Presentation Information
[C09-03]Fungi's polymorphism is driven by virus even if there are inter-strain competitions in fungi
*Shun Minami1,3, Akira Sasaki, Hisashi Ohtsuki1,2 (1. The Graduate University for Advanced Studies (Japan), 2. Research Center for Integrative Evolutionary Science (Japan), 3. Integrative Evolutionary Science (Japan))
Keywords:
Red Queen Dynamics,Polymorphism,Immunology,Virus,Allorecognition
Recent empirical studies show a remarkably high degree of polymorphism in fungal compatibility types. The diversity is thought to arise from pathogen-mediated selection by mycovirus, which is a virus that infects fungi. However, it is controversial because diversification can lead to strong inter-strain competition and exclusion of each other.
We explore evolutionary origin of fungi polymorphism by using a multi-strain epidemiological and ecological population dynamics model. The identity of a fungal colony is determined by Vegetative Compatibility system which genetically recognizes self/non-self (VC type). Fungi can share nutrients with the same VC type colony by cell fusion. If colonies have different VC types, cell death occurs and restricts cytoplasmic exchange, resulting in two colonies being separated. Therefore, we assume that inter-VC type competition is stronger than intra-VC type competition. Segregation by the VC system also acts against viral infection by restricting cytoplasmic exchange, so we assume that inter-VC type infection rate is lower than that of intra-VC type infection. We analyze whether a mycovirus promotes VC type coexistence and, if so, how many VC types can coexist.
As a result, we find that a mycovirus promotes an extremely high degree of fungal polymorphism when there is inter-VC type infection. This is because imperfect segregation by the VC system allows the virus to spread in fungus population and causes negative frequency-dependent selection. This result is the opposite to the previous prediction from empirical studies that imperfectness of protection by the VC system leads to low VC diversity because it can reduce the intensity of negative frequency-dependent selection caused by virus. Furthermore, we find that the diversity is determined by the balance between the strength of inter-strain competition and the efficiency of protection from viral infection by the VC system. Our result is in line with the prediction by some field studies that geographical difference in VC diversity can be caused by regional difference in viral intensity.
We explore evolutionary origin of fungi polymorphism by using a multi-strain epidemiological and ecological population dynamics model. The identity of a fungal colony is determined by Vegetative Compatibility system which genetically recognizes self/non-self (VC type). Fungi can share nutrients with the same VC type colony by cell fusion. If colonies have different VC types, cell death occurs and restricts cytoplasmic exchange, resulting in two colonies being separated. Therefore, we assume that inter-VC type competition is stronger than intra-VC type competition. Segregation by the VC system also acts against viral infection by restricting cytoplasmic exchange, so we assume that inter-VC type infection rate is lower than that of intra-VC type infection. We analyze whether a mycovirus promotes VC type coexistence and, if so, how many VC types can coexist.
As a result, we find that a mycovirus promotes an extremely high degree of fungal polymorphism when there is inter-VC type infection. This is because imperfect segregation by the VC system allows the virus to spread in fungus population and causes negative frequency-dependent selection. This result is the opposite to the previous prediction from empirical studies that imperfectness of protection by the VC system leads to low VC diversity because it can reduce the intensity of negative frequency-dependent selection caused by virus. Furthermore, we find that the diversity is determined by the balance between the strength of inter-strain competition and the efficiency of protection from viral infection by the VC system. Our result is in line with the prediction by some field studies that geographical difference in VC diversity can be caused by regional difference in viral intensity.