scholarly journals Competition and the origins of novelty: experimental evolution of niche-width expansion in a virus

2013 ◽  
Vol 9 (1) ◽  
pp. 20120616 ◽  
Author(s):  
Lisa M. Bono ◽  
Catharine L. Gensel ◽  
David W. Pfennig ◽  
Christina L. Burch

Competition for resources has long been viewed as a key agent of divergent selection. Theory holds that populations facing severe intraspecific competition will tend to use a wider range of resources, possibly even using entirely novel resources that are less in demand. Yet, there have been few experimental tests of these ideas. Using the bacterial virus (bacteriophage) ϕ 6 as a model system, we examined whether competition for host resources promotes the evolution of novel resource use. In the laboratory, ϕ 6 exhibits a narrow host range but readily produces mutants capable of infecting novel bacterial hosts. Here, we show that when ϕ 6 populations were subjected to intense intraspecific competition for their standard laboratory host, they rapidly evolved new generalist morphs that infect novel hosts . Our results therefore suggest that competition for host resources may drive the evolution of host range expansion in viruses. More generally, our findings demonstrate that intraspecific resource competition can indeed promote the evolution of novel resource-use phenotypes.

2020 ◽  
Author(s):  
Vance Difan Gao ◽  
Sara Morley-Fletcher ◽  
Stefania Maccari ◽  
Martha Hotz Vitaterna ◽  
Fred W. Turek

AbstractCompetition for resources often contributes strongly to defining an organism’s ecological niche. Biological rhythms are important adaptations to the temporal dimension of niches, but the role of other organisms in determining such temporal niches have not been much studied, and the role specifically of competition even less so. We investigate how interspecific and intraspecific competition for resources shapes an organism’s activity rhythms. For this, communities of one or two species in an environment with limited resource input were simulated. We demonstrate that when organisms are arrhythmic, one species will always be competitively excluded from the environment, but the existence of activity rhythms allows niche differentiation and indefinite coexistence of the two species. Two species which are initially active at the same phase will differentiate their phase angle of entrainment over time to avoid each other. When only one species is present in an environment, competition within individuals of the species strongly selects for niche expansion through arrhythmicity, but the addition of an interspecific competitor facilitates evolution of increased rhythmic amplitude when combined with additional adaptations for temporal specialization. Finally, if individuals preferentially mate with others who are active at similar times of day, then disruptive selection by intraspecific competition can split one population into two reproductively isolated groups. In summary, these simulations suggest that biological rhythms are an effective method to temporally differentiate ecological niches, and that competition is an important ecological pressure promoting the evolution of rhythms and sleep.Author summaryWhy do we sleep? We are interested in the ecological factors which promote the evolution of biological rhythms like the sleep-wake cycle, focusing especially on competition. When animals compete with each other for resources, they often evolve to avoid each other by specializing to use different resources or separating their activity in other ways. To test hypotheses about how competition shapes rest-activity rhythms, we performed computer simulations of a community of animals who move, reproduce, and compete for resources. We show that biological rhythms let two species divide time so that one species is active while its competitor is resting, thus avoiding depleting shared resources. When a species has no competitors in the simulation, competition between members of the same species cause population and individual rhythms to decrease, since resource availability is low when everybody is active at the same time. However, having competitors allows strong rhythms to evolve from originally arrhythmic organisms. Competition can even cause a single population to split into two species which are separated in time. In summary, these results suggest that competition is a strong factor promoting rest-activity rhythms.


1995 ◽  
Vol 177 (12) ◽  
pp. 3443-3450 ◽  
Author(s):  
E Mellado ◽  
J A Asturias ◽  
J J Nieto ◽  
K N Timmis ◽  
A Ventosa

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2275
Author(s):  
Yanxi Liu ◽  
Mengjiao Liu ◽  
Ran Hu ◽  
Jun Bai ◽  
Xiaoqing He ◽  
...  

Bacteriophages are viruses that specifically infect target bacteria. Recently, bacteriophages have been considered potential biological control agents for bacterial pathogens due to their host specificity. Pseudomonas syringae pv. actinidiae (Psa) is a reemerging pathogen that causes bacterial canker of kiwifruit (Actinidia sp.). The economic impact of this pest and the development of resistance to antibiotics and copper sprays in Psa and other pathovars have led to investigation of alternative management strategies. Phage therapy may be a useful alternative to conventional treatments for controlling Psa infections. Although the efficacy of bacteriophage φ6 was evaluated for the control of Psa, the characteristics of other DNA bacteriophages infecting Psa remain unclear. In this study, the PHB09 lytic bacteriophage specific to Psa was isolated from kiwifruit orchard soil. Extensive host range testing using Psa isolated from kiwifruit orchards and other Pseudomonas strains showed PHB09 has a narrow host range. It remained stable over a wide range of temperatures (4–50 °C) and pH values (pH 3–11) and maintained stability for 50 min under ultraviolet irradiation. Complete genome sequence analysis indicated PHB09 might belong to a new myovirus genus in Caudoviricetes. Its genome contains a total of 94,844 bp and 186 predicted genes associated with phage structure, packaging, host lysis, DNA manipulation, transcription, and additional functions. The isolation and identification of PHB09 enrich the research on Pseudomonas phages and provide a promising biocontrol agent against kiwifruit bacterial canker.


