While investigating some of the research I do in the lab, I came across this article by Dr. Hibbett at Clark University;
Mycorrhizae, the symbiotic associations of plant roots and fungal hyphae, are classic examples of mutualisms. In these ecologically important associations, the fungi derive photosynthetic sugars from their plant hosts, which in turn benefit from fungus-mediated uptake of mineral nutrients. Early views on the evolution of symbioses suggested that all long-term, intimate associations tend to evolve toward mutualism. Following this principle, it has been suggested that mycorrhizal symbioses are the stable derivatives of ancestral antagonistic interactions involving plant parasitic fungi(1). Alternatively, mutualisms have been interpreted as inherently unstable reciprocal parasitisms, which can be disrupted by conflicts of interest among the partners(2-5). To determine the number of origins of mycorrhizae, and to assess their evolutionary stability, it is necessary to understand the phylogenetic relationships of the taxa involved. Here we present a broad phylogenetic analysis of mycorrhizal and free-living homobasidiomycetes (mushroom-forming fungi). Our results indicate that mycorrhizal symbionts with diverse plant hosts have evolved repeatedly from saprotrophic precursors, but also that there have been multiple reversals to a free-living condition. These findings suggest that mycorrhizae are unstable, evolutionarily dynamic associations.
Evolutionary instability of ectomycorrhizal symbioses in basidiomycetes, 2000, Nature 407(6803): 506-508.
I thought this was intriguing because I had assumed that this “avirulence hypothesis” only referred to microbial communities. It was interesting to see the theory pop up in this article, and further more, to be shot down like it was in the microbial community.
Podcast “Bacterial Infection Defy Treatment” 4/16/2010
Look up in the sky!
Ok, so you really can’t see these superbugs but they are everywhere. On science Friday, 4/16/2010, a group of researchers and academics from all over the nation discuss the problems associated with antibiotic resistant. Antibiotic resistant strains, such as MRSA, are prevalent in hospitals. Other strains are beginning to surface such as CDIF, and gram negative bacteria are also becoming a problem as they are becoming increasingly resistant to antibiotic treatment. Many of these bacteria are found everywhere, such as S. aureus found on your skin and in your nose. Douglas Adams might describe these species as “mostly harmless.” So, while they are a natural part of your body’s microbial community, certain strains are lethal if they get a chance to invade. Even pneumonia, caused by a common bacterium, is actually opportunistic when the immune system begins to go down the drain.
MRSA surfaced in 1961 in hospitals and has since become prevalent on large farm feeding operations where antibiotics are administered regularly to the livestock. Being able to combat these superbugs is an ongoing process as adaptation occurs rapidly as it has done so over the past two billion years. One scientist stated that these bacteria won’t ever stop adapting as coexistence was really the thing we as humans must strive for. Of course, the bacteria could care less as their genes continue to mutate. This scientist made no mention of the virulence hypothesis previously mentioned in the last post. (Refresher—it was assumed for a long time that bacteria strive to coexist rather than become more virulent. However, we know today that this is not the case and there is no proof to back this statement up.)
Most interestingly, one woman from New York stated the lack of cleanliness as the main contagion. Doctors, she explains, will wash their hands and then touch the patient’s bedpost before touching the patient. Cleanliness in hospitals is undervalued. Doctors and staff will often forget to wash their hands or come into contact with a fomites or inanimate objects that transfer disease.
So why have pharmaceutical industries not stayed one step ahead of what some consider “microbiotic warfare”? One researcher gives two reasons: economics and statistics. Economics states that there isn’t enough money involved in the production of novel antibiotics to make production worthwhile. Why would pharmaceutical industries produce antibiotics when they could be producing drugs that the client must take long term? It is more financially savvy to produce a drug that must be bought time and time again.
Researchers began to quibble over the best method of antibiotic production. Some feel it should be a non-profit production but details are still as shaky as the legislature behind the actions. Legislature, most of the participants agreed, tended to be slow on the uptake, and does not respond to scientific findings as quickly as one would like. So making certain practices “legislative practices” leaves the door shut to potential novelties.
Aside from cleanliness, the participants describe how there are many new methods in curing these superbugs that have yet to be discovered. One such method are plaques. Still, the best method is the preventative method. This means, in many cases, feeling empowered to ask the doctor to wash their hands before touching you. In Norway, one woman who called in explained, they prevented the spread of MRSA by going directly to the source and eradicating it.
Alizon et al. in their review “Virulence evolution and the trade-off hypothesis: history, current state of affairs and the future” investigate the problems associated with the trade-off hypothesis in measuring and quanitfying factors such as virulence (and various definitions). Below is a outline of the history of virulence.
History of virulence
Pasteur and Koch (1881) looked into parasite virulence but this data was overlooked–concept of strain specific virulence.
