Tracking plant pathogens is no simple matter. Due to their possible environmental hidey holes being in the soil, the air, other plants, or the host plants themselves lying dormant, any and every possibility must be accounted for. And the triggers that begin active pathogenicity and harm to the plant is connected to a convoluted system of interactions between the pathogen, its host, and environmental conditions. Just a single one of these pathogens can become a scientist’s entire career focus and they will leave behind plenty to still discover.

The Epoch of Plant Warfare

If a pathogenic bacteria is to be thwarted in its attempts to make a meal out of its host plant, then every part of its lifestyle needs to be understood down to the minute details to find places to counter them. A single small chemical change has the potential to allow a pathogen to thrive or expire in its target host.

Unfortunately, bacteria are among the worst kinds of pathogens to deal with in plants, as they don’t cause the same overt responses that others like fungi or eukaryotic oomycetes do. Instead of a immediate hypersensitive response and development of specialized cell types, the fight between bacteria and plants is one done in subterfuge, relying on chemical and enzyme defenses that often can be the sole source of resistance against invasion. Only if the pathogen accidentally reveals itself do the stronger responses come into play.

As with animals, plants can become more susceptible to infection when they are less healthy than they could be. Though they don’t have a direct immune system, per se, like humans do with our roaming white blood cells and structured antigen system, they do have an interlocked system of chemical-based responses and enzymatic processes that help to protect them. Even so, negative abiotic stresses can still overtax the capabilities of plants and make them slow to respond to pathogens. On the opposite hand, a positive symbiosis with microorganisms can prove protective against others with a more parasitic mindset, as the symbiosis often comes with chemical and genetic protections, along with simple blocking off of the plant cells from being reached by the pathogenic bacteria.

Another point to consider is how the internal plant ecosystem alters after infection. If a prolonged battle is being fought between plant and bacteria, the multiple and ongoing generational descendants of the bacteria can lead to a tipping of the fight in their favor. In addition to slowly and steadily developing resistance to a plant’s methods of defense due to natural selective pressures, bacteria are also capable of altering the cells surrounding them to leave them more open to assault, not to mention hijacking them for the purposes of replication.

Funny enough, one of the most classic examples of this behavior would be the original GMO tool, Agrobacterium tumefaciens, which creates a gall tumor on any plant it infects in order to manipulate and form an environment that best suits its offspring to grow, full of rich nutrients from rapidly dividing plant cells. Of course, all of this can also produce the opposite response over time. Rather than increasing the survivability of the pathogen’s environment, the wrong action can cause the plant to undergo a systemic response or to even warn other plants around about the attack, allowing them to begin building even more extreme defenses and thereby limiting the ability of the pathogen to spread.

As one might expect, the multilayered complexity of all of this makes studying it seem nigh impossible. The best bet for scientists is to focus on a small segment of the overall interaction, work that out, and proceed from there. Over dozens of experiments and published studies, a better model of how the pathogen-plant structure is organized can be made. A further problem includes how bacterial pathogen actions can often only be seen when in a host plant and not in a lab culture, but studying them within their host plant makes it difficult to distinguish the processes that are conducted by the plant or by the pathogen.

A method that can help this sort of research is testing the effectiveness of a pathogen on a plant that is not normally a host for its attacks. If the infection fails to take hold, then it is easier to find out what defenses the plant has that are different from the usual host plant and how this protects against the pathogen in question. Alternatively, if the non-host plant has little resistance against the pathogen, then that tells quite a bit more about the generality of its methods.

Before getting into a deep discussion of a study looking into this very experiment, we should first go over the most common pathogen it applies to, one of the more deadly plant bacteria out there, and a model organism in its own right: Pseudomonas syringae.

The Widespread Disaster That Is P. syringae

To start, it should be noted that the specific strains, named pathovars, of P. syringae are seemingly as numerous as the stars. Many of its subtypes were actually incorporated into other Pseudomonas species lines due to the high interconnectivity between them in lineage. But, as a whole, this species and all of its subtypes and close relatives infect an innumerable swath of crops and plants around the world.

