Cells Recognize and Respond to Pathogens

close up of maple leaves with black splotches indicting disease against a blurry background

Biological Strategy

Plants

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Protect From Microbes

In living systems, microbes play important roles, such as breaking down organic matter and maintaining personal and system health. But they also pose threats. Bacteria can be pathogens that cause diseases. Some bacteria create colonies called biofilms that can coat surfaces, reducing their effectiveness–for example, inhibiting a leaf’s ability to photosynthesize. Living systems must have strategies for protecting from microbes that cause disease or become so numerous that they create an imbalance in the system. At the same time, living systems must continue living in harmony with other microbes. Some living systems kill microbes. Others repel without killing to reduce the chances that microbes will adapt to the lethal strategy and become resistant to it. For example, some pea seedlings exude a chemical that inhibits biofilm buildup.

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Plants

Phylum Plantae (“plants”): Angiosperms, gymnosperms, green algae, and more

Plants have evolved by using special structures within their cells to harness energy directly from sunlight. There are currently over 350,000 known species of plants which include angiosperms (flowering trees and plants), gymnosperms (conifers, Gingkos, and others), ferns, hornworts, liverworts, mosses, and green algae. While most get energy through the process of photosynthesis, some are partially carnivores, feeding on the bodies of insects, and others are plant parasites, feeding entirely off of other plants. Plants reproduce through fruits, seeds, spores, and even asexually. They evolved around 500 million years ago and can now be found on every continent worldwide.

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Cells of plants detect pathogens and promote rapid cell death around the infection, keeping the plant alive, using Hypersensitive Response (HR).

“When a plant is attacked and there is a gene-for-gene recognition, the HR [Hypersensitive Response] response leads to very rapid cell death around the site of attack. This seals off the wounded tissue to prevent the pathogen or pest from moving into the rest of the plant. Hydrogen peroxide and nitric oxide are produced and may signal a cascade of biochemical events resulting in the localized death of host cells.” (Raven et al. 2002:834)

“In the case of virulent invaders (no R gene recognition), there are changes in local cell walls that at least partially block the movement of the pathogen or pest farther into the plant. In this case there is not an HR response and the local plant cells are not suicidal.” (Raven et al. 2002:834)

“Certain proline-rich s of the cell wall become oxidatively cross-lined after pathogen attack in an H₂O₂ – mediated reaction. This process strengthens the walls of the cells in the vicinity of the infection site, increasing their resistance to microbial digestion.” (Taiz and Zeiger 2010:392)

“The hypersensitive response behaves in the following manner: before the HR is triggered, reactive oxygen and nitric oxide (NO) rapidly accumulates in the cells. The accumulated oxygen then reduces, forming hydroxide ion (OH^–) and hydrogen peroxide (H₂O₂). These compounds contribute to death of the infected host cells. The NO is the activator of HR and triggers the reduction of oxygen. Accumulation of both oxygen and NO are needed to trigger the HR, an increase in one of these will not trigger a response by the plant cells. In addition, HR only responds to and pathogenic invasions, virulent attacks gain no response from the plant cell.” (Taiz and Zeiger 2010)

Raven, Peter H., and George B. Johnson. “How Plants Grow in Response to Their Environment.” Biology. Boston: McGraw-Hill, 2002. 834-35. ; “An Overview of Plant Defenses against Pathogens and Herbivores.” Overview of Plant Defenses. N.p., n.d. Web. 16 Sept. 2012. http://www.apsnet.org/edcenter/intropp/topics/Pages/OverviewOfPlantDiseases.aspx. ; Taiz, L., and E. Zeiger. “Secondary Metabolites and Plant Defense.” Plant Physiology.
USA: Sinauer Associates, 2010. 386-94. Print.