Or Why I'm confused.
This is a painless discussion of plant injury and response.
Sorry, but I couldn't resist this attractive, color-coordinated diagram. Just notice the top edge (with the caterpillar) and know that "JA" stands for jasmonate. A bug bite triggers a cascade of responses.
Complete technical article: http://www.plantphysiol.org/content/146/4/1459.full
Here's what I find interesting. While most plants possess genes that enable the plant to fight off infections and injuries, these genes are normally switched off. Their default status is "non-functional." The same thing is true in humans and other animals. When something bad happens, a plant (or your cousin Vinnie) must initiate the process of mounting a response. In addition, the plant (or Vinnie) may want to signal to its (his) neighbors to be on the alert, because something bad is going on. [See those little purple bubbles at the top of the diagram? That's the alert message.]
In plants, the flagman for cranking up the response (say, increasing alkaloid levels, like the level of nicotine) is jasmonate (JA) signaling. It initiates a response by switching on some idle genes. But it also must ultimately switch them back to their "off" position, so the whole affair becomes rather complex--too complex for me to follow. In animals, a group of compounds that are structurally similar to jasmonate, and function in starting and stopping defensive tools, is called prostaglandins (PG). It turns out that anti-inflammatory drugs, like aspirin, directly affect levels of the various PGs.
Curiouser and curiouser.
Studies have demonstrated that healthy people are able to smell certain infections and metabolic abnormalities in other people. Plants apparently do the same thing, through the JA Signaling system, which releases certain volatile chemicals from the leaf surface, and which are "sensed" and responded to by neighboring plants. The response in the injured plant, as well as in the alerted neighbors, includes the production of some chemicals that are unpleasant to insects, or that induce suicide in virus infected leaf.
As it turns out, herbivorous insects try hard not to trigger a big JA response. Small hornworms, for example, avoid eating the vein of a leaf, which will trigger a significant JA response. Full size hornworms throw caution to the wind, and eat all but the thickest veins.
For flying insect herbivores, the smell of the volatile chemicals of the JA response cause them to chose to go elsewhere, regardless of the actual plant defenses. These insects do not respond to, say, nicotine levels, but only to the "smell" of the jasmonate response in the air, when they decide which plant to land on for feeding.
Another impact of the JA cascade is that root elongation is slowed. This means that the roots grow more dense, a change which apparently enables them to devote more energy to alkaloid production, and the synthesis of other compounds that assist in resistance to attack or disease.
When I clip my seedlings, I am triggering the JA response. The JA response fades after a few days to a week. My impression is that the clipped transplants have thicker stalks, denser root systems, and are less likely to be attacked by slugs and bugs. So a final clipping a day or two prior to transplant should allow the seedlings a bit of a head start.
The same applies to denying the seedlings water for several days prior to transplant to the field. Water restriction triggers the JA pathways. Watering them well on the evening prior to transplant will make the process of transplantation easier, without reducing the "drought" effect.
Although I have included the entire, colorful diagram of the JA system, I have a clear understanding of only that caterpillar part at the top.
Much of the research from which these biochemical pathways were deduced was performed on tobacco derived from ARS-GRIN seed.
Bob
This is a painless discussion of plant injury and response.
Sorry, but I couldn't resist this attractive, color-coordinated diagram. Just notice the top edge (with the caterpillar) and know that "JA" stands for jasmonate. A bug bite triggers a cascade of responses.
Complete technical article: http://www.plantphysiol.org/content/146/4/1459.full
Here's what I find interesting. While most plants possess genes that enable the plant to fight off infections and injuries, these genes are normally switched off. Their default status is "non-functional." The same thing is true in humans and other animals. When something bad happens, a plant (or your cousin Vinnie) must initiate the process of mounting a response. In addition, the plant (or Vinnie) may want to signal to its (his) neighbors to be on the alert, because something bad is going on. [See those little purple bubbles at the top of the diagram? That's the alert message.]
In plants, the flagman for cranking up the response (say, increasing alkaloid levels, like the level of nicotine) is jasmonate (JA) signaling. It initiates a response by switching on some idle genes. But it also must ultimately switch them back to their "off" position, so the whole affair becomes rather complex--too complex for me to follow. In animals, a group of compounds that are structurally similar to jasmonate, and function in starting and stopping defensive tools, is called prostaglandins (PG). It turns out that anti-inflammatory drugs, like aspirin, directly affect levels of the various PGs.
Curiouser and curiouser.
Studies have demonstrated that healthy people are able to smell certain infections and metabolic abnormalities in other people. Plants apparently do the same thing, through the JA Signaling system, which releases certain volatile chemicals from the leaf surface, and which are "sensed" and responded to by neighboring plants. The response in the injured plant, as well as in the alerted neighbors, includes the production of some chemicals that are unpleasant to insects, or that induce suicide in virus infected leaf.
As it turns out, herbivorous insects try hard not to trigger a big JA response. Small hornworms, for example, avoid eating the vein of a leaf, which will trigger a significant JA response. Full size hornworms throw caution to the wind, and eat all but the thickest veins.
For flying insect herbivores, the smell of the volatile chemicals of the JA response cause them to chose to go elsewhere, regardless of the actual plant defenses. These insects do not respond to, say, nicotine levels, but only to the "smell" of the jasmonate response in the air, when they decide which plant to land on for feeding.
Another impact of the JA cascade is that root elongation is slowed. This means that the roots grow more dense, a change which apparently enables them to devote more energy to alkaloid production, and the synthesis of other compounds that assist in resistance to attack or disease.
When I clip my seedlings, I am triggering the JA response. The JA response fades after a few days to a week. My impression is that the clipped transplants have thicker stalks, denser root systems, and are less likely to be attacked by slugs and bugs. So a final clipping a day or two prior to transplant should allow the seedlings a bit of a head start.
The same applies to denying the seedlings water for several days prior to transplant to the field. Water restriction triggers the JA pathways. Watering them well on the evening prior to transplant will make the process of transplantation easier, without reducing the "drought" effect.
Although I have included the entire, colorful diagram of the JA system, I have a clear understanding of only that caterpillar part at the top.
Much of the research from which these biochemical pathways were deduced was performed on tobacco derived from ARS-GRIN seed.
Bob