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[Encephalization of the marine lamprey, Petromyzon marinus (L.). Quantitative analysis of the principle brain subdivisions].

The measure of both the somatic weight (S) and the brain weight (E) on a sample of 13 adult individuals of Petromyzon marinus (L.) leads for this species to the determination of its brain-body weight coefficient of allometry and to the knowledge of its index of encephalization. The value of the first one is 0.556. Its locates the Sea-Lamprey at the highest level of a scale of decreasing values belonging one after the other to Chondrichthyes (0.551), to Teleost fishes (0.487), to Anurans (0.458), to Reptiles (0.43) and at last to Mammals (0.25). This result revalues our previous hypothesis which gives to this kind of statistic a phylogenetic meaning (RIDET et al. 1977). The index of encephalization has been arbitrarily fixed at the 10 value; it is the lowest of all the other indices previously known and consequently it points the Sea-Lamprey as the less encephalized Vertebrate species. The histological study carried out on the brain allows to the knowledge of the volumes of the main encephalic subdivisions. It leads to various results as: 1. The study the relative volumes (that is to say the volume of each subdivision expressed in percentage of the volume of the whole brain) emphasizes the olfactory bulbs and the Tegmentum + Medulla oblongata which have together the highest values amongst the brain percentages of Petromyzon marinus (and also of Lampetra planeri). This peculiarity has no equivalence in the brain structure of the other studied species of Vertebrates and we consider it as the expression of a primitive brain pattern. 2. The isoponderal indices locate also the Sea-Lamprey at the lowest level for all its encephalic subdivisions, as it was previously the case for the whole brain expressed by the index of encephalization. Such an unanimity seems also to be related to a fundamental brain organization. Comparisons between Petromyzon marinus, Lampetra planeri and Myxine glutinosa corroborate the paraphyletic status of the last one in the Agnathes. The differences pointed also between the two first species are less obvious but justify meanwhile a more detailed study of this group (Petromyzontidae) which shall be given soon.

Animals↗

Silent mutations in the gene encoding the p53 protein are preferentially located in conserved amino acid positions and splicing enhancers.

The last release of p53 somatic mutation database contains more than 20,000 of mutation among which 951 are silent (synonymous). This striking amount of silent mutations is much more than what would be expected if synonymous mutations were effectively neutral. The prevalent explanation to reconcile this vast amount of silent mutations with the neutral expectation is that they are just the subproduct of the hypermutability process that affect cancer cells. Some evidences have been presented in this direction, and the explanation has been taken as granted. Assuming that silent mutations are effectively neutral has major implication in the investigation of mutational processes that affect the gene encoding the p53 protein, since on the basis of this assumption they are considered the Null hypothesis, for instance for measuring and comparing among tissues the endogenous mutability. From this it follows that determining whether silent mutations in the p53 gene, and in all disease genes in general, are or not basically mutational noise, is of paramount importance. In this paper we readdress this topic by testing whether there is a relationship between the spatial distribution of silent mutations inside the p53 gene and functional significant features of the gene. For this purpose we divided the population of silent mutations in three groups: those that are found accompanied by other mutations (doublets and multiplest), those that were isolated as singlets, but the same mutation was also isolated as being part of a doublet (or multiplet) in another individual. And the last group is composed by those that were always found as singlets and never as being part of a doublet or a multiplet. This last group was expected to be enriched in functionally significant silent mutations. We found that all silent mutations, but particularly those of the last group, are preferentially located in conserved amino acid positions (i.e. functionally important amino acids) and also tend to be located inside suspected splicing enhancers. Noteworthy, this association remains even after eliminating the possible contribution of mutation hotspots. Besides, we present additional evidence in the direction that these putative splicing enhancers are real functional enhancers.

Amino Acid Sequence↗

The ecology of fish parasites with particular reference to helminth parasites and their salmonid fish hosts in Welsh rivers: a review of some of the central questions.

