Bacteriophage experimental evolution: Difference between revisions
imported>John J. Dennehy No edit summary |
mNo edit summary |
||
| (20 intermediate revisions by 7 users not shown) | |||
| Line 1: | Line 1: | ||
{{subpages}} | |||
[[Experimental evolution]] studies are a means of testing [[evolution]]ary theory under carefully designed, reproducible experiments. Although theoretically any organism could be used for experimental evolution studies, those with rapid [[generation time]]s, high [[mutation rate]]s, large [[population size]]s, and small sizes increase the feasibility of experimental studies in a laboratory context. For these reasons, [[bacteriophage]]s (i.e. [[virus]]es that infect [[bacteria]]) are especially favored by experimental evolutionary biologists. Bacteriophages, and microbial organisms, can be frozen in stasis, facilitating comparison of evolved strains to ancestors. Additionally, microbes are especially labile from a molecular biologic perspective. Many [[molecular tool]]s have been developed to manipulate the [[genetic material]] of microbial organisms, and because of their small [[genome]] sizes, [[sequencing]] the full genomes of evolved strains is trivial. Therefore, comparisons can be made for the exact molecular changes in evolved strains during [[adaptation]] to novel conditions. This article explains how such experiments are conducted, and contains annotated references for [[experimental evolution]] studies conducted with bacteriophages, as well as an expansion of a table presented by Breitbart et al. (2005). | |||
= Experimental studies, by category = | == Experimental studies, by category == | ||
== Laboratory [[phylogenetics]] == | === Laboratory [[phylogenetics]] === | ||
Phylogenetics is the study of the evolutionary relatedness of organisms. Laboratory phylogenetics is the study of the evolutionary relatedness of laboratory-evolved organisms. | Phylogenetics is the study of the evolutionary relatedness of organisms. Laboratory phylogenetics is the study of the evolutionary relatedness of laboratory-evolved organisms. An advantage of laboratory phylogenetics is the exact evolutionary history of an organism is known, rather than estimated as is the case for most organisms. | ||
=== [[Epistasis]] === | |||
Epistasis is the dependence of the effect of one [[gene]] or [[mutation]] on the presence of another gene or mutation. Theoretically epistasis can be of three forms: no epistasis (additive inheritance), synergystic (or positive) epistasis and antagonistic (or negative) epistasis. In synergystic epistasis, each additional mutation has increasing negative impact on [[fitness]]. In antagonistic epistasis, the effect of each mutation declines with increasing numbers of mutation. Understanding whether the majority of genetic interactions are synergistic or antagonistic will help solve such problems as the [[evolution of sex]]. | |||
Epistasis is the dependence of the effect of one [[gene]] or [[mutation]] on the presence of another gene or mutation. | |||
The phage literature provides many examples of epistasis which are not studied under the context of experimental evolution nor necessarily described as examples of epistasis. | The phage literature provides many examples of epistasis which are not studied under the context of experimental evolution nor necessarily described as examples of epistasis. | ||
== [[Experimental adaptation]] == | === [[Experimental adaptation]] === | ||
Experimental adaptation involves [[selection]] of [[organisms]] either for specific [[traits]] or under specific conditions. For example, strains could be evolved under conditions of high temperatures to observe the molecular changes that facilitate survival and [[reproduction]] under those conditions. | |||
The reader should be aware that numerous phage experimental adaptations were performed in the early decades of phage study. | The reader should be aware that numerous phage experimental adaptations were performed in the early decades of phage study. | ||
=== [[Adaptation]] to usual [[hosts]]. = | ==== [[Adaptation]] to usual [[hosts]]. ==== | ||
==== Adaptation to new or modified hosts. ==== | |||
The older phage literature, e.g., pre-1950s, contains numerous examples of phage adaptations to different hosts. | The older phage literature, e.g., pre-1950s, contains numerous examples of phage adaptations to different hosts. | ||
=== Adaptation to modified conditions === | ==== Adaptation to modified conditions ==== | ||
The older phage literature, e.g., pre-1950s, also contains examples of phage adaptations to different [[culture conditions]], such as [[phage T2]] adaptation to low salt conditions. | The older phage literature, e.g., pre-1950s, also contains examples of phage adaptations to different [[culture conditions]], such as [[phage T2]] adaptation to low salt conditions. | ||
=== Adaptation to high temperatures. === | ==== Adaptation to high temperatures. ==== | ||
==== Adaptation as compensation for [[deleterious mutations]]. ==== | |||
There are many examples in the early phage literature of phage adapting and compensating for deleterious mutations. | There are many examples in the early phage literature of phage adapting and compensating for deleterious mutations. | ||