Its incorporation into the model organism category was an easy decision, as the generalist nature of its functions lends itself to studying how bacterial pathogen interactions with plants take place on the broadest of scales. Especially since the bacteria is capable of surviving away from its host plants as well and has been recovered from multiple habitats and environmental soils.

Infection by P. syringae causes necrosis of leaf tissue and also chlorosis that results in white and yellowed leaves incapable of making enough chlorophyll for photosynthesis. The focus on leaves and the ubiquity of the pathogen has resulted in this particular area becoming one of the more well-studied avenues of pathogen assault. Though the bacteria are, of course, not limited just to leaf tissue, with other pathovars being known for infecting seeds, fruit, and bark, depending on the type of plant that specific pathovar focuses on. Science just currently knows the most about the leaf interaction, so that is what we will be speaking about in more detail.

The term that has to be explained right away when discussing P. syringae and its host is the word apoplastic. The apoplast is a special space outside of the plasma membrane, but inside the cell wall of plant cells. Diffusion of nutrients and other materials often happens through this space and into this space in cells next door as well. In one sense, it is an interconnected space between all plant cells, a continuum that continues on at each junction point. Water and solutes are transported through it in a fashion referred to, appropriately enough, as apoplastic transport.

All of this, you might guess, makes it the perfect point of access into a plant’s systems, giving a pathogen free rein to go to any tissue it so chooses. Our model organism is one of those that takes advantage. Its access to leaf cells is facilitated by any open wounds or through natural openings like the stomata pores for gas exchange. Once inside the apoplast, they travel into the mesophyll, the inner layer of cells filled with chloroplasts. The bacteria feeds on the nutrients in the apoplastic fluid surrounding it, which is especially rich nearby to the chlorophyll-heavy cells.

The next landmark of interest in pathogen biology is the specific secretion system used by P. syringae. This bacteria uses the Type III Secretion System (T3SS) and if you want to know more about bacterial secretion systems in general, look forward to a future at some point long-form article on them.

It uses this secretion system to inject effector proteins into its surroundings, which can have varying roles to play. Their primary function is to work with the other virulence factors the bacteria uses, such as toxins and purposefully derived phytohormones in order to weaken the host plant immune system and to alter the plant cell physiology around the bacteria to give them more nutrients and a desired environment.

While some of these manipulations may only be localized and affect the cells that the bacteria are currently inhabiting, some of the signal proteins produced do generate systematically throughout the entire leaf and possibly the rest of the plant. There is even the potential for these signals to be unwillingly or unwittingly propagated by the host plant into the surrounding air and to other host plants presumably growing nearby, making them more susceptible to attack by the pathogen. The full extent of how phytohormones are utilized like this is poorly understood and much research is still ongoing.

An Unhelpful Result of Non-Host Resistance

When discussing generalist bacterial pathogens like P. syringae that have pathovars that frequent numerous host types, with all of them theoretically having the potential to infect any of their relatives’ host plants as well, there are questions raised about growth efficiency and how optimal virulence is achieved in a non-host plant. There is a presumption with generalists versus specialists that the former have lower overall replication success and speed due to their nature of using only general chemicals and compounds, rather than targeted ones against a specific host plant like specialists do.

Past evidence has shown that natural selection pressures on pathogens would tend toward the best possible level of virulence to maximize infection rate. Decades of experiments have verified this as true for the majority of cases. Therefore, one would expect a pathogen infecting a non-host to exhibit suboptimal results in their fitness and capability. And this is also true in most cases. But, when it comes to biology, there are always exceptions to consider.

Though, with multi-host parasites such as this, things become more complicated in the first place, with varying trends of fitness between the multiple hosts they can infect. It is necessary information to uncover, however, as pathogens cannot be managed unless all of their potential reservoirs of hiding are laid out in the open and dealt with. When it comes to P. syringae, it is also the environmental holdouts that can be an issue, giving additional source populations to come back from. It is likely both nonhost plants and soil environments that contribute to the evolutionary development of so many strains of the species focused on new plant cultivars as hosts.