1995 ◽  
Vol 9 (6) ◽  
pp. 617-632 ◽  
Author(s):  
Loyal A. Mehrhoff ◽  
Roy Turkington

2015 ◽  
Vol 282 (1821) ◽  
pp. 20151932 ◽  
Author(s):  
Lisa M. Bono ◽  
Catharine L. Gensel ◽  
David W. Pfennig ◽  
Christina L. Burch

Competition for resources is thought to play a critical role in both the origins and maintenance of biodiversity. Although numerous laboratory evolution experiments have confirmed that competition can be a key driver of adaptive diversification, few have demonstrated its role in the maintenance of the resulting diversity. We investigate the conditions that favour the origin and maintenance of alternative generalist and specialist resource-use phenotypes within the same population. Previously, we confirmed that competition for hosts among φ 6 bacteriophage in a mixed novel (non-permissive) and ancestral (permissive) host microcosm triggered the evolution of a generalist phenotype capable of infecting both hosts. However, because the newly evolved generalists tended to competitively exclude the ancestral specialists, coexistence between the two phenotypes was rare. Here, we show that reducing the relative abundance of the novel host slowed the increase in frequency of the generalist phenotype, allowing sufficient time for the specialist to further adapt to the ancestral host. This adaptation resulted in ‘evolutionary rescue’ of the specialists, preventing their competitive exclusion by the generalists. Thus, our results suggest that competition promotes both the origin and maintenance of biodiversity when it is strong enough to favour a novel resource-use phenotype, but weak enough to allow adaptation of both the novel and ancestral phenotypes to their respective niches.


1994 ◽  
Vol 28 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Rodolphe Boivin ◽  
Guy Bellemare ◽  
Patrice Dion

2006 ◽  
Vol 51 (2) ◽  
pp. 796-799 ◽  
Author(s):  
Ângela Novais ◽  
Rafael Cantón ◽  
Raquel Moreira ◽  
Luísa Peixe ◽  
Fernando Baquero ◽  
...  

ABSTRACT The spread of CTX-M-1-like enzymes in Spain is associated with particular plasmids of broad-host-range IncN (bla CTX-M-32, bla CTX-M-1), IncL/M (bla CTX-M-1), and IncA/C2 (bla CTX-M-3) or narrow-host-range IncFII (bla CTX-M-15). The identical genetic surroundings of bla CTX-M-32 and bla CTX-M-1 and their locations on related 40-kb IncN plasmids indicate the in vivo evolution of this element.


1981 ◽  
Vol 59 (9) ◽  
pp. 1836-1846 ◽  
Author(s):  
Murray J. Kennedy

Previous experimental and field studies have shown that variations within the genus Haematoloechus may result from differences in age and degree of maturity, extent of crowding, species of host, and other factors.Based on these observations, only 6 of the 15 previously known species from Canada and the United States are considered valid. The valid species and their synonyms are as follows: Haematoloechus longiplexus Stafford, 1902; H. breviplexus Stafford, 1902; H. varioplexus Stafford, 1902 (= H. parviplexus, = H. buttensis, = H. similiplexus, = H. floedae, and H. uniplexus); H. kernensis Ingles, 1932 (= H. tumidus); H. medioplexus Stafford, 1902; and H. complexus (Seely, 1906) (= H. coloradensis, = H. confusus, = H. oxyorchis).The existence of three species groups is hypothesized. Haematoloechus longiplexus and H. breviplexus constitute one group, characterized by little geographical variation and a narrow host range. They are typically parasites of Rana catesbeiana and R. clamitans. Haematoloechus varioplexus and H. kernensis constitute the second group. These species have a wider host range and greater variation in characters purported to be specific differences. The third group includes those lung flukes which do not contain extracaecal loops (H. medioplexus and H. complexus). Of these, only H. medioplexus had little geographical variation and was found to occur in a single frog host.


2016 ◽  
Vol 91 (4) ◽  
Author(s):  
Qiang Ding ◽  
Markus von Schaewen ◽  
Gabriela Hrebikova ◽  
Brigitte Heller ◽  
Lisa Sandmann ◽  
...  

ABSTRACT Hepatitis C virus (HCV) causes chronic infections in at least 150 million individuals worldwide. HCV has a narrow host range and robustly infects only humans and chimpanzees. The underlying mechanisms for this narrow host range are incompletely understood. At the level of entry, differences in the amino acid sequences between the human and mouse orthologues of two essential host factors, the tetraspanin CD81 and the tight junction protein occludin (OCLN), explain, at least in part, HCV's limited ability to enter mouse hepatocytes. We have previously shown that adenoviral or transgenic overexpression of human CD81 and OCLN facilitates HCV uptake into mouse hepatocytes in vitro and in vivo. In efforts to refine these models, we constructed knock-in mice in which the second extracellular loops of CD81 and OCLN were replaced with the respective human sequences, which contain the determinants that are critical for HCV uptake. We demonstrate that the humanized CD81 and OCLN were expressed at physiological levels in a tissue-appropriate fashion. Mice bearing the humanized alleles formed normal tight junctions and did not exhibit any immunologic abnormalities, indicating that interactions with their physiological ligands were intact. HCV entry factor knock-in mice take up HCV with an efficiency similar to that in mice expressing HCV entry factors transgenically or adenovirally, demonstrating the utility of this model for studying HCV infection in vivo. IMPORTANCE At least 150 million individuals are chronically infected with hepatitis C virus (HCV). Chronic hepatitis C can result in progressive liver disease and liver cancer. New antiviral treatments can cure HCV in the majority of patients, but a vaccine remains elusive. To gain a better understanding of the processes culminating in liver failure and cancer and to prioritize vaccine candidates more efficiently, small-animal models are needed. Here, we describe the characterization of a new mouse model in which the parts of two host factors that are essential for HCV uptake, CD81 and occludin (OCLN), which differ between mice and humans, were humanized. We demonstrate that such minimally humanized mice develop normally, express the modified genes at physiological levels, and support HCV uptake. This model is of considerable utility for studying viral entry in the three-dimensional context of the liver and to test approaches aimed at preventing HCV entry.


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