=== Adaptation as toward change in phage [[virulence]] === | ==== Adaptation as toward change in phage [[virulence]] ==== | ||
Virulence is the negative impact that a [[pathogen]] (or [[parasite]]) has on the [[Darwinian fitness]] of a harboring organism (host). For phage, virulence results either in reduction of bacterial division rates or, more typically, in the death (via [[lysis]]) of individual bacteria. A number of theory papers exist on this subject, especially as it applies to the evolution of phage latent period | Virulence is the negative impact that a [[pathogen]] (or [[parasite]]) has on the [[Darwinian fitness]] of a harboring organism (host). For phage, virulence results either in reduction of bacterial division rates or, more typically, in the death (via [[lysis]]) of individual bacteria. A number of theory papers exist on this subject, especially as it applies to the evolution of phage [[latent period]]. | ||
The older phage literature contains numerous references to phage virulence, and phage virulence evolution. However, the reader should be warned that virulence is often used as a synonym for "not temperature", a usage which is neither employed here nor to be encouraged generally. | The older phage literature contains numerous references to phage virulence, and phage virulence evolution. However, the reader should be warned that virulence is often used as a synonym for "not temperature", a usage which is neither employed here nor to be encouraged generally. | ||
== Impact of [[sex]]/[[coinfection]] == | === Impact of [[sex]]/[[coinfection]] === | ||
More than one phage can [[coinfect]] the same bacterial cell. When this happens, the phage can exchange genes, which is equivalent to "sex." Note that a number of the immediately following studies employ sex to overcome [[Muller's ratchet]] while papers that demonstrate Muller's ratchet (i.e., without employing sex to overcome the result) are instead presented under that heading. | More than one phage can [[coinfect]] the same bacterial cell. When this happens, the phage can exchange genes, which is equivalent to "sex." Note that a number of the immediately following studies employ sex to overcome [[Muller's ratchet]] while papers that demonstrate Muller's ratchet (i.e., without employing sex to overcome the result) are instead presented under that heading. | ||
=== Muller’s ratchet === | |||
Muller’s ratchet is the gradual, but irreversible accumulation of deleterious mutations in [[asexual organisms]]. [[Asexual]] organisms do not undergo gene exchange and therefore can't recreate mutation-free genomes. Chao, 1997, provides a phage-emphasizing review of the subject. | |||
=== [[Prisoner’s dilemma]] === | |||
Prisoner's dilemma is a part of [[game theory]] which involves two individuals choosing to [[cooperate]] or [[defect]], reaping differential rewards. During phage coinfection, it pertains to viruses which produce more [[protein]] products than they use (cooperators) and viruses which use more [[protein]] products than they produce (defectors). | |||
== | === Coevolution === | ||
== | |||
[[Coevolution]] is the study of the evolutionary influence that two [[species]] have upon each other. Phage-bacterial coevolution is typically studied within the context of [[phage community ecololgy]]. | [[Coevolution]] is the study of the evolutionary influence that two [[species]] have upon each other. Phage-bacterial coevolution is typically studied within the context of [[phage community ecololgy]]. | ||
== Historical considerations == | == Historical considerations == | ||
| Line 145: | Line 59: | ||
The following is quoted from [[d'Hérelle]] and Smith, 1924. | The following is quoted from [[d'Hérelle]] and Smith, 1924. | ||
ADAPTATION AND THE BACTERIOPHAGE | |||
{{Quotation|All authors admit that the virulence of the bacteriophage may increase for a given bacterium, or that it may diminish, according to the condition of the moment. This is then a phenomenon of adaptation analogous to that observed with all [[parasite]]s.}} | |||
{{Quotation|The fact of [[attenuation]] and of exaltation of virulence is sufficient by itself to show that the bacteriophage is an autonomous parasite. Certain authors ([[Seiffert]]) while admitting the fact, have tried to maintain that it is not the bateriophage which adapts itself, but rather the bacterium. An obvious reply would be that it is not the bacterium with which the passages are made, since each passage involves the action of the filtrate of a preceding lysed culture upon a fresh normal suspension of bacteria. By virtue of the fact that only the filtrate is concerned in the passages the adaptation must be something which is found in the filtrate.}} | |||
