The evolution of spectrum in antibiotics and bacteriocins
A key property of many antibiotics is that they will kill or inhibit a diverse range of microbial species. This broad-spectrum of activity has its evolutionary roots in ecological competition, whereby bacteria and other microbes use antibiotics to suppress other strains and species. However, many ba...
| Main Authors: | , |
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| Format: | Journal article |
| Language: | English |
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National Academy of Sciences
2022
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| _version_ | 1826308941382942720 |
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| author | Palmer, JD Foster, KR |
| author_facet | Palmer, JD Foster, KR |
| author_sort | Palmer, JD |
| collection | OXFORD |
| description | A key property of many antibiotics is that they will kill or inhibit a diverse range of microbial species. This broad-spectrum of activity has its evolutionary roots in ecological competition, whereby bacteria and other microbes use antibiotics to suppress other strains and species. However, many bacteria also use narrow-spectrum toxins, such as bacteriocins, that principally target conspecifics. Why has such a diversity in spectrum evolved? Here, we develop an evolutionary model to understand antimicrobial spectrum. Our first model recapitulates the intuition that broad-spectrum is best, because it enables a microbe to kill a wider diversity of competitors. However, this model neglects an important property of antimicrobials: They are commonly bound, sequestered, or degraded by the cells they target. Incorporating this toxin loss reveals a major advantage to narrow-spectrum toxins: They target the strongest ecological competitor and avoid being used up on less important species. Why then would broad-spectrum toxins ever evolve? Our model predicts that broad-spectrum toxins will be favored by natural selection if a strain is highly abundant and can overpower both its key competitor and other species. We test this prediction by compiling and analyzing a database of the regulation and spectrum of toxins used in inter-bacterial competition. This analysis reveals a strong association between broad-spectrum toxins and density-dependent regulation, indicating that they are indeed used when strains are abundant. Our work provides a rationale for why bacteria commonly evolve narrow-spectrum toxins such as bacteriocins and suggests that the evolution of antibiotics proper is a signature of ecological dominance. |
| first_indexed | 2024-03-07T07:26:49Z |
| format | Journal article |
| id | oxford-uuid:0da1288a-971d-4b8d-ad30-c7f708af3112 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T07:26:49Z |
| publishDate | 2022 |
| publisher | National Academy of Sciences |
| record_format | dspace |
| spelling | oxford-uuid:0da1288a-971d-4b8d-ad30-c7f708af31122022-12-02T16:52:32ZThe evolution of spectrum in antibiotics and bacteriocinsJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:0da1288a-971d-4b8d-ad30-c7f708af3112EnglishSymplectic ElementsNational Academy of Sciences2022Palmer, JDFoster, KRA key property of many antibiotics is that they will kill or inhibit a diverse range of microbial species. This broad-spectrum of activity has its evolutionary roots in ecological competition, whereby bacteria and other microbes use antibiotics to suppress other strains and species. However, many bacteria also use narrow-spectrum toxins, such as bacteriocins, that principally target conspecifics. Why has such a diversity in spectrum evolved? Here, we develop an evolutionary model to understand antimicrobial spectrum. Our first model recapitulates the intuition that broad-spectrum is best, because it enables a microbe to kill a wider diversity of competitors. However, this model neglects an important property of antimicrobials: They are commonly bound, sequestered, or degraded by the cells they target. Incorporating this toxin loss reveals a major advantage to narrow-spectrum toxins: They target the strongest ecological competitor and avoid being used up on less important species. Why then would broad-spectrum toxins ever evolve? Our model predicts that broad-spectrum toxins will be favored by natural selection if a strain is highly abundant and can overpower both its key competitor and other species. We test this prediction by compiling and analyzing a database of the regulation and spectrum of toxins used in inter-bacterial competition. This analysis reveals a strong association between broad-spectrum toxins and density-dependent regulation, indicating that they are indeed used when strains are abundant. Our work provides a rationale for why bacteria commonly evolve narrow-spectrum toxins such as bacteriocins and suggests that the evolution of antibiotics proper is a signature of ecological dominance. |
| spellingShingle | Palmer, JD Foster, KR The evolution of spectrum in antibiotics and bacteriocins |
| title | The evolution of spectrum in antibiotics and bacteriocins |
| title_full | The evolution of spectrum in antibiotics and bacteriocins |
| title_fullStr | The evolution of spectrum in antibiotics and bacteriocins |
| title_full_unstemmed | The evolution of spectrum in antibiotics and bacteriocins |
| title_short | The evolution of spectrum in antibiotics and bacteriocins |
| title_sort | evolution of spectrum in antibiotics and bacteriocins |
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