, Richard Karban and other researchers from the University of California showed that a cut sagebrush “told” nearby, downwind wild tobacco plants about its injury, and the tobacco plants apparently responded to protect themselves from damage. Over three seasons, researchers clipped leaves of sagebrush plants to mimic insects eating their leaves. The cut sagebrush released volatile chemicals (methyl jasmonate), which the wind carried to nearby downwind plants. The tobacco plants apparently sensed the chemicals-at least the tobacco plants increased production of a defensive agent-that caused their leaves to taste bad to insects. These downwind tobacco plants experienced less than half the leaf damage from grasshoppers and cutworms than control plants (Anon.). In one case study an acacia tree responded to browsing, or being beaten with a stick, by increasing the levels of tannin in its leaves within minutes. Amazingly, the tannin levels then rise in neighboring trees, and, due to its bitter taste, repel the browsers before they can do any further damage (Jacob 2001; Anon.).

What’s more is that plants can also talk to mammals. A study done by Professor Steven Johnson and his research team from the University of KwaZulu-Natal, South Africa, demonstrated how ground-dwelling mammal pollinators are attracted by a rare parasitic plant’s unique “perfume.” This specific floral aroma is comprised of over 30 compounds, especially ketones, fatty-acid derivatives, mono- and sesquiterpenoids. The three most abundant scent chemicals were 1-hexen-3-one, 3-hexanone, and ethyl butyrate. When the impact of these chemicals was tested on mice, it turned out that mice, like humans, find 3-hexanone to have a pleasant smell. The molecule is routinely used in artificial flavoring to produce a sweet fruity grape-like flavor. In addition, 3-hexanone has also been found in some bat-pollinated flowers, so it may be a general mammal attractant. Remarkably, scent cues are particularly important to plants pollinated by small ground-dwelling mammals because these animals are usually around at night when visual cues are less effective (Johnson et al. 2011; Anon.).

In addition to pests, plants have to deal with numerous microbial pathogens such as bacteria, fungi and oomycetes, and viruses in the natural environment. A proper response to pathogens can lead to resistance mechanisms that enable plants to survive. Plants can recognize potential pathogens by detecting pathogen-associated molecular patterns (PAMPs). This recognition activates a defense mechanism. A well-organized communication between the pathogen-invaded plant tissues and non-invaded ones is essential for the timely manifestation of defense mechanisms that limit the systemic spread of pathogens (Shah 2009). Salicylic acid, an important mobile signal, is transported from infected tissue to the rest of the plant body. It activates the systemic acquired resistance, which is a “whole-plant” resistance response that occurs following an earlier localized exposure to a pathogen. Plants not only communicate within themselves about a microbial invasion, they also talk to one another. For example, Tobacco plants warn each other against tobacco mosaic virus attack by releasing methyl salicylate, which is then converted to the protective salicylic acid in uninfected plants (Jacob 2001).

In contrast to harmful pathogenic interactions, there are also symbiotic, advantageous interactions between some microorganisms and plants. Establishment of such a beneficial symbiosis (which literally means “living together” in Greek) is complex. For successful infections, a molecular dialogue between partners is essential (Vadassery and Oelmüller 2009). Among these kinds of interactions, legume-Rhizobium symbiosis is of particular importance in agriculture, because by forming the symbiosis, atmospheric nitrogen can be used to sustain the growth of legume crops, such as soybean, pea, and bean, which occupy 12% to 15% of the land that can be used for growing crops throughout the world (Sugiyama, Shitan, and Yazaki 2007). Rhizobia are soil bacteria that fix nitrogen (diazotrophs) after becoming established inside root nodules of legumes such as alfalfa, clover, peas, beans, lentils, lupins, mesquite, carob, soy, and peanut.

Rhizobia require a plant host, since they cannot independently fix nitrogen (Anon.). Plant roots secrete signaling molecules (e.g. flavonoids) to attract Rhizobia. When Rhizobia sense these chemicals, they colonize around root tissues of the host legume plant. So, the rhizobial infection in legumes is an invasion by invitation (Murray 2011). The attached rhizobia secrete Nod factors, which are perceived by the plant. This initiates a series of events that leads to the formation of nodule, where Rhizobia fix nitrogen. Thus, Rhizobia make legume independent of soil nitrogen and the legume supplies nutrients to the bacteria. In addition, the legume plant supplies one critical component of nitrogenase, which is the key enzyme for fixing nitrogen. It all happens because the plant can talk to the bacteria.

The plant has many interests in being colonized by mycorrhizal fungi. Apart from providing nutrients such as phosphorus and nitrogen, the fungi protect plants from diseases, parasites, and other stresses. Plants even grow as much as 40% more when colonized. In laboratory experiments, carrots that were colonized grew 20 times more than the carrots that were not! In fact, they are such close “friends” that the fungus cannot live without a plant, and between 80-90% of all plants on earth are somehow associated with mycorrhizal fungi. The origin of this incredible friendship is communication (Montréal 2012).

