It was a beautiful day in the garden. There was a slight breeze moving my petals and leaves and making them flip back and forth. I was watching the butterflies basking in the sun with open wings and enjoying the company of chirping birds. Their songs were so relaxing and soothing. I was very happy and thought that nothing could stress me out today. Oh well, I was wrong. It all started with a tiny microbe!

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

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