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Cooperation, competition and enforcement in transposon evolution.

Transposons are powerful drivers of genome evolution, but we lack a clear understanding of how these selfish genetic elements evolve and co-evolve with their hosts. Here, we develop a new general model of transposon-host co-evolution that incorporates key details of transposon and host biology. Our model reveals that the way that transposons replicate is critical for their evolutionary prognosis. Publicly-replicating transposons (such as DNA transposons), which cooperatively share their replication machinery, are predicted to be self-limiting. However, privately-replicating transposons (such as long interspersed nuclear elements, or LINEs), which do not replicate cooperatively, are under continual selection to increase their duplication rate even to the point of host extinction, a so-called tragedy of the commons. Neither selection against transposons' deleterious effects nor exploitation by parasitic elements is sufficient to prevent host extinction. Instead, our analysis shows that only active suppression by hosts avoids population collapse. In particular, suppression must act post-transcriptionally in order to prevent continuous escalation of the transposon-host genetic conflict. We argue that only with host enforcement of transposons can complex life exist.

DNA Transposable Elements

The evolution of a universal genetic code.

Some of the basic problems presented by the rapid evolution of a universal genetic code can be resolved by a mechanism of co-evolution of the code and the amino acids it serves.

Amino Acids

Altruism: its characteristics and evolution.

Altruism is a group phenomenon in which some genes or individuals, which must be presumed to be selfish, benefit others at cost to themselves. The presumption of selfishness and the fact of altruism are reconciled by kin-group selection and by reciprocal altruism. Kin-group selection is clearly visible only in special cases; its role even among social insects may be overestimated; it is probably usually inhibited by competition. However, reciprocal altruism is ubiquitous. All altruism is: (i) potentially reciprocal; (ii) potentially profitable to altruists as well as to recipients; (iii) environmentally determined, usually by position of individuals in group or environmental situations; and (iv) a net-gain lottery. These generalizations are illustrated by four idealized cases; the difficulty of applying them to real cases is illustrated by alarm-calling in groups of birds. Although altruism is a group phenomenon, it evolves by individual selection, by processes equivalent to co-evolutions. Its evolution is: (i) opposed by competition; (ii) costly, complex, and slow, and tending to produce an imprecise flexible altruism rather than a precisely detailed one; and (iii) supplemented by group selection (differential extinction of groups). That altruism in human beings conforms to these generalizations is a good working hypothesis. However, analysis does not "take the altruism out of (human) altruism." Humans do not calculate it, but behave altruistically because they have human altruistic emotions.

Altruism

Transition of Staphylococcus aureus tetracycline resistance plasmid pT181 from independent multicopy replicon to predominantly integrated chromosomal element over 65 years.

Mobile genetic elements (MGEs), including plasmids, phages and genome islands, are major sources of bacterial genetic diversity. The small plasmid pT181 confers tetracycline resistance in bacterial pathogen Staphylococcus aureus via an efflux pump, TetK. pT181 was one of the earliest sequenced S. aureus plasmids, and has been isolated in both clinical and livestock-associated strains for decades, both as an independent replicon and integrated in the chromosome as part of staphylococcal cassette chromosome mec (SCCmec). Bacterial genome analysis tools and high-quality sequences with metadata are publicly available, but these resources remain underleveraged for examining historical data, especially when studying the spread of MGEs across a species and over time. Using publicly available reads and metadata, we explored the evolution of pT181 over almost seven decades of samples to identify temporal trends in sequence evolution, copy number changes, and spread across S. aureus and beyond. pT181 was prevalent across S. aureus (found in 9.5% of 83,366 genomes tested), with a conserved sequence outside of three hypervariable regions. The history of pT181 since 1954 is characterized by spread across strains, significant variation in plasmid copy number of the independent replicon, and increasing frequency of integration of the plasmid into the S. aureus chromosome. We have identified multiple chromosomal integration locations of the plasmid, including outside of the previously characterized SCCmec. We find that pT181 has been transferred across staphylococcaceae and into a Gram-negative species. The repeated integration of pT181 into the chromosome may indicate co-evolution of the plasmid and the host, potentially to facilitate increased antibiotic resistance.