As a result, plants can talk to microorganisms, pests, and mammals, but do they communicate with people? Are they intelligent creatures who can communicate with us? In 1848, Dr. Gustav Theodor Fechner, a German professor, suggested that plants are capable of emotions and that one could promote healthy growth with talk, attention, and affection. An Indian scientist, Sir Jagdish Chandra Bose, conducted experiments on plants in 1900. Bose found that plants grew more quickly amidst pleasant music and more slowly amidst loud noise or harsh sounds (Sir Patrick Geddes and Geddes 1920).

Moreover, according to Royal Horticultural Society, talking to plants helps them grow, especially if the one talking to the plant is a woman. Even though there are lots of divisive experiments done with plants to understand if they can talk to human beings, there is no serious finding about this subject yet. Even if, plant biologists do not currently know how to talk to plants, they strive to comprehend how plants communicate with other organisms in order to use this new and exciting language for improving the resistance of plants against pests or pathogens. Instead of using chemical pesticides, genetically engineered plant defense and communication pathways in crops are a preferred avenue.

Communication of plants with other organisms is such a complex problem. Plants can have a network with so many different creatures. They pass on information to each other or to other organisms that speak other languages. How did they obtain these amazing communication skills? Even the most advanced creatures, human beings, experience problems in communication, how can plants have robust communication systems in a heterogeneous environment?

The next time you hear a strange rustling among your garden plants, maintain distance. They might be having an argument. Plants also talk and they respond to attacks like we do. So, be careful and do not hurt plants as they might even curse or scream to you (Anon.).

Safiye Arslan is a research fellow in the area of molecular biology in Nevada.

References

• Adler, Frederick R. 2011. Plant signalling: the opportunities and dangers of chemical communication. Biology Letters. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3061173tool=pmcentrez&rendertype=abstract.
• Anon. Do plants talk? What are the chances it’s a boy? – USATODAY.com. http://www.usatoday.com/tech/columnist/aprilholladay/2006-07-24-plant-talk-baby-boys_x.htm.
• Anon. jacobson’s organ and the remarkable nature of smell. http://books.google.com/books/about/Jacobson_s_Organ_and_the_Remarkable_Natu.html?id=liKKQgAACAAJ.
• Anon. BBC – Earth News – “Perfumed” parasitic plant lures in pollinating mammals. http://news.bbc.co.uk/earth/hi/earth_news/newsid_9376000/9376474.stm.
• Anon. What is Rhizobia. http://www.bionewsonline.com/y/what_is_rhizobia.htm.
• Anon. Biotechnology: Plantlinguistic: – “Plants Communicate With Each Other.” http://bioinformations4all.blogspot.com/2009/08/plantlinguistic-plants-communicate-with.html.
• Jacob, Tim. 2001. “The science and myths of smell.” EMBO Reports 2 (10): 880. http://www.nature.com/embor/journal/v2/n10/full/embor301.html.
• Johnson, Steven D, Priscilla M Burgoyne, Lawrence D Harder, Stefan Dötterl, and Proc R Soc. 2011. “Mammal pollinators lured by the scent of a parasitic plant Subject collections Mammal pollinators lured by the scent of a parasitic plant.” Society 278 (January): 2303-10. doi:10.1098/rspb.2010.2175. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3119003&tool=pmcentrez&rendertype=abstract.
• Montréal, Jardin botanique de. 2012. “Chatting with a plant’s best friend – Science +” (June 3). http://www.aucoeurdelarbre.ca/en/thematics-texts/thematics-texts-details.php?id=8.
• Murray, Jeremy D. 2011. “Invasion by invitation: rhizobial infection in legumes.” Molecular plantmicrobe interactions MPMI 24 (6): 631-639. http://www.ncbi.nlm.nih.gov/pubmed/21542766.
• Shah, Jyoti. 2009. “Plants under attack: systemic signals in defence.” Current Opinion in Plant Biology 12 (4): 459-464. http://www.ncbi.nlm.nih.gov/pubmed/19608451.
• Sir Patrick Geddes, and Sir Patrick Geddes. 1920. The life and work of Sir Jagadis C. Bose. Longmans, Green. http://books.google.com/books?id=EPtCAAAAIAAJ&pg=PA97&q=”continuous”#v=twopage.
• Sugiyama, Akifumi, Nobukazu Shitan, and Kazufumi Yazaki. 2007. “Involvement of a soybean ATP-binding cassette-type transporter in the secretion of genistein, a signal flavonoid in legume-Rhizobium symbiosis.” Plant physiology 144 (4) (August): 2000-8. doi:10.1104/pp.107.096727. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1949875&tool=pmcentrez&rendertype=abstract.
• Vadassery, Jyothilakshmi, and Ralf Oelmüller. 2009. “Calcium signaling in pathogenic and beneficial plant microbe interactions: what can we learn from the interaction between Piriformospora indica and Arabidopsis thaliana.” Plant signaling & behavior 4 (11) (November): 1024-7. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2819509&tool=pmcentrez&rendertype=abstract.