{{Quotation|But this is not all. It is certain that the bacterium, which is also a living being, must react, must likewise undergo adaptation. Constant experience shows that this is just what happens, but the adaptation which takes place, far from tending toward a destructive action, as would be the case if the bacterium adapted itself to the secretion of a lytic substance, reacts against the bacteriophage by a process of adaptation tending to hinder the action of the bacteriophage. The bacterium acquires a [[resistance]]. This resistance may, indeed, reach to a completely refractory condition, and, in such a case, it is the bacterium which destroys the bacteriophage (d'Herelle, Flu).}} | |||
{{Quotation|The bacteriophage adapts itself to a more and more vigorous attack against the bacterium, and the bacterium accustoms itself to resist this attack. Considering only experimental facts this is clearly evident when no pretense is made to interpret these facts to make them fit into a preconceived theoretical scheme.}} | |||
{{Quotation|But there are still other points. The bacteriophage adapts itself to harmful effects of the medium. I have shown that the bacteriophage can gradually adapt itself to the harmful action of [[glycerol]] and of [[acids]]. Asheshov has habituated a bacteriophage, originally unable to effect bacteriophagy in an acid medium, to act very strongly after a number of passages in a medium of increasing [[acid]]ity. Wolff and Janzen have succeeded in adapting it to different antiseptics.}} | |||
{{Quotation|We have already seen that the bacteriophage functions as an [[antigen]] and that the [[serum]] of an animal which has received serial injections of a bacteriophage possesses the property of inhibiting bacteriophagous actions. Prausnitz has shown further that it is possible to adapt the bacteriophage to resist the inhibiting action of an [[antiserum]]. Once this adaptation is accomplished bacteriophagy takes place in any quantity of antiserium, although prior to the adaptation, an amount of a thousandth of a cubic centimeter or even less paralyzed bacteriophagy completely.}} | |||
{{Quotation|The proofs are then multiple: The bacteriophage possesses the power of adaptation. We have seen that it also possesses that of assimilation. It possesses likewise the two corollaries of these powers; the faculties of multiplication and variability as everyone admits. (pp. 267-268)}} | |||
{{Quotation|The bacteriophagous corpuscles are endowed with the powers of assimilation and adaptation, the faculties of multiplication and of variation. They are this necessarily living beings since they possess all of the characteristics of other living things.}} | |||
{{Quotation|A single bacteriophage is usually virulent, at the same time, for a certain number of bacterial species. This virulence is variable and is subject to increase or attenuation. Increase may always be secured [[in vitro]] by the method of passages at the expense of the bacterium for which it is desired to increase the virulence.}} | |||
{{Quotation|The bacterium does not remain passive before the attack of the bacteriophage. It is capable of resistance. It is even able, when the conditions for it are favorable, to acquire a complete [[immunity]]. (pp. 269-270)}} | |||
== References == | == References == | ||
| Line 176: | Line 75: | ||
Breitbart, M., F. Rohwer, and S. T. Abedon. 2005. Phage ecology and bacterial pathogenesis, p. 66-91. In M. K. Waldor, D. I. Friedman, and S. L. Adhya (eds.), Phages: Their Role in Bacterial Pathogenesis and Biotechnology. ASM Press, Washington DC. ISBN 1-55581-307-0 | Breitbart, M., F. Rohwer, and S. T. Abedon. 2005. Phage ecology and bacterial pathogenesis, p. 66-91. In M. K. Waldor, D. I. Friedman, and S. L. Adhya (eds.), Phages: Their Role in Bacterial Pathogenesis and Biotechnology. ASM Press, Washington DC. ISBN 1-55581-307-0 | ||
d'Hérelle, F., and G. H. Smith. 1924. Immunity in Natural Infectious Disease. Williams & Wilkins Co., Baltimore. | d'Hérelle, F., and G. H. Smith. 1924. Immunity in Natural Infectious Disease. Williams & Wilkins Co., Baltimore.[[Category:Suggestion Bot Tag]] | ||
Latest revision as of 16:01, 15 July 2024
Experimental evolution studies are a means of testing evolutionary theory under carefully designed, reproducible experiments. Although theoretically any organism could be used for experimental evolution studies, those with rapid generation times, high mutation rates, large population sizes, and small sizes increase the feasibility of experimental studies in a laboratory context. For these reasons, bacteriophages (i.e. viruses that infect bacteria) are especially favored by experimental evolutionary biologists. Bacteriophages, and microbial organisms, can be frozen in stasis, facilitating comparison of evolved strains to ancestors. Additionally, microbes are especially labile from a molecular biologic perspective. Many molecular tools have been developed to manipulate the genetic material of microbial organisms, and because of their small genome sizes, sequencing the full genomes of evolved strains is trivial. Therefore, comparisons can be made for the exact molecular changes in evolved strains during adaptation to novel conditions. This article explains how such experiments are conducted, and contains annotated references for experimental evolution studies conducted with bacteriophages, as well as an expansion of a table presented by Breitbart et al. (2005).