Journal Article

RNA Virus Diversity, Cross-Species Transmission, and Molecular Constraints in Two Closely Related Rat Species.

Viral infection involves co-evolution with hosts, yet the molecular determinants that constrain viral cross-species transmission remain poorly understood. Here, we established conspecific and heterospecific co-housing models for two closely related rat species, Rattus norvegicus (RN) and Rattus tanezumi (RT), both maintained in laboratory settings for over 10 generations, together with wild-caught RT individuals. Using meta-transcriptomic sequencing and population genomic analyses, we compared their RNA virus profiles and investigated the potential molecular constraints on cross-species viral transmission. From 63 rats, we characterized an extensive RNA virome comprising more than 600 viruses, including 7 zoonotic viruses, 29 viruses with cross-species transmission potential, and 335 novel viruses. Notably, the prevalence of Seoul orthohantavirus (SEOV) was significantly higher in RN than in RT. Population genomic analysis revealed that RN exhibited higher heterozygosity in Itgb3 (the gene encoding the SEOV receptor, β3-integrin) and Tlr7 (the gene encoding the receptor for viral ssRNA, Toll-like receptor 7) compared to RT. These genetic variations likely represent the molecular determinants responsible for the differential susceptibility to SEOV between the two species. Our findings clarify the diversity and prevalence of RNA viruses in closely related rodent species and highlight host genetic barriers that may influence zoonotic spillover risk.

Animals

The factory enters the fray: how mitochondrial protein trafficking shapes the host response to infection.

Beyond textbook functions in homeostatic metabolism, mitochondria are now recognized as central coordinators of cell-intrinsic and cell-extrinsic immune responses to infection. Directed trafficking of proteins and other molecules between mitochondria and the rest of the cell underlies a growing catalog of these activities. Some are pro-host; others are antagonized by viral effectors or co-opted by viruses entirely. How host and viral factors rewire the mitochondrial proteome during infection to shape these outcomes remains incompletely understood. The evolutionary history of this system adds another dimension: mitochondria retain biochemical signatures of their α-proteobacterial endosymbiotic origin, and ongoing co-evolution between viral, host, and mitochondrial genomes continues to shape the proteins that traffic to and from the organelle. Using published examples, we highlight general principles, mechanisms, and consequences of host and viral protein localization to and from the mitochondria. To support discovery, we present integrated gene lists identifying host mitochondrial factors with evidence for type I interferon stimulation, interactions with viral proteins, and signatures of positive selection. Together, these resources and the principles within offer a framework for understanding mitochondria not as passive metabolic machinery but as actively contested cellular territory whose protein composition is continuously negotiated between the host and the pathogen.

adaptation

Tracking Nongenetic Evolution from Primary to Metastatic ccRCC: TRACERx Renal.

While the key aspects of genetic evolution and their clinical implications in clear cell renal-cell carcinoma (ccRCC) are well-documented, how genetic features co-evolve with the phenotype and tumor microenvironment (TME) remains elusive. Here, through joint genomic-transcriptomic analysis of 243 samples from 79 patients recruited to the TRACERx Renal study, we identify pervasive non-genetic intratumor heterogeneity, with over 40% not attributable to genetic alterations. By integrating tumor transcriptomes and phylogenetic structures, we observe convergent evolution to specific phenotypic traits, including cell proliferation, metabolic reprogramming and overexpression of putative cGAS-STING repressors amid high aneuploidy. We also uncover a co-evolution between the tumor and the T cell repertoire, as well as a longitudinal shift in the TME from an anti-tumor to an immunosuppressive state, linked to the acquisition of recurrently late ccRCC drivers 9p loss and SETD2 mutations. Our study reveals clinically-relevant and hitherto underappreciated non-genetic evolution patterns in ccRCC.