After Pasteur’s experiment, the avirulence hypothesis was formed along with other theories to explain parasite virulence
Topley (1919) hypothesized that populations in high density had a greater propensity to replicate and migrate more rapidly.
Kostitzin (1934) challenges avirulence hypothesis, stating that virulence may occur from a completely mutualistic interaction.
Ball (1943) old host-parasite interactions are still virulenty
G C Williams, J Maynard Smith, and W. D. Hamilton (1960/1970) field of evolutionary ecology founded
Hamilton (1964) challenged avirulence hypothesis
Levin and Pimentel (1981) evidence that virulent and avirulent strains can coexist
May and Anderson (1983) avirulence hypothesis which was universally accepted although there was lack of evidence due to the fact that old host-parasite associations do not tend to be virulent. May and Anderson found a connection between recovery and virulence.
Ewald (1983) virulence depends on how the mechanism is transmitted.
So, the long accepted “common knowledge” avirulent hyypothesis went down the drain as lack of evidence supported the trade-off hypothesis. The trade-off hypothesis basically states simply that more transmissible parasite strains must remain with the host for a longer period of time. In the abstract, Alizon states that “the trade-off hypothesis states that virulence is an unavoidable consequence of parasite transmission.”
There is a lack of evidence for the trade-off hypothesis which is one reason why it is increasily challenged. However, on the same note, the authors argue that lack of evidence is often times not due to lack of study. Rather, investigations that fail to see a significant trend are not published. Furthermore, defining virulence in its most crude state is also a debate among biologists. Many factors are involved and the trade-off hypothesis may be “too simple” to encompass virulence. Indeed, the trade-offs that exist may not be the trade-offs that are “usually assumed.”
Ultimately, Alizon et. al argue that although this statement may be considered a sweeping generlization for parasites, it is an important theory for predicting virulence.
If you’re going to cheat, you have to do it right. Cheating is a problem for any social system, Velicer explains in his article “Developmental cheating in the social bacterium Myxococcus xanthus.” Cheating isn’t something new to just bacteria. Ectomycorrhizal fungi, for example, assist trees in nutrient uptake but often “cheaters” or saprotrophic fungi take advantage of the relationship (Mayor, Elucidating the nutritional dynamics of fungi using stable isotopes 2008). Likewise, lightening bugs fluoresce in such a way to attract a female. Some lightening bugs take advantage of this signal and flash a deceptive signal. The male, thinking he has attracted the eye of a female, is led into a trap and eaten by the predator species.
M. xanthus is a type of microbe that lives in soil and exhibits both adventurous and social behavior. Social behavior involves cooperative behavior among the clones and while some may not win out in the end, they aid in the common good. In this case, being the only cheater in a band of cooperators seems to be the way to go.
Six strains originated from the original ancestor, DK1622. The strains were evolved for 1,000 generations from the original where the microbe was unable to exhibit social behavior. The ability to sporulate and its efficiency in sporulation then reflects its ability to potentially cheat.
H1 states that “defective strain may sporulate with the same efficiency as it does in the pure culture” and H2 states that “an evolved clone behaves as would a neutrally marked variant of the wildtype.” In both cases, the null hypothesis is rejected. Three cheaters appeared, GVB2063, GVB2083, and GVB143. When the evolved clones were mixed at low concentrations with the wildtype, they fared better than expected than on pure agar, where they exhibited defects in sporulation. As the mixing ratio went up, and the cheaters became more common, the sporulation efficiency went down. Also, cheaters that are not as “bad” as other cheaters tended to have more success at higher mixing ratios than those that were obligate cheaters. Being a cheater is effective but it also has some cost since cheaters harm the whole.
This experiment ultimately tested to see if variability amongst colonies could exist and if cheaters would contribute to the population. Velicer argues that, through this research, M. xanthus probably does has a low subpopulation of known cheaters in vivo.
I am most interested in the way in which this microbe might try to combat the cheaters. What kind of “policing mechanisms” would prevent cheaters from entering into a population? Furthermore, how can a reproductive cycle be unfavorable to a cheater? Can the bacteria develop some sort of allopathic technique to dissuade a strain so similar to their own? Velicer only mentions these techniques but does not go into detail. What kind of genotype would a wildtype strain have to have in order to repress these known cheaters? However, at the same time, would it be worth the extra effort to repress a subpopulation that does not threaten to take over the population? Basically, is it worth it to throw a microbe out of your game just because they don’t play nice?
Researchers in New Zealand investigate the evolution of sex based on different fitness habitats. The relationship between genotype and fitness is known as the fitness landscape.
These researchers investigated three types of fitness landscapes, smooth random, and NK (rugged landscape). Using computer simulations, they found that the evolution of sex is different for different landscapes. They also describe the difficulty of predicting the evolution of sex experimentally which leads to a vast number of theories as to “why sex?” The authors state that there is a two-fold cost to sex and their models attempt to predict when sex will be beneificial and when it will not be.