A study in April of last year sought to find out whether passing the model organism through a nonhost species would affect its virulence on its original host later on. Their expectation and hypothesis was that the loss of infectivity and growth speed from infecting the nonhost plant would then also negatively impact both of those factors when passed through the original host afterwards. For this experiment, they used the pathovar variant of P. syringae that uses tomatoes as a host, as this is one of the most studied pathovars of the species and is already known to be capable of infecting the nonhost model organism Arabidopsis thaliana.

The pathogen was inoculated in 18 tomato and 18 Arabidopsis plants and their densities after growth were measured, along with whole genome resequencing being done to check for any obtained mutations in the separate populations that may contribute to new phenotypes and traits. After this was done with four passages over 20 days through each plant of ongoing strains collected from the prior passage, the bacterial densities were measured. Passages through the plants were also mixed, such as going through tomato first and then Arabidopsis later or vice versa.

The goal of this was, as noted, to see if passage through certain hosts altered the optimal virulence levels when going through another. Their results were extremely interesting and showed that passage through Arabidopsis first resulted in significantly increased pathogen growth through later passages, regardless of whether the later ones were tomato or Arabidopsis again. This was not the case if tomato was passed through first.

For some reason, a first pass through Arabidopsis was increasing the growth capability of the pathogen in a manner that continued through generations and subsequent hosts. An example the scientists gave of why this could be the case is that the flagellin receptor, which is an immune system receptor that recognizes flagellin proteins of bacteria and alerts the plant of an impending attack, is different between the two plant species and the specific type of protein that Arabidopsis searches for could cause the pathogen to select for certain alternative formations that also give it a benefit against tomato plants.

This in general showcases the effect that selective host decisions have on the generational growth of pathogens and their virulence. Evolution within a host definitely occurs and can result in making a pathogen even more deadly toward other hosts if certain traits are selected for within the first one. Virulence is a shifting landscape of success and seemingly minor or major interactions can alter how dangerous a pathogen becomes, for better or for worse.

A Fungus To Catch A Bacteria

Not all pathogenic activity stands alone. It’s a competitive sphere of influence, where different pathogens compete with each other for more space and access to their desired host. You can find both situations where pathogens symbiotically team up to better improve their virulence on a host and also times where pathogens release specialized chemicals meant to inhibit or kill their competition.

As mentioned earlier, effector proteins are the primary way by which all such actions are conducted. And it is through recognizing the presence of some of these proteins that the plant immune system jumps to its job. For those that reveal to the plant that certain cells have been infected, the response often calls for the “hypersensitive response” (HR), otherwise known as one form of programmed cell death.

Since causing the death of the cells they are in wouldn’t be good for the pathogens, the effector proteins that cause this response are referred to as avirulence factors, or factors that are harmful to the virulence of a pathogen. Thus, the cataloging and understanding of effector proteins that may turn out to be avirulent and helpful to scientists is a top priority in pathogen research. There are, unfortunately, no clear-cut methods to discovering whether a given protein is or is not an effector protein, however, and there is usually a reliance on functional analysis programs to determine the probability of any one protein being as such based on its amino acid composition.

In February of last year, researchers in Brazil were desiring to decipher the effector status of proteins from the fungus Hemileia vastatrix that causes coffee leaf rust disease. An analysis of its possible effector proteins had never been performed before and they had to decide how they were going to go about the process. There aren’t yet good options for genetically manipulating the activity of both a host and its pathogen, so they would have to work on a single protein level. The other possibility was to use the candidate effector proteins as a molecular probe in the host to see if they caused a phenotypic effect, thus confirming that the candidate is indeed an effector. Even avirulence effectors can be found this way, as host detection of them results in rapid programmed cell death of nearby cells.