Experimental studies, by category
Laboratory phylogenetics
Phylogenetics is the study of the evolutionary relatedness of organisms. Laboratory phylogenetics is the study of the evolutionary relatedness of laboratory-evolved organisms. An advantage of laboratory phylogenetics is the exact evolutionary history of an organism is known, rather than estimated as is the case for most organisms.
Epistasis
Epistasis is the dependence of the effect of one gene or mutation on the presence of another gene or mutation. Theoretically epistasis can be of three forms: no epistasis (additive inheritance), synergystic (or positive) epistasis and antagonistic (or negative) epistasis. In synergystic epistasis, each additional mutation has increasing negative impact on fitness. In antagonistic epistasis, the effect of each mutation declines with increasing numbers of mutation. Understanding whether the majority of genetic interactions are synergistic or antagonistic will help solve such problems as the evolution of sex.
The phage literature provides many examples of epistasis which are not studied under the context of experimental evolution nor necessarily described as examples of epistasis.
Experimental adaptation
Experimental adaptation involves selection of organisms either for specific traits or under specific conditions. For example, strains could be evolved under conditions of high temperatures to observe the molecular changes that facilitate survival and reproduction under those conditions.
The reader should be aware that numerous phage experimental adaptations were performed in the early decades of phage study.
Adaptation to usual hosts.
Adaptation to new or modified hosts.
The older phage literature, e.g., pre-1950s, contains numerous examples of phage adaptations to different hosts.
Adaptation to modified conditions
The older phage literature, e.g., pre-1950s, also contains examples of phage adaptations to different culture conditions, such as phage T2 adaptation to low salt conditions.
Adaptation to high temperatures.
Adaptation as compensation for deleterious mutations.
There are many examples in the early phage literature of phage adapting and compensating for deleterious mutations.
Adaptation as toward change in phage virulence
Virulence is the negative impact that a pathogen (or parasite) has on the Darwinian fitness of a harboring organism (host). For phage, virulence results either in reduction of bacterial division rates or, more typically, in the death (via lysis) of individual bacteria. A number of theory papers exist on this subject, especially as it applies to the evolution of phage latent period.
The older phage literature contains numerous references to phage virulence, and phage virulence evolution. However, the reader should be warned that virulence is often used as a synonym for "not temperature", a usage which is neither employed here nor to be encouraged generally.
Impact of sex/coinfection
More than one phage can coinfect the same bacterial cell. When this happens, the phage can exchange genes, which is equivalent to "sex." Note that a number of the immediately following studies employ sex to overcome Muller's ratchet while papers that demonstrate Muller's ratchet (i.e., without employing sex to overcome the result) are instead presented under that heading.
Muller’s ratchet
Muller’s ratchet is the gradual, but irreversible accumulation of deleterious mutations in asexual organisms. Asexual organisms do not undergo gene exchange and therefore can't recreate mutation-free genomes. Chao, 1997, provides a phage-emphasizing review of the subject.
