How plants responded to bacterial attack was still a complete mystery though. One of the main things that distinguishes plants from animals is that animal cells are a lot more motile, they can move through the body. Animal cell movement is crucial during the development of the embryo and even once the body is fully formed cells still rush around the blood stream and slide around in the epithelial layers. The correct functioning of the immune system relies on cells being able to do this, dendritic cells and macrophages will pick up bits of bacteria at the site of infection and go running back with them to the lymph nodes which will start organising the best way to deal with the infection.
A macrophage in the lungs, from Wikimedia commons. The macrophage engulfs bacteria and eats them, which requires it to be able to move.
With a few odd exceptions plant cells do not move. Not at all. There is no movement of cells during the seed development, and even the movement of plants towards sources of light and water is caused by cells growing rather than moving. How then does the plant respond and react to bacterial infections?
There are several different ways, which is why this is a three-part post series:
Part One: Deadly Chemicals
One of the simpler ways to remove a bacterial infection is to release a chemical that is harmful to the bacteria. There are quite a lot of plants that produce antibacterial products as normal secondary metabolites, an example of which is saponins, a group of compounds which have soap-like properties. As saponins are lipid soluble they can break up bacterial membranes by binding to sterol compounds within the membrane and disrupting the structure. Studies done on oats (reference one) have shown that reducing the natural levels of saponin made the oat plants much more vulnerable to fungal infections.
Rather more excitingly, plants can also release certain chemicals in response to a bacterial attack. When bacteria attack plants have been shown to release an assortment of hydrolytic enzymes - glucanases, chitinases, etc that break down cell walls and membranes. These are known as pathogenesis-related proteins as they are specific to bacterial or fungal attack. One of the better researched is a group of chemicals called phytoalexins. In normal conditions neither the phytoalexins themselves, nor the enzymes used to make them, are found within plant cells. It is only after a microbial invasion that the enzymes are transcribed and translated and the phytoalexins synthesised.
In order to respond specifically to bacterial attack, the plant needs to be able to recognise bacteria as invading elements. Like many animals, plants have what are known as "Toll-like receptors" that recognise bacterial pathogen molecules (which in animals are referred to as PAMPS Pathogen-Associated Molecular Patterns but in plants seem to be called elictors) such as bits of protein and polysaccharide fragments from the bacterial cell wall. [EDIT - I have since been informed that PAMP is used quite widely among plantscis now as well]
Comparison of the plant and animal TOLL receptors. The blue and red lines are the receptors, and the blobs attached to them are the bits of pathogen. The yellow boxes labelled PK stand for 'protein kinase cascade' which carries the message through the cell to turn on the genes required. Diagram adapted from reference two.
By recognising pathogens as they invade, the plant cells can launch a deadly chemical attack against them, without requiring any movement. None of this requires the cells to travel around, and until the bacteria develop resistance to the chemicals being used, it can be highly affective. Chemical warfare however, is only one of the strategies that plant cells can adopt to protect themselves against invading microorganisms, and my next post will cover the second - depriving the bacteria of valuable nutrients by committing cellular suicide.
1) Papadopoulou, K. (1999). Compromised disease resistance in saponin-deficient plants Proceedings of the National Academy of Sciences, 96 (22), 12923-12928 DOI: 10.1073/pnas.96.22.12923
2) Nürnberger, T., & Scheel, D. (2001). Signal transmission in the plant immune response Trends in Plant Science, 6 (8), 372-379 DOI: 10.1016/S1360-1385(01)02019-2
3) Taiz, Zeiger, Plant Physiology, third edition Sinauer Associates 2002.
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