But how to get the candidates into the host? Agrobacterium, while being available, is a poor fit for being used on hosts like coffee plants, as coffee mesophyll cells can resist infection by the bacteria fairly strongly. So the scientists went with the other, other alternative, an effector detector vector (EDV). Catchy, isn’t it? These EDV’s require a nonpathogenic bacteria to be used or an adapted pathogen with a Type III Secretion System and that is capable of translocating the candidate effectors into the cell cytoplasm of the host.

They found a quite unique opportunity because they were working with coffee plant hosts. What about using the P. syringae subtype that specifically preys on coffee and causes bacterial leaf blight? Using this system of having the alternative vector express single candidate effector genes, along with taking leaf samples at various stages to increase the probability of obtaining potential effector samples while they are active, the researchers were able to confirm 94 effector sequences, 46 of which were previous confirmed, 34 for which were partially known, and 14 that were completely new.

In the process, they found a single very interesting effector protein from the fungus named HvEC-016. When it was introduced by P. syringae into hosts with a known SH1 resistance gene, the effects of the vector bacteria in causing bacterial blight and leaf necrosis was significantly reduced. This included a huge decrease in bacterial concentration and growth in the leaf tissues.These results were not seen in coffee plants lacking the resistance gene, indicating that there appears to be some sort of dependent response the resistance gene confers that allows the fungal effector gene to act as a avirulence factor against bacterial blight.

But, since we don’t currently have ways to genetically transform either coffee plants or fungi reliably, it will be difficult to confirm this hypothesis on why these effects are happening. The researchers are, however, working on a different way by cultivating a large amount of coffee plants with resistance phenotypes in order to better test this outcome. We’ll just have to wait for the results from that upcoming experiment.

Like A Moth To Citrus

Moving on to the completely separate topic of citrus fruits, these plants and the produce they produce have long been subjected to a horrible disease worldwide that they have little to no resistance to. Known as citrus greening disease, or Huanglongbing in Asia, it is easily the most devastating disease in citrus out there. The bacteria that causes it is Candidatus Liberibacter asiaticus, a particular subtype that formed in Asian regions among the citrus they grow there. A quirk of this bacteria is that, when it infects its host plant, it localizes the infection to the nutrient-carrying phloem region in the center of the plant stem.

The bacteria, however, doesn’t spread on its own. It has a special vehicle that it rides upon, a vector named Diaphorina citri, an aphid-like bug species originally from Asia, but which has since spread worldwide. It reached North American shores in the late 90’s and now has spread across the continent. Worse still, it infects far more than just citrus plants, delving into several other important crops. For its main greening disease, it causing yellow shoot growth, mottling of leaves, and inverse fruit coloring, before eventually causing twigs to no longer grow and starting a long decline for the host plant toward death.

There is no known direct cure other than quarantine and isolation of infected trees or just cutting them all down outright. The process is difficult, expensive, and might not even work, as the bug vectors could still manage to find their way to another tree eventually. So, scientists and agronomists have been hard at work trying to develop resistant citrus cultivars by any means possible. And genetic modification techniques have been extremely promising in recent studies toward that end.

Traditional breeding methods have seen far less success, not only because of how much longer they take, but also because no known resistance genes have been found in the genomes of citrus trees thus far. Even GM attempts with antibiotic genes from other bacteria and other host resistance pathways hasn’t seen much progress, though they do confer a stronger plant immune response. Antimicrobial peptides (AMPs) are the best way to deal with bacterial diseases, though the trouble is always finding the right one and complement gene to use.

One of the better of these general peptides are cecropins, special peptides that cause lysis of bacterial cells. Only small amounts need to be produced, on the level of micromoles, in order to be effective, saving on production and energy costs for the plants made to use them. Since these peptides don’t affect eukaryotic cells, insects, other plants, and the animal kingdom at large aren’t at risk from them.

