The "co-" in coevolution.
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A model which equates oxygen transport to hemoglobin concentration and molecular weight is used to demonstrate that high concentrations of hemoglobin will augment oxygen transport only if the molecular weight of the hemoglobin is low. The evolution of corpuscles is a necessary counterpart to having high concentrations of the low molecular weight hemoglobins. corpuscles prevent loss of the small molecules by way of excretory filters and prevent the development of exceedingly high plasma osmotic pressures.
Plectonema boryanum, a filamentous blue-green alga, was cloned and then allowed to reach a steady state in a quasi-continuous culture in the presence of the algal virus, LPP-1. The culture was maintained for 3.5-month period during which time at least four distinct culture lysings were evident. After the fourth lysis the culture reached a steady-state level which was identical in its algal concentration to the preinfection level. Upon testing the characteristics of the evolved alga and virus variants, the following was determined: cell variants resistant to both the original virus and the derived virus had evolved, and there was no evidence of lysogeny present amony these cells. The evolved virus strains still grew on the parental algal strain, though with altered plaque morphology. Furthermore, they were antigenically similar to the parental virus, and showed no significant difference in adsorption rate or growth characteristics on parental cells. However, a low-grade chronic viral infection persisted in the culture. Rapid re-establishment of a dense, stable culture is apparantly the normal laboratory response of a procaryotic cell-virus system.
We have amplified by the polymerase chain reaction, cloned, and sequenced genomic segments of 118 human papillomavirus type 16 (HPV-16) isolates from 76 cervical biopsy, 14 cervical smear, 3 vulval biopsy, 2 penile biopsy, 2 anal biopsy, and 1 vaginal biopsy sample and two cell lines. The specimens were taken from patients in four countries--Singapore, Brazil, Tanzania, and Germany. The sequence of a 364-bp fragment of the long control region of the virus revealed 38 variants, most of which differed by one or several point mutations. Phylogenetic trees were constructed by distance matrix methods and a transformation series approach. The trees based on the long control region were supported by another set based on the complete E5 protein-coding region. Both sets had two main branches. Nearly all of the variants from Tanzania were assigned to one (African) branch, and all of the German and most of the Singaporean variants were assigned to the other (Eurasian) branch. While some German and Singaporean variants were identical, each group also contained variants that formed unique branches. In contrast to the group-internal homogeneity of the Singaporean, German, and Tanzanian variants, the Brazilian variants were clearly divided between the two branches. Exceptions to this were the seven Singaporean isolates with mutational patterns typical of the Tanzanian isolates. The data suggest that HPV-16 evolved separately for a long period in Africa and Eurasia. Representatives of both branches may have been transferred to Brazil via past colonial immigration. The comparable efficiencies of transfer of the African and the Eurasian variants to the New World suggest pandemic spread of HPV-16 in past centuries. Representatives of the African branch were possibly transferred to the Far East along old Arab and Indonesian sailing routes. Our data also support the view that HPV-16 is a well-defined virus type, since the variants show only a maximal genomic divergence of about 5%. The small amount of divergence in any one geographic location and the lack of marked divergence between the Tanzanian and Brazilian African genome variants two centuries after their likely introduction into the New World suggest a very slow rate of viral evolution. The phylogenetic tree therefore probably represents a minimum of several centuries of evolution, if not an age equal to that of the respective human races.
Parasites may employ particular strategies of eluding an immune response by taking advantage of those mechanisms that normally guarantee immunological self-tolerance. Much in the way as it occurs during the establishment of self-tolerance, live pathogens may induce clonal deletion, functional inactivation (anergy) and immunosuppression. At this latter level, it appears that certain pathogens produce immunosuppressive cytokine-like mediators or provoke the host to secrete cytokines that will compromise the anti-parasite immune response. It appears that immune responses that preferentially involve T helper 1 cells (secretors of interleukin-2-and interferon-gamma) tend to be protective, whereas T helper 2 cells (secretors of IL-4, IL-5, IL-6, and IL-10), a population that antagonizes T helper cells, mediate disease susceptibility and are involved in immunopathological reactions. Cytokines produced by T helper 2 cells mediate many symptoms of infection, including eosinophilia, mastocytosis, hyperimmunoglobulinemia, and elevated IgE levels. Administration of IL-2 and IFN-gamma has beneficial effects in many infections mediated by viruses, bacteria, and protozoa. The use of live vaccinia virus might be an avenue for the treatment of or the vaccination against infection. We have found that a vaccinia virus expressing the gene for human IL-2, though attenuated, precipitates autoimmune disease in immunodeficient, athymic mice. Thus, although T helper 1 cytokines may have desired immunostimulatory properties, they also may lead to unwarranted autoaggressive responses.
