Years ago, a group led by Dr. Fritig in IBMP-CNRS in Strasbourg, France, was working on the defense reaction (hypersensitive response, HR, see below) of tobacco infected by the tobacco mosaic virus. The team did a pioneer work in the characterization of many tobacco defense proteins and chemical messengers involved in setting up plant defense. I had a chance to do my PhD in the group of Dr. Fritig.
One day, Dr. Fritig told us about a coming popularization talk he had to prepare and asked for possible support in illustrating the hypersensitive response phenomena. Though I don’t remember how this has exactly happened, I ended up drawing cartoons to illustrate plant induced defense responses. After the talk, those cartoons remained silently stored for two decades in floppy disks that followed me up to Rovaniemi.
I rediscovered them a few months ago, and I thought they could help me to discuss plant defense responses. My aim is definitely not to make a scientific review of a complex topic in 5 cartoons, but just to show some mechanisms that plants have developed to fight against pathogen attacks to those who don’t know about plant defense responses.
Cartoon 1: Plant enemies
Plants are sessile and have many enemies. They have developed a large set of mechanisms to defend themselves against pathogen attacks using a combination of constitutive (pre-existing organs or chemicals, e.g. resin in conifers) and induced defences (e.g. de novo production of antimicrobial compounds).
Most plants are not normally colonized by most pathogens; they are non-host for these pathogens mainly due to basic resistance. To induce a defense reaction in a host plant, the plant needs to recognize the pathogen: the plant has to carry a resistance gene and the pathogen, an avirulance gene.
If the recognition takes place, the defense mechanisms are activated in the plant; the interaction is incompatible. If the plant or the pathogen does not carry that gene, there is no recognition, no induction of defense response, development of disease symptoms, reduced vitality and eventually death of the plant; the interaction is compatible.
The plant cell is like a fortified castle, the ramparts the cell walls and the nucleus the keep.
The incompatible interaction is thus highly specific to a particular plant-pathogen combination. It is characterized by the rapid induction of plant cell death at the site of infection that ultimately leads to the sequestration of the pathogen in necrotic lesions at the site of penetration, thus limiting its spread.
A commonly activated defense strategy in case of incompatible interaction is the hypersensitive response (HR). After recognition of specific pathogen-produced signal molecules (elicitors), some responses occur within minutes (oxidative burst and strengthening of the cell wall) and others within hours, such as the de novo synthesis of specific proteins, the pathogenesis-related proteins (PR-proteins).
If the plant cell is depicted as a fortified castle, the ramparts are the cell walls and the nucleus the keep. So let’s see how the plant cell starts fighting the pathogen…
Cartoon 2: Plant cell wall thickening
Among the first responses upon elicitation is a massive oxidative burst. The reactive oxygen species produced are damaging the cells of invading organisms but as well induce cross-linking of preexisting cell wall structural proteins (hydroxyproline-rich glycoproteins, proline-rich proteins and glycine-rich proteins), strengthening the cell wall. Local lignin-like impregnation may also occur to improve membrane strengthening.
Plant cells also respond to microbial attack by rapidly synthesizing and depositing callose (β-1,3-glucan) between the cell wall and cell membrane adjacent to the invading pathogen. Callose deposits, called papillae, are polysaccharide polymers that impede cellular penetration at the site of infection. Phenolics, reactive oxygen species, cell wall proteins, and cell wall polymers may also be found in papillae.
Plasmodesmata are small channels that directly connect the cytoplasm of adjacent plant cells. The inner diameter and, thus, the size of the molecules trafficking via plasmodesmata are regulated by reversible deposit of callose. Elicitation induces a deposit of callose in plasmodesmata, which reduces the spread of some pathogens like viruses, which move from cell to cell via plasmodesmata.