The strongest of the available ones against Gram-negative bacteria is called cecropin B and it has previously been used and found to be competent against multiple bacterial diseases. A study in March of last year looked into genetically engineering a Tarocco blood orange to give it resistance against citrus greening disease. The three cecropin B production genes were synthesized from the Chinese oak silkworm (also known as the tasar moth) genome, along with a separate promoter for them that specifically promotes activation of the gene in phloem tissues, the home of the bacteria in question.

GUS and NptII were used as the selectable antibiotic markers to show success in the transformation and Agrobacterium was chosen as the vector to insert the gene sequences. After transformation, several blotting techniques were used to confirm the insertion of the gene, the production of the peptide protein from the gene, and that that production was only happening in phloem cells.

The results were striking. The peptides were able to strongly reduce infection and growth rates of the bacteria, the first accomplishment ever recorded in dealing with citrus greening disease. The researchers were very happy for the success, as cecropin B had seen variable results in other studies in regards to bacterial resistance, with it doing nothing in tobacco, but it working fine in rice and tomatoes.

They attribute part of their success due to the specific design of their insertion, targeting only the necessary cells, and also having them secret the peptides into the apoplastic space of the cells in the phloem, preventing the bacteria from using proteolytic chemicals against the peptides. Since the aforementioned rice study saw triumph once they had localized the expression to the ER of the cells, the researchers suggest further subcellular localization attempts in the future when using cecropin peptides, as it may improve the changes and efficiency of the peptides in dealing with pathogenic bacteria.

An Orange-Based Defense

Plant phytohormones and other defenses often rely on volatile organic compounds to act as signaling molecules and usually in many other growth and regulation pathways as well. These compounds are characterized by having a low boiling point and are thus prone to vaporization, making them “volatile”. This volatility can be seen in several methyl forms of common acids used as regulators, such as salicylic acid and jasmonic acid.

In addition to these acids are terpenes, which are secondary metabolites that can help with induction of microbial plant defenses. They can also regulate and trigger the above acid pathways and all the proteins that result from those. So it is clear that there is at least some amount of interaction between volatile phytohormones and volatile terpenoids, with citrus plants especially producing high amounts of the latter through their oil-soaked tissues.

Terpenes have already been long known to be antimicrobials and can commonly be found in cleaning supplies. Limonene is one of the more common and creates what is the definitive and characteristic smell of oranges. Among these terpenes, linalool is one that has seen prior research involving antibacterial mechanisms against Xanthomonas citri, which causes citrus canker. It accumulates at high levels in certain citrus plants, like the Ponkan mandarin.

Since citrus canker is such a deadly disease, especially for grapefruit, Mexican lime, and various orange growers, there is a great desire for research into providing linalool resistance into them as well. Thus, in May of last year, scientists in Japan looked into conferring this resistance upon sweet oranges. The priority was to find a way to make a transgenic sweet orange that built up enough linalool in its tissues to be an effective defense.

Hamlin sweet oranges from Florida were used, along with a linalool synthase gene (CuSTS3-1) from the Miyagawawase satsuma mandarin. Overaccumulation of the molecule was confirmed and measured and showed strong resistance generation against citrus canker. The amount of resistance related directly to the amount of linalool that was produced and reached levels equivalent to the original mandarin source.

The scientists found that the concentrations heavily reduced the multiplication rate of the bacteria and, based on how linalool appeared to work in other studies using it in other manners, they hypothesized that it acts as a direct toxin to the bacteria and doubly as a signal molecule for the plant immune system. Thanks to these results, they suggest that more research is done into volatile organic compounds, especially those from citrus plants, which appear to have unique compounds useful against a general range of bacterial infections.

Bringing Heat To The ER

The tools available to biological science today were all derived from nature in some form and fashion. While CRISPR is the most well known for its original function as a bacterial immune defense against viral bacteriophages, the older genetic engineering tools also had a similar origin. One such tool is TALENs, which stands for transcription activator-like effector nucleases. They are capable of cutting up specific parts of DNA due to their restriction enzyme activity.