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Recently reported P1, P2 and metabacteria line sequences of transposition-type 'A' proteins, equivalent to Escherichia coli ribosomal protein L7/L12, were examined using a correlation method which evaluates the sequence similarity quantitatively. As the sequences could be aligned along the alignment previously constructed for 25 various 'A' proteins, the inclusive alignment further supports the previous claims concerning the rule of "preservation units" and the transpositional regeneration for metabacterial and eukaryotic 'A' proteins. Yeasts contain multispecies of P1 and P2 line genes and their P1 line sequences show low correlation coefficient values compared to other P1 line sequences, indicating a great evolutionary distance between lower and higher eukaryotes. Five sequences of protein P0 from metabacteria, yeast, and human, of which about 20 residues at the C termini are homologous with those of their own transposition-type 'A' proteins, were similarly examined. The N-terminal three-quarters of the sequences align naturally and the first two-thirds of the alignment could involve the E. coli L10 (EL10) sequence. An alignment of the remaining sequences at the C termini was established, relying on the well-matching sequence similarities between the metabacteria 'A' protein and their P0 protein sequences. Finally, the C-terminal halves of P0 protein sequences corresponded with almost overall sequences of the transposition-type 'A' proteins. The gene fusion of a protein might have resulted in the formation of the P0 proteins. A coupling of this gene fusion and the transposition of prototype 'A' proteins may have given rise to the complementary molecular transformations required for the development toward higher organism cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Paleontologic and zoogeographic data speak in favour of Mesozoic origin of ixodid ticks. The absence of strict restrictions for the feeding on unusual species of hosts has caused the domination of polyphagy and oligophagy over monophagy among ixodid ticks. The same peculiarities of ixodid ecology are responsible for a restricted part or absence of phylogenetic parallelism with hosts in their evolution. Primary food relations with reptiles are, apparently, preserved only in the genus Aponomma and in many species of Amblyomma while hosts for most species of other genera are mammals and, to a lesser extent, birds. The number of potential hosts in these species can be much greater than that of real ones. Restrictions in the distribution of some species are connected rather with direct effect of unfavourable environmental factors on their nonparasitic stages of the life cycle than with the absence of suitable hosts. During the evolution of natural landscapes and at a shorter stages under the influence of successions or anthropogenic factors ixodids easily adapt themselves to feeding on new species of hosts. So the differentiation of primary and secondary hosts of these parasites is rather difficult.
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Mitochondrial function depends on tight coordination between mitochondrial and nuclear genomes, which requires long-term coevolution to maintain mitonuclear coadaptation. While mitonuclear incompatibility is typically studied in the context of hybridization, other evolutionary scenarios that may disrupt coadaptation between the two genomes remain less explored. Here, we propose that extreme ecological niche shifts may disrupt mitonuclear coadaptation, which we test in carnivorous Miletinae butterflies with an extreme dietary transition. By generating high-quality genome assemblies, we found that Miletinae exhibit extensive chromosomal rearrangements. Comparative phylogenomic analyses revealed a striking asymmetric mitonuclear evolutionary response: Miletinae exhibit elevated mitochondrial nucleotide substitution rates compared to phytophagous relatives, whereas nuclear rates remain stable. This shift reverses the typical lepidopteran pattern where nuclear rates exceed mitochondrial rates. Interestingly, this mitochondrial acceleration is driven primarily by relaxed purifying selection rather than positive selection. To sustain mitochondrial function, the nuclear genome of Miletinae underwent pervasive, multilayered compensatory evolution. We detected strong signatures of positive selection and accelerated evolution in nuclear genes directly interacting with mitochondrial components across oxidative phosphorylation (OXPHOS) complexes, the mitochondrial translation, and replication and transcription machinery. Furthermore, this nuclear compensatory response extends to systems governing mitochondrial homeostasis, including protein quality control and RNA degradation and stabilization. Our results support a model in which extreme ecological transitions can disrupt ancestral mitonuclear coadaptation and promote the emergence of a new coadapted state through systemic nuclear compensation. This study broadens the conceptual framework of mitonuclear coevolution and highlights its role in facilitating evolutionary persistence after major ecological shifts.
