PubMed · 745430
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M R Rose. 1978-11-07. Cheating in evolutionary games.. https://doi.org/10.1016/0022-5193(78)90200-x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Rapid adaptive evolution can increase the competitive ability of invasive species in their non-native ranges. However, whether this increase is a general response and what drives it remain uncertain because the evidence is largely based on studies with limited sampling, inadequate consideration of population co-ancestry, and oversimplified estimates of competitive ability. We conduct a large-scale glasshouse experiment testing the effects of competition and drought on 100 native and 165 non-native populations of Erigeron canadensis, all genotyped to account for co-ancestry. Plants from non-native populations are significantly more competitive against other species than the conspecifics from native populations under both mesic and dry conditions. Genetic clustering indicates that the rapid evolution of competitive ability occurs independently in two out of four clusters in the non-native range. This advantage is present only during interspecific interactions and is absent during intraspecific competition. Repeated evolution of increased competitive ability suggests that adaptation following introduction can reshape species interactions and promote invasion success, even under future drought conditions, highlighting the importance of rapid evolution in determining the ecological impacts of invasive plants.
Despite a long-standing interest since Darwin's time, the genomic implications of obligate self-fertilization remain elusive. Complete cleistogamy-the obligate production of closed, self-pollinating flowers-represents an extreme reproductive strategy. Here, we present the genomic profiles and evolutionary history of two lineages of the mycoheterotrophic orchid Gastrodia, both of which independently acquired complete cleistogamy, based on detailed sampling and a combination of simple sequence repeat (SSR), multiplexed ISSR genotyping by sequencing (MIG-seq) and RNA-seq data. Our analysis reveals clear species delimitation, with no evidence of introgression between the completely cleistogamous species and their co-occurring allogamous sisters. Intriguingly, all analyses indicate that both the completely cleistogamous Gastrodia species and their allogamous sisters exhibit genetic profiles typical of self-pollinating plants. This pattern suggests that their ancestors, probably bearing allogamous flowers, had already evolved mechanisms to mitigate the deleterious effects of selfing, potentially facilitating the emergence of complete cleistogamy through benefits such as reproductive assurance, enhanced colonization ability and species reinforcement. Meanwhile, further analyses suggest that complete cleistogamy evolved very recently (possibly within the last 1000-2000 years) in these two Gastrodia lineages. Combined with the scant evidence of complete cleistogamy outside Gastrodia, our findings imply a limited and ephemeral role for complete cleistogamy in plant speciation.
Oncogene amplification on extrachromosomal DNA (ecDNA) is a common event, driving aggressive tumor growth, drug resistance and shorter survival. Currently, the impact of nonchromosomal oncogene inheritance-random identity by descent-is poorly understood. Also unclear is the impact of ecDNA on somatic variation and selection. Here integrating theoretical models of random segregation, unbiased image analysis, CRISPR-based ecDNA tagging with live-cell imaging and CRISPR-C, we demonstrate that random ecDNA inheritance results in extensive intratumoral ecDNA copy number heterogeneity and rapid adaptation to metabolic stress and targeted treatment. Observed ecDNAs benefit host cell survival or growth and can change within a single cell cycle. ecDNA inheritance can predict, a priori, some of the aggressive features of ecDNA-containing cancers. These properties are facilitated by the ability of ecDNA to rapidly adapt genomes in a way that is not possible through chromosomal oncogene amplification. These results show how the nonchromosomal random inheritance pattern of ecDNA contributes to poor outcomes for patients with cancer.