This tool was derived from TALE, the transcription activator-like effectors obtained from the bacterial genus Xanthomonas You might notice we were just talking about a pathogen species from said genus. These effector proteins make up a large family excreted by the pathogen’s Type III secretion system and have some related groups found throughout the rest of the bacterial kingdom.

The purpose of these TALE proteins is to be injected into the host plant cells, identify their connected effector elements in the plant genome ahead of promoter sequences, and activate those genes. As one might guess, the genes targeted are usually those that make the plants susceptible to pathogen infection. The host plants haven’t taken this lying down though. Over time, breeds with resistance or R genes have evolved to counteract the functions of TALE proteins. Thus far, there have been 3 types of R genes that have been found.

The first is the recessive type, which have mutations in their effector elements ahead of their susceptibility genes, meaning that the TALE proteins can no longer recognize their connection point and turn on those genes. The second is the dominant non-transcriptional-based type, which only one plant in nature has been found to have, the tomato. As a counterpart sequence to two specific TALE genes, this tomato gene is able to activate its resistance function even without the full TALE protein being around, as even the other truncated avirulence form also sets it off.

The final third type is the dominant transcriptional-based R genes, also known as executor R genes. These genes have upstream effectors that purposefully match the sequences the TALE proteins are looking to activate and, upon doing so, these genes create proteins that activate the hypersensitive response system and eventual cell death, depriving the pathogen of its host cell. Since these genes and their defenses are based around effector sequences ahead of the actual gene sequence, they are actually quite easy to swap out with other genes that scientists may want to be activated by TALE proteins. Or, new effector regions could be added or multiple of them in order to increase the number of TALE proteins that will activate the death gene sequences, giving even broader pathogen resistance to the host plant.

When it comes to bacterial blight of rice, it is TALE proteins that Xanthomonas oryzae uses to cause the disease. While rice does have three known executor R genes, they are each attuned to only an individual avirulence TALE gene, though they do offer some amount of protection. Once activated, the protein forms localize themselves to the endoplasmic reticulum (ER) of the cell, where they disrupt its calcium homeostasis, causing cell death.

As a part of their research on both peppers and rice, researchers from Singapore published a study in March of this year. Their original focus was on the two known executor genes found in peppers, one of which, Bs4C-R, appeared to create a protein that has no homology to any other known proteins. This made them unsure on how it functioned in causing cell death. To find out more and to test the cross-species effectiveness of such genes, they decided to transgenically confer the gene and its three protein products onto rice plants. CFP (Cyan Fluorescent Protein) was used as a marker to detect where the proteins localized themselves in the cell.

Upon completing the procedure, they confirmed that the proteins localized themselves to the ER, but did not use the same calcium disruption method the rice executor R proteins did. In fact, the mechanism of action that was used by the pepper R proteins is still unclear. Either way, within 24 hours of purposeful introduction of avirulence pathogen TALEs, the cells had undergone programmed death and the rice plants as a whole exhibited strong resistance to bacterial blight due to this.

Even if more research is needed, the scientists were able to show that transgenic crossing of R genes can be successful at conferring strong pathogen resistance even to very unrelated plant species. By adding more than a single effector element region to the genes, even broader resistance may be possible and provide new options for dealing with disease outbreaks in plants as a whole.

The Wide Span of Bacterial Pathogens

Even from just the few we’ve covered here in this article, I hope it has helped to expand your worldview on what kinds of bacterial pathogens are out there and what they’re capable of. At the same time, the main focus has been on what plants (and scientists) can do to combat those same pathogens and prevent the diseases they cause. The solution isn’t always the same and it is rarely simple, but there are answers out there for any problem.

It’s commonly the task for us humans to find the interactions that exist between different plants, their genomes, and how they deal with bacterial infections. In a way, we can help to bridge the gap between parts of nature and help develop a more full-fledged coterie of plants that can deal with any situation. One issue at a time.


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Photo CCs: Syngonium auritum- Bacterial leaf blight from Wikimedia Commons

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