Journal Article

Diversification, loss, and virulence gains of the major effector AvrStb6 during continental spread of the wheat pathogen Zymoseptoria tritici.

Interactions between plant pathogens and their hosts are highly dynamic and mainly driven by pathogen effectors and plant receptors. Host-pathogen co-evolution can cause rapid diversification or loss of pathogen genes encoding host-exposed proteins. The molecular mechanisms that underpin such sequence dynamics remains poorly investigated at the scale of entire pathogen species. Here, we focus on AvrStb6, a major effector of the global wheat pathogen Zymoseptoria tritici, evolving in response to the cognate receptor Stb6, a resistance widely deployed in wheat. We comprehensively captured effector gene evolution by analyzing a global thousand-genome panel using reference-free sequence analyses. We found that AvrStb6 has diversified into 59 protein isoforms with a strong association to the pathogen spreading to new continents. Across Europe, we found the strongest differentiation of the effector consistent with high rates of Stb6 deployment. The AvrStb6 locus showed also a remarkable diversification in transposable element content with specific expansion patterns across the globe. We detected AvrStb6 gene losses and evidence for transposable element-mediated disruptions. We used virulence datasets of genome-wide association mapping studies to predict virulence changes across the global panel. Genomic predictions suggested marked increases in virulence on Stb6 cultivars concomitant with the spread of the pathogen to Europe and the subsequent spread to further continents. Finally, we genotyped French bread wheat cultivars for Stb6 and monitored resistant cultivar deployment concomitant with AvrStb6 evolution. Taken together, our data provides a comprehensive view of how a rapidly diversifying effector locus can undergo large-scale sequence changes concomitant with gains in virulence on resistant cultivars. The analyses highlight also the need for large-scale pathogen sequencing panels to assess the durability of resistance genes and improve the sustainability of deployment strategies.

Ascomycota

[Organization of the psychotherapy-psychosomatic department and its integration into the University Pediatric Clinic].

With regard to the 20 years history of our psychotherapeutic unit some essential feed-back-loops between medical pediatric work and our systemic thinking are presented. So-called objective tasks interfere with group dynamics and subjective task formulations. If two models (the biomedical and the systemic-therapeutic) collide, both of them get "contaminated" and should be changed in a co-evolutive process--for the sake of the patients and their families. In our experience this is only possible, if autonomy of the unit is present, then the unit can wait for "perturbations".

Austria

The ecology and evolution of microbial immune systems: a look on the wild vibrio side.

Natural populations of vibrio beyond the well-studied pandemic strains of Vibrio cholerae, provide a powerful model for investigating the eco-evolutionary dynamics of microbial immune systems. Their genetic diversity, ecological versatility, ease of culturability and the availability of time-series data enable detailed studies of phage-host interactions in natural contexts. This review synthesizes recent advances in vibriophage research, highlighting key findings and emerging tools. High-throughput assays and genomic tools have offered new perspectives on phage specificity, host range and the evolutionary pressures shaping these interactions. Theoretical frameworks, such as arms race and fluctuating selection dynamics, are informed by empirical data from vibrio-phage systems, with time-series sampling providing crucial insights into their temporal and spatial dynamics. A major finding is the role of mobile genetic elements (MGEs) in encoding bacterial defence systems, which shape phage-host coevolution. Discoveries like the phage satellite PICMI illustrate how MGEs facilitate the transfer of antiviral systems, influencing ecological and evolutionary dynamics. The paradox of generalist vibriophages, rare despite their broad host ranges, is also explored. By integrating experimental approaches with field observations, vibriophage research advances microbial ecology and informs sustainable applications in aquaculture and phage therapy, reinforcing vibrios as a versatile model system.This article is part of the discussion meeting issue 'The ecology and evolution of bacterial immune systems'.

Bacteriophages