Artificial photosynthesis transforms CO₂ into liquefiable fuels

Yu and Jain. Plasmonic photosynthesis of C1–C3 hydrocarbons from carbon dioxide assisted by an ionic liquid. Nature Communications, May 2019.

Scientists have recently established a reliable “artificial photosynthesis” paradigm to produce fuels from water, carbon dioxide, and visible light. With the help of sunlight, chemical reactions between water and CO₂ are catalyzed in plants to generate and store solar energy in the form of glucose. This process is called photosynthesis. In the new study, the researchers developed an artificial process that uses the same mechanisms of natural photosynthesis to convert CO₂ and water into liquid fuel by using electron-rich gold nanoparticles as a catalyst. Gold nanoparticles function in the same role as chlorophyll in natural photosynthesis in the absorbing of light and transferring electrons and protons to catalyze the chemical reactions between CO₂ and water. They are known to be efficient at absorbing light and do not break down or degrade like other metals. The energy stored in the bonds of the hydrocarbon fuel can be freed by the conventional method of combustion or by new-generation, environmentally-friendly power fuel cells, thus producing electrical current. By converting CO₂ into more complex molecules like propane, green-energy technology is now one step closer to using excess CO₂ to store solar energy for use when the sun is not shining and in times of peak demand. While the development of this CO₂-to-liquid fuel may be exciting for proponents of green-energy technology, the artificial photosynthesis process is nowhere near as efficient as it is in plants. New methods should be developed to increase the efficiency of the catalysts and downstream chemical reactions at much higher scales.

Brain area that watches for walls identified

Henriksson et al. Rapid Invariant Encoding of Scene Layout in Human OPA. Neuron, May 2019.

Neuroscientists have identified the part of the human brain whose duty is to help us perceive the barriers which define the navigable space around us, such as walls or ceilings, so that so we can avoid bumping into things and navigate safely through our environment. By way of vision we have an almost instant sense of where we are in space. Although this process feels effortless, it requires the coordinated activity of multiple brain regions and neurons working together to give us this sense of our surroundings. This process has remained unknown. But thanks to a new study, we are a step closer to solving the puzzle. Using cutting-edge brain-imaging technologies, researchers examined the mental responses of volunteers as they were shown images of various three-dimensional scenes. The images depicted a typical room with three walls, a ceiling, and a floor, but then were abruptly changed by the removal of a wall or a ceiling. By doing this repeatedly, the team could pinpoint how the participant’s brain encoded every scene. In the brain scans of the volunteers, one brain area called the occipital place area (OPA) clearly stood out. OPA activity represented the geometry of the scenes and activity patterns, reflected the presence or absence of each component, such as a ceiling or a wall, and projected a detailed picture of the overall configuration. Interestingly, OPA seemed to ignore the surface appearance of the various components such as colors or textures in order to focus only on the geometric patterns. The OPA managed to perform all the necessary computations needed to get a sense of a room’s layout extremely fast – in just 100 milliseconds. In the future, the research team plans to incorporate virtual reality technology to create more realistic 3D environments for participants to experience, hopefully achieving much deeper insights into how our brains process and makes sense of the visual information.

Gut segments are organized by function

Esterházy D. et al. Compartmentalized gut lymph node drainage dictates adaptive immune responses. Nature, April 2019.

As food enters our intestine, it goes through a windy and lengthy journey. A new study provides new insights into how our intestines maximize nutrient uptake while protecting the body from potentially dangerous invading microbes. At first glance, the intestines appear to have a uniform tissue structure. But when scientists looked at them closer, they found that our food-processing canal seems to consist of multiple compartments that pace the immune system’s reactions to the food passing through. Scientists uncovered these functional intestine segments in mice when they examined the intestinal structures called gut draining lymph nodes, which orchestrate immune responses. The researchers found that nodes in different parts of the intestines had different cell composition, and they saw different immune responses between segments when they challenged the mice with a pathogen. They observed less aggressive defenses in the first segments where nutrients are absorbed, and more forceful responses at the end, where pathogens are eliminated. Researchers plan to exploit these immunological differences between the gut segments for treating gastrointestinal disorders. For example, by targeting immune-suppressing drugs to the specific gut segment where they’ll have the most effect, it might be possible to dampen their side-effects. The spectrum of immune responses along the intestines could also be used to make new and better oral vaccines. Thus far, scientists’ efforts to design oral vaccines have been hampered by the difficulty of generating a robust immune response; it is possible that the muted immune response at the beginning of the intestines might be part of the reason why oral vaccines tend to be less effective than injections. Thus, targeting the distant end of the intestine might be much more efficient way of inducing the immune response required.

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.