Ecological studies carried out in Welsh rivers on the feeding behaviour of salmonid fish, their helminth parasites and intermediate hosts in the early 1950s and in 1998 have been used as a basis to review the literature dealing with the following questions. First, how are the helminth populations dispersed in space-time? Second, to what extent are the distributional patterns and the life history strategies of the parasites influenced by physicochemical factors? Third, to what extent are populations of helmith parasites in salmonid fish influenced by host characteristics including the genome, sex, age, size, social position and Feeding behaviour? Fourth, are the populations of parasites regulated in a density-dependent manner? Fifth, do the parasites influence the survival and wellbeing of their salmonid hosts and the evolution of sex? Sixth, to what extent is the parasite community influenced by environmental changes including those of an anthropogenic nature and can the parasites be used as bioindicators of pollution? As with most parasites the helminth species found were highly overdispersed thus making it necessary to undertake a log10 (1 + x) conversion for statistical analyses. Statistical analyses confirm that the genome, age and sex of salmonid fish hosts, the station and seasonal change in radiation levels were significant factors in predicting the number of parasites. The evidence given supports the hypothesis that the feeding behaviour and habitat selection by the host fish, their position in the social hierarchy and the overdispersed nature of the transmission sites are the key factors in causing differences in the parasitic fauna related to host species, age, size and sex. Differences in the helminth parasite community related to station can be explained on the basis of differences in water types, sediments and chemistry. Although the evidence presented is in accord with the consensus view that temperature is correlated with seasonal changes in the abundance of many species of helminth parasites, it is argued that it may not be the direct causative mechanism. It is postulated that the life history strategy that results in a decline in abundance of the more vulnerable adult parasites in the gut of the salmonid hosts during the summer has arisen as a result of evolutionary pressures. At this time, the gut environment is particularly inhospitable because of the temperature-related enhancement of the host's immune mechanism and the increased gut turnover rate. In contrast, the larval stages in the immunologically and metabolically more benign intermediate host would be under less intensive selective pressures. It is postulated therefore that evolutionary pressures have caused the parasites to leave the definitive host and concentrate their reproductive efforts in the intermediate hosts during the warmer months. Evidence is given in support of the hypothesis that the parasite populations are regulated in a density-dependent manner and that the regulatory mechanisms may involve the host's immune mechanisms and intraspecies competition and interspecies competition of an exploitative or interference nature. Quantitative studies using 'K' factor analysis and biochemical research to elucidate the nature of the interference mechanisms are required to test this hypothesis. The absence of age-related resistance indicates an old and stable relationship in which the immunosuppressive and immunoavoidance mechanisms of the parasites and hosts, respectively, are in balance. This indicates that the introduction of novel parasites or new genetic strains of host fish could result in harmful epidemics. Despite causing tissue damage, there was no evidence of parasite-induced mortality among the salmonids in the Teifi. This finding is in accord with the generally accepted view that most freshwaters are not troubled by parasite problems. although parasites are present in abundance. In fact, parasite abundance in the salmonid fish in the Teifi was positively correlated with the condition factor and the adipose index. Two testable hypotheses were advanced to explain these observations. First, the more dominant well-conditioned fish in the hierarchy are more likely to acquire parasites because they ingest more food items and spend more time in sheltered habitats with depositing sediments where transmission mainly occurs. Second, the parasites may release factors that stimulate the host's immune and endocrinological systems to produce factors that enhance somatic growth and inhibit reproduction of the host. This benign relationship is considered to be indicative of long-term coevolution. The sex of the fish had a significant influence on the abundance of the parasites in total and also on particular species with the bias in all cases being in favour of the female fish. This review shows that sex bias in parasitism is generally not strong and that male bias in parasitism is not a general rule. Taken as a whole, the results fail to support most of the predictions based on the Hamilton-Zuk and the immunocompetence hypotheses. Possible hypotheses to explain why parasitism tends to be higher in female than in male trout include testosterone immunosuppression, corticosteroid-based immune suppression and differences between the size and behaviour of the sexes. However, the latter two hypotheses have more credence, although testosterone levels are higher in female than male trout. Between the early 1950s and 1998 there has been a marked decline in the prevalence, abundance and diversity of the helminth parasite communities in salmonid fish as well as their intermediate hosts. Possible reasons for these declines include heavy metal pollution, increased acidity and habitat degradation linked to changes in land use. It is concluded that although helminth parasites can provide supplementary information on pollution. the use of biotic indices based on the Biological monitoring working party (BMWP) or River invertebrate prediction and classification system (RIVPACS) methods are preferable. However, as these methods were designed to measure the impact of organic pollution they lack the sensitivity for measuring metal pollution. It is advocated therefore that new biomonitoring methods should be developed to measure the impact of heavy metal pollution using biotic indices based on the sampling of the susceptible invertebrate communities inhabiting depositing sediments in the transmission sites of helminth parasites.

Animals↗

The reserve-capacity hypothesis: evolutionary origins and modern implications of the trade-off between tumor-suppression and tissue-repair.

Antagonistic pleiotropy, the evolutionary theory of senescence, posits that age related somatic decline is the inevitable late-life by-product of adaptations that increase fitness in early life. That concept, coupled with recent findings in oncology and gerontology, provides the foundation for an integrative theory of vertebrate senescence that reconciles aspects of the 'accumulated damage' 'metabolic rate', and 'oxidative stress' models. We hypothesize that (1) in vertebrates, a telomeric fail-safe inhibits tumor formation by limiting cellular proliferation. (2) The same system results in the progressive degradation of tissue function with age. (3) These patterns are manifestations of an evolved antagonistic pleiotropy in which extrinsic causes of mortality favor a species-optimal balance between tumor suppression and tissue repair. (4) With that trade-off as a fundamental constraint, selection adjusts telomere lengths--longer telomeres increasing the capacity for repair, shorter telomeres increasing tumor resistance. (5) In environments where extrinsically induced mortality is frequent, selection against senescence is comparatively weak as few individuals live long enough to suffer a substantial phenotypic decline. The weaker the selection against senescence, the further the optimal balance point moves toward shorter telomeres and increased tumor suppression. The stronger the selection against senescence, the farther the optimal balance point moves toward longer telomeres, increasing the capacity for tissue repair, slowing senescence and elevating tumor risks. (6) In iteroparous organisms selection tends to co-ordinate rates of senescence between tissues, such that no one organ generally limits life-span. A subsidiary hypothesis argues that senescent decline is the combined effect of (1) uncompensated cellular attrition and (2) increasing histological entropy. Entropy increases due to a loss of the intra-tissue positional information that normally regulates cell fate and function. Informational loss is subject to positive feedback, producing the ever-accelerating pattern of senescence characteristic of iteroparous vertebrates. Though telomere erosion begins early in development, the onset of senescence should, on average, be deferred to the species-typical age of first reproduction, the balance point at which selection on this trade-off should allow exhaustion of replicative capacity to overtake some cell lines. We observe that captive-rodent breeding protocols, designed to increase reproductive output, simultaneously exert strong selection against reproductive senescence and virtually eliminate selection that would otherwise favor tumor suppression. This appears to have greatly elongated the telomeres of laboratory mice. With their telomeric failsafe effectively disabled, these animals are unreliable models of normal senescence and tumor formation. Safety tests employing these animals likely overestimate cancer risks and underestimate tissue damage and consequent accelerated senescence.

Aging↗