Microbes, in particular bacteria, are associated with many diseases, being the deadliest pathogens along with viruses. But, this doesn’t mean that all bacteria are harmful. Indeed, most bacterial colonies that reside in our gut have mutualistic relationship with humans. Our intestines carry approximately ten times more bacteria than the total number of cells in human body. This vast number of bacteria residing in our intestines are not only harmless, but they are also beneficial for us in many ways, by digesting food to supply energy for the body, by outcompeting the disease-causing bacteria in the intestines, and by producing vitamins and hormones. This study brings a new dimension to our understanding of the interactions between the host immune system with the gut microflora. The main components of immune system are the T cells that can recognize the pathogens. Each T cell recognizes one particular pathogen and distinguishes self-cells from the pathogens. In the thymus, T cells that recognize self-molecules are either eliminated or transformed into a special category of T-cells called regulatory T cells (Tregs), whose job is to maintain tolerance towards self-antigens. Lathrop and colleagues demonstrated for the first time that naïve T cells are developed into Tregs in the gut upon encounter of commensal gut bacteria. What is striking is that these Tregs responded to the bacterial antigens, unlike the thymus originated Tregs that were generated by self-antigen recognition. These data suggest that gut bacteria train host’s immune system to be silent against themselves and act only against invading pathogens. Mechanisms involved in distinguishing harmful vs. beneficial bacteria by the immune system may provide new ways of tackling with bacterial diseases.

2- Cancer meets memory

Original Article: Odajima, J. et al., Developmental Cell 21, 655 (2011).

The recent discovery in the field of neuroscience reminded us the phrase “context is everything.” A study conducted by the scientists of Dana-Farber Cancer Institute and Harvard Medical School addressed somewhat contradictive observation that why human brain has high levels of cyclin E protein, a well-known culprit in many cancers. Cyclin E protein plays an important role in cell cycle where it helps to regulate the timing and the frequency of cell division in normally growing cells. However, overexpression of cyclin E has been associated with uncontrolled cell growth in various cancer types. It is surprising that the human brain, which has a group of non-dividing cells, also express cyclin E at high levels. The study showed that when cyclin E deficient mice were analyzed, there was a serious defect in the formation of nerve connections as well as the formation of memory. “It is overexpressed in many different cancers, but it also is expressed in high levels in the human brain. We have found that cyclin E is needed for memory formation and is a very important player,” said senior author Peter Sicinski, PhD, a cancer biologist at Dana-Farber. The study showed that cyclin E achieves its functions in the brain by binding to Cdk5 enzyme whose activity is associated with Alzheimer’s disease. “There is good evidence that hyperactivity of Cdk5 contributes to Alzheimer’s disease and inhibiting this enzyme can ameliorate symptoms in animals,” said Sicinski. “Manipulating cyclin E levels might be another way to accomplish this,” he added.

3- Designing perfect plastic 

Original Article: Read, D.J. et al., Science 333, 1871 (2011).

Plastic is used everywhere in our daily lives. Up until now, production of different types of plastic was done by trial and error. Only a small fraction of these trials give rise to a usable product. After ten years of hard work, scientists have now developed a computer program that can predict properties of plastic without actually manufacturing it. The program has two parts. The first part can predict how a specific polymer will flow based on the connections between the macromolecules that make up the polymer. The second part predicts the shape of these macromolecules when they are made at a chemical level. Using this code, one can effectively construct a recipe book for plastic. This will make it possible to design plastic that can better handle a specific job. It will also be possible to make plastic out of renewable materials instead of oil based materials which will be easy to recycle.

4- The key to long life?

Original Article: Kim, E.B. et al., Nature (published online before print, 2011).

Who would want to live a long life at the cost of looking ugly? One type of rodent species, naked mole rat, seems to have said “yes” to this intricate question. While an average rodent, a house mice or a rat living on streets, can live up to 4 years, naked mole rats can live up to 30 years. Mole rats are hairless, buck-toothed and almost blind rodents that are only found in dry sections of the Horn of Africa. They live in underground colonies with a social structure similar to ant colonies. There is a queen rat that chooses to mate with only few males, and rest of the colony takes the big responsibility of maintaining and protecting the colony. Scientists have always been puzzled with the extraordinary life span of these exotic animals and they finally generated the complete gene map of these intriguing animals. A quick look of the genomic map revealed that many genes associated with vision, circadian rhythms, perception of pain and perception of bitter tastes seem to be completely turned-off. Perhaps, these specific modifications allow animals to tolerate harsh living conditions and help them to adapt a lifestyle which lacks so-called the luxuries and expectations of a normal animal. Scientists believe that comprehensive analyses of naked mole’s genetic map might shed light on fundamental cellular mechanisms that are disrupted in aging and aging-related diseases.

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

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