Prisoner’s dilemma
Prisoner's dilemma is a part of game theory which involves two individuals choosing to cooperate or defect, reaping differential rewards. During phage coinfection, it pertains to viruses which produce more protein products than they use (cooperators) and viruses which use more protein products than they produce (defectors).
Coevolution
Coevolution is the study of the evolutionary influence that two species have upon each other. Phage-bacterial coevolution is typically studied within the context of phage community ecololgy.
Historical considerations
The following is quoted from d'Hérelle and Smith, 1924.
ADAPTATION AND THE BACTERIOPHAGE
All authors admit that the virulence of the bacteriophage may increase for a given bacterium, or that it may diminish, according to the condition of the moment. This is then a phenomenon of adaptation analogous to that observed with all parasites.
The fact of attenuation and of exaltation of virulence is sufficient by itself to show that the bacteriophage is an autonomous parasite. Certain authors (Seiffert) while admitting the fact, have tried to maintain that it is not the bateriophage which adapts itself, but rather the bacterium. An obvious reply would be that it is not the bacterium with which the passages are made, since each passage involves the action of the filtrate of a preceding lysed culture upon a fresh normal suspension of bacteria. By virtue of the fact that only the filtrate is concerned in the passages the adaptation must be something which is found in the filtrate.
But this is not all. It is certain that the bacterium, which is also a living being, must react, must likewise undergo adaptation. Constant experience shows that this is just what happens, but the adaptation which takes place, far from tending toward a destructive action, as would be the case if the bacterium adapted itself to the secretion of a lytic substance, reacts against the bacteriophage by a process of adaptation tending to hinder the action of the bacteriophage. The bacterium acquires a resistance. This resistance may, indeed, reach to a completely refractory condition, and, in such a case, it is the bacterium which destroys the bacteriophage (d'Herelle, Flu).
The bacteriophage adapts itself to a more and more vigorous attack against the bacterium, and the bacterium accustoms itself to resist this attack. Considering only experimental facts this is clearly evident when no pretense is made to interpret these facts to make them fit into a preconceived theoretical scheme.
But there are still other points. The bacteriophage adapts itself to harmful effects of the medium. I have shown that the bacteriophage can gradually adapt itself to the harmful action of glycerol and of acids. Asheshov has habituated a bacteriophage, originally unable to effect bacteriophagy in an acid medium, to act very strongly after a number of passages in a medium of increasing acidity. Wolff and Janzen have succeeded in adapting it to different antiseptics.
We have already seen that the bacteriophage functions as an antigen and that the serum of an animal which has received serial injections of a bacteriophage possesses the property of inhibiting bacteriophagous actions. Prausnitz has shown further that it is possible to adapt the bacteriophage to resist the inhibiting action of an antiserum. Once this adaptation is accomplished bacteriophagy takes place in any quantity of antiserium, although prior to the adaptation, an amount of a thousandth of a cubic centimeter or even less paralyzed bacteriophagy completely.
The proofs are then multiple: The bacteriophage possesses the power of adaptation. We have seen that it also possesses that of assimilation. It possesses likewise the two corollaries of these powers; the faculties of multiplication and variability as everyone admits. (pp. 267-268)
The bacteriophagous corpuscles are endowed with the powers of assimilation and adaptation, the faculties of multiplication and of variation. They are this necessarily living beings since they possess all of the characteristics of other living things.
A single bacteriophage is usually virulent, at the same time, for a certain number of bacterial species. This virulence is variable and is subject to increase or attenuation. Increase may always be secured in vitro by the method of passages at the expense of the bacterium for which it is desired to increase the virulence.
The bacterium does not remain passive before the attack of the bacteriophage. It is capable of resistance. It is even able, when the conditions for it are favorable, to acquire a complete immunity. (pp. 269-270)
References
Breitbart, M., F. Rohwer, and S. T. Abedon. 2005. Phage ecology and bacterial pathogenesis, p. 66-91. In M. K. Waldor, D. I. Friedman, and S. L. Adhya (eds.), Phages: Their Role in Bacterial Pathogenesis and Biotechnology. ASM Press, Washington DC. ISBN 1-55581-307-0
d'Hérelle, F., and G. H. Smith. 1924. Immunity in Natural Infectious Disease. Williams & Wilkins Co., Baltimore.