An extension of J. Roughgarden's [1979, Theor. Pop. Biol. 9, 388; 1979, "An Introduction to Evolutionary Ecology and Population Genetic Theory," Macmillan, New York] formalism for investigating the effects of coevolution on community structure is presented. The extension assumes the result that a coevolved community is asymptotically stable when coevolution takes place at a genetically noninvasible boundary. This is proved for the general case of n interacting species. From this a community persistence function, phi (P), is defined that allows measuring the domain of attraction for the community as well as the resilience time, that is, the time taken for a perturbation to decay to 1-1/e (63%) of its initial value.
Darwinian theory has yet to explain adequately the fact of sex. If males provide little or no aid to offspring, a high (up to 2-fold) extra average fitness has to emerge as a property of a sexual parentage if sex is to be stable. The advantage must presumably come from recombination but has been hard to identify. It may well lie in the necessity to recombine defenses to defeat numerous parasites. A model demonstrating this works best for contesting hosts whose defense polymorphisms are constrained to low mutation rates. A review of the literature shows that the predictions of parasite coevolution fit well with the known ecology of sex. Moreover, parasite coevolution is superior to previous models of the evolution of sex by supporting the stability of sex under the following challenging conditions: very low fecundity, realistic patterns of genotype fitness and changing environment, and frequent mutation to parthenogenesis, even while sex pays the full 2-fold cost.
More than 100 published and four unpublished papers recording virus isolations of California (CAL) serogroup viruses from mosquitoes and other arthropods were analyzed, followed by a comparison of a contemporary classification of mosquitoes of the genus Aedes with a contemporary classification of CAL serogroup viruses. Using criteria of five or more total isolations of a given virus from a given species of mosquito, and a minimum infection rate of 1:10,000 or greater (more frequent), Aedes, and to a lesser extent Culiseta, species were found to be the arthropods most frequently involved as vectors. Such a comparison could not explain all virus-vector associations on the basis of coevolution of viruses in Aedes mosquito species, probably because of the crossing over of viruses to other mosquito species through horizontal transmission and because of deficiencies in currently available classifications. Coevolution of host-parasite systems is discussed, as are the inadequacies of contemporary taxonomic treatments of viruses and Aedes mosquitoes. The paper ends with hypothetical reconstructions of virus-mosquito relationships over time and possible routes of dispersal of California serogroup viruses to their present geographical distributions.
It is generally assumed that conservation and divergence of DNA signify function (selection) and no function (drift), respectively. This assumption is based on the view that a mutation is a unique event on a single chromosome, the fate of which depends on selection or drift. Knowledge of the rates, units and biases of widespread mechanisms of non-reciprocal DNA exchange, in particular within multigene families, provides alternative explanations for conservation and divergence, notwithstanding biological function. Such mechanisms of DNA turnover cause continual fluctuations in the copy-number of variant genes in an individual and, hence, promote the gradual and cohesive spread of a variant gene throughout a family (homogenization) and throughout a population (fixation). The dual processes (molecular drive) of homogenization and fixation are inextricably linked. Data are presented of the expected stages of transition in the spread of variant repeats by molecular drive in some non-genic families of DNA, seemingly not under the influence of selection. When a molecularly driven change in a given gene family is accompanied by the coevolution (mediated by selection) of other DNA, RNA or protein molecules that interact with the gene family then biological function is observed to be maintained despite sequence divergence. Conversely, the mechanics of DNA turnover and a turnover bias in favour of ancestral sequences can dramatically retard the rate of sequence change, in the absence of function. Examples of the maintenance of function by molecular coevolution and conservation of sequences in the absence of function, are drawn mainly from the rDNA multigene family.