Some pathogens are content to focus on their one host and live in their niche of evolutionary propagation. They go about their ongoing generational fight to one-up their host, just as their host works to outperform and prevent infection by the pathogen. Occasionally, one of these sorts of pathogens will branch off and appropriate one or two additional hosts, which may in turn lead to eventual speciation of the pathogen. And then there are other kinds of pathogens.
The Scourge Continues
For those of you with a long memory of this page (or are rampant bingers of its content), you may remember an article from early last year that discussed a certain scourge that goes by the name Xylella fastidiosa. Its colloquial names are many and varied, thanks to the array of crops and plants it infects around the world, spreading like a one-bacteria plague. New forms of it continue to crop up, such as the olive quick decline syndrome version discussed in the article above. The amount of damage varies from host to host, soil type, environmental condition, and so on, but it is almost always still devastating to a local plant population for those that are susceptible to the pathogen.
When it comes to the grapevine, scientific name Vitis vinifera, the impact of the disease-causing bacteria is among the worst. The specific form of death that is created between them is referred to as Pierce’s disease, thanks to its discovery in 1892 by scientist Newton B. Pierce near Anaheim, California. The infection here is quite a bit different from other common pathogenic diseases. The first thing to note is that Xylella fastidiosa lacks the Type III Secretion System (T3SS) that is found in most other similar pathogens. Without it, its evolutionary makeup had to get a bit crafty to find ways for it to actually access the plant cells it needs to infect.
The Impact of Vectors
This required assistance is offered by its insect vector for grapes, which was the blue-green sharpshooter (Graphocephala atropunctata) upon its initial discovery and later a transmission to a related insect, the glassy-winged sharpshooter (Homalodisca vitripennis). This alteration to its intermediate host in 1996 was no small, inconsequential jump. This new insect was more voracious, more reproductive, and, overall, was a far better spreader of Pierce’s disease than the old insect had ever been. The straightforward mechanism by which it works is that the insect bites into the xylem level of a plant stem using their needle-like mouth parts in order to consume the nutrient rich fluid inside. By doing so, they release the bacterial pathogen into the plant.
The bacteria quickly go about producing a gel-like substance that block water flow from rising further through the xylem, allowing them to better collect nutrients for themselves. By doing so, they prevent those same nutrients from reaching and feeding the leaves, causing them to slowly become a sickly yellow color. They’ll eventually turn brown and fall off, with an entire upper stem dying. Thus far, there are no known cultivars of Vitis vinifera that have any sort of resistance to the pathogen.
The Results of Infection
Researchers at the University of California wanted to look into the grapevine responses to infection by the Pierce’s disease bacteria, a topic that has yet to be properly investigated. They started by inoculating some grapevine samples with the bacteria and then taking leaf samples 12 weeks later, allowing infection to set in. Imaging was also done during the process of infection, with the stem being imaged into three sections, both infected and non-infected areas. Next, RNA samples were produced from the collected leaves and a transcriptome analysis run to see what RNA products, and thus activated genes, were working during the plant response to the bacterial invasion. A proteome and metabolomic analysis followed to also see which genes coded for a protein involved in the response.
What is known about Xylella fastidiosa is that the pathogen lacks a T3SS system, as previously mentioned, along with the normal flagella indicators used by plant immune defenses as signals. However, the bacteria does have a T2SS process that secretes hydrolytic enzymes and it is these that appears to cause the visual leaf symptoms on the plants. With this as a starting point, the scientists were able to identify how the PAMP immune response occurs and is activated by the plant, how strong oxidative stress appears to happen even despite antioxidant metabolites being produced by the plant, and how the cell wall is remodeled and lignified during this time period.
On the flip side, the bacteria is involved by forcing only the PAMP system to activate, but blocking the salicylic acid-mediated immune response from triggering, a major part of proper plant defense. They also use the lignification to reduce the flow of sap in the xylem, further concentrating water and nutrients at their location. All of the genes used by the plant in these systems were recorded by the scientists for later use.
With this deeper understanding of the genetic and molecular components used by the grapevine to defend itself and the ways in which the pathogen exploits and abuses those same defenses, it is hopeful that the found molecular markers and relevant genes can be made to provide a true resistant cultivar in the future. The scientists acknowledge that this data is very basic for now and requires both more data and better integration of said data to isolate methods in which to improve plant resistance or, on the other side, inactivate the genes that make the plant susceptible to attack.
They nonetheless find their results promising for further expansion in the fight against deadly crop pathogens like Xylella fastidiosa.
Photo CCs: Ripatella 4644 from Wikimedia Commons