Several theories come into play; The Red Queen Hypothesis, Fisher Muller, Hill Robertson (identically to Fisher Muller), and Mutational Deterministic Hypothesis. Fisher-Muller states that sex is advantageous because “it allows for beneficial mutations that arise in different lineages to recombine, thereby reducing clonal interferences and speeding up adaptation (Cooper 2007).” The Red Queen Hypothesis however describes an arms race between individuals. The latter hypothesis assumes that the deleterious genes are only slightly deleterious and adding a mutation has a great effect. This is known as synergistic epistatis.
For the record, the Red Queen’s Race actually took place in Lewis Carroll’s book “Through the Looking Glass” not Alice in Wonderland. These two books are known collectively as the Annotated Alice despite what Hollywood and Tim Burton might believe.
With all these theories in mind, it seems almost impossible to test theoretically or experimentally. I am curious to know whether there is a true theory to back up the mystery of sexual evolution. Could it be at all these theories can come into play? Are some organisms driven by one theory, such as the Red Queen Hypothesis, while other organisms conform to the Mutualistic determinism theory, or is there one simple overall “answer” that describes why sex evolved countless times in very different organisms. Or can all these theories play a small role in sex evolution?
Researchers studying tripartite mutualism in ant species at the University of Wisconsin found in vitro antagonistic reactions between the actinobacteria and cultivar fungus while in vivo reactions were less understood. Fungus was paired with a specific strain of the bacteria and interactions were measured through biomass inhibition/accumulation. Although in vivo results yielded less conclusive data, Acromyrmex sp. preferentially chose and recognized their indigent Pseudonocardia.
Mutualistic symbiosis is an important ecological concept since the evolution of one organism is mutually dependent on the evolution of another. This may also be true in predator-prey relations as well. The tripartite relationship between ants, fungus, and bacteria was thought to have originated 50 million years ago. Ants cultivate the fungus for food and supply it with the necessary nutrients. This fungus, often specific to the ant colony, is hosts to a number of species of bacteria in the genus Escovopsis. Ants developed a way to combat the antifungal microbe by producing the bacteria Pseudonocardia. This bacteria, found on cuticle of the worker ants and the queen, produces secondary metabolites that exhibit antibiotic resistance to Escovopsis. Ants typically house a monoculture of the Pseudonocardia bacteria and a monoculture of the fungus. When new strains are introduced to the specific fungus (horizontal transmission), inhibitory growth responses may occur. Antagonism between the two species yields less biomass in some cases. Strains are typically introduced vertically from parents to offspring. The combination of the ant and the cultivar fungus could indeed impact the survival of the ant colony. This study observed the ant colonies in vitro through sub colonization. Sub colonies began collapsing after three weeks due to time rather than do to the secondary metabolites produced by the host’s microbial symbiont. The extent of the in vivo impacts was harder to determine and there was no direct negative impact. This result may have been do to a number of factors, such a the location separation between the cultivar and the bacteria. More work needs to be done on the in vivo results to draw a better conclusion.
What can this article tell us about the species definition in co-evolution? Different strains of bacteria are competing against each other and ants are associated typically with few or only one strain of bacteria and one cultivar. Does this make each strain a different species due to antagonism responses within what are considered mutual symbionts? Interestingly, in the article, the author mentions that the fungal cultivar “defends its monopoly by imprinting ant fecal droplets with incompatibility compounds that aid in the detection of non-native fungal strains” (Poulsen 2010).
The question “why do species definitions matter in light of your favorite microbe or microbiological issue?” interests me since we have yet to discuss the importance of the co-evolution of species. It seems that we were always asking, “what makes a species a species?” Physiologically, these species are similar and a few genetic mutations are the only difference between what wins out in the end. The line is harder to distinguish than eukaryotic organisms and at what point are you able to draw the line? Even the fungus cultivar behaves similarly and excludes related fungus from the nest.
It seems that trying to phylogenetically classify bacterial species might be a lost cause since there is too much grey. As humans, we attempt to classify everything to make order out of chaos. As sentient beings, we must philosophize and attempt to create a bridge from the known to the unknown but perhaps there is no way to fully classify certain organisms. Can we accept that the difference between a species and an ecotype is less cut and dry than we’d originally like it to be? It is easy to expect a dualism between all things but can we always make things so cut and dry? Download
Previously, I had defined a species in terms of the ability to reproduce. However, the eukaryotic definition will not hold true for prokaryotes and researchers are left with interpreting the jargon left after millions upon millions of years of evolution through mutations and horizontal gene transfer (HGT). Hanage, et al. tested several isolates of the Neisseria bacteria: N. meningitides, N. lactamica, and N. gonorrhoeae. What they found ultimately was some “fuzz to the puzz” and delineating between species was almost as good as a guessing game.
A bacterial species has apparently plagued systematists for a long while. Hanage goes on to explain that attempts to define species by DNA extraction have been somewhat futile. Using a multilocus approach may be the best method for resolution. Some labs, however, are using a DNA-DNA hybridization approach as the gold standard, a method which still has its own quarks. The multilocus sequence approach, known as MLST (multilocus sequence typing) may not be so good for highly recombinogenic bacteria but may serve its purpose in the ability to draw the line between distinct species.
So is there such thing as a universal species? What evidence do we have for or against this concept? Ben Stiller once said something along the lines of “if we take away all our differences, we’re really all the same.” How can this line, with Ben Stiller’s infinite wisdom, affect the universal species law? What would you have to take away from the bacteria in order to create a universal species and at what point is it not like the other? The line is becoming more arbitrary once phenotype is taken out of the equation.
In class, we talked about adaptations and different means in which to measure it. We saw that adaptation would increase logarithmically and ultimately would plateau after a certain number of generations. How many generations and the extent of the exponential growth were determined by the environment. I am curious to know if genetic load plays the same role as genetic load in say, a plant. Plants that have a low genetic load run less risk of homozygous mutations or “bad” mutations and may continue to propagate through selfing or apomixes. Plants that have a high genetic load tend to have defenses against self-fertilization, such as preventing pollen tube formation by species with genomes too similar to their own, dioeciously, or even separating the pollen grain from the pistil through space or time. A plant may exhibit any multitude of preventative measures from self-fertilization. To draw a comparison, the genetic load of a bacterium is much smaller. Is there a limit to the number of mutations it can really attain?
Researchers Whitaker, Grogan, and Taylor tested the Sulfolobus species, an extremophile bacteria growing in hot springs. Hot springs located around the world included Mutnovsky, Uzon Caldera, Geyser Valley, Brokeoff Caldera, Devil’s Kitchen, Norris Geyser Basin, and Geyser Creek. Segments from the bacteria were sequenced at nine loci and AMOVA was used to group the strains regionally and to test for possible population structure. What Whitaker, et al. ultimately found was that these strains were grouped base on locale rather than through environmental selection. The Baas-Becking Hypothesis, which states; everything is everywhere, the environment selects, would have been hard pressed to interpret the findings otherwise. It had long been accepted that bacteria, unlike other kingdoms, were limited by environmental conditions rather than dispersal method. This was due, in part, to their small size, ubiquity, and large metabolic capacity. Had the Baas-Becking Hypothesis been supported, researchers would have found genetic differences based on hot spring character such as pH, temperature, and nutrient availability. Because the hot spring environment is rare, bacteria are limited based on dispersal, in some cases they are isolated. These findings muddle the Baas-Becking Hypothesis while at the same time, shedding light on microbial biodiversity.
A variety of methods could have been used to improve and strengthen the study’s findings. Testing more hot springs, sequencing different loci on the genome, and more characteristics about the hot spring (e. g. elevation and size) would all contribute to a stronger statistical test. The genes sequenced in this study were not as involved in cellular processes, nicknamed “boring genes.” Looking at a greater abundance of genes necessary for survival in this extreme environment may lead to greater understanding of the biodiversity within regions or through hot spring characteristic.
Using extremophiles is an extreme example used to call into question the merits of the Baas-Becking Hypothesis. Are these two approaches black and white or is there some grey? Are most microbes disperse limited or is this a trend only found in extreme environments?
The Baas-Becking Hypothesis was a vague concept when first presented in class. Originally I had translated it as everything has the capacity to live everywhere, but environmental conditions and competition will decide who “takes the cake.” It seems that with any organism, there is still a limit to the species richness within an environment. Can there be infinite bacterial species in a given niche if the environment allows? Despite their small size, bacteria should still be space limited if this were the case. Likewise, dispersal limitation would depend on the type of bacteria. Choosing an extreme bacterium such as Sulfolobus to prove a dispersal limitation seems a little like choosing Hitler to disprove the merits of communism. If a more common strain of E. coli was examined in depth, would there be any trends between geographic locations? How does the heterogeneity of the environment play a role in the selection of the organism? More insight into the study will lead to better questions and hopefully to better answers into microbial population dispersal and ecology.
Whitaker, et al. Geographic Barriers Isolate Endemic Population of Hyperthermophilic Archaea. Science Magazine 2003
This is my New Post. I’m Rachel. Looking forward to a great last semester.
More about me per request!
I am a super senior, therefore I save old ladies from crossing the street at the wrong time, I pull cats out of trees, breath fire, and can unscramble an egg. The merits of being a super senior.
I am a General Biology and a Classics major. Currently I am finishing up the my Biology major and this course is a requirement. Otherwise, I enjoy being active, hanging out with friends, long walks on the beach, etc. I am hoping to be involved with plant biology in the future.
