Health Effects of Toxin-Producing Cyanobacteria: “The CyanoHABs”

Increasingly, harmful algal blooms (HABs) are being reported worldwide due to several factors, primarily eutrophication, climate change and more scientific monitoring. All but cyanobacteria toxin poisonings (CTPs) are mainly a marine occurrence. CTPs occur in fresh (lakes, ponds, rivers and reservoirs) and brackish (seas, estuaries, and lakes) waters throughout the world. Organisms responsible include an estimated 40 genera but the main ones are Anabaena, Aphanizomenon, Cylindrospermopsis, Lyngbya, Microcystis, Nostoc, and Oscillatoria (Planktothrix). Cyanobacteria toxins (cyanotoxins) include cytotoxins and biotoxins with biotoxins being responsible for acute lethal, acute, chronic and sub-chronic poisonings of wild/domestic animals and humans. The biotoxins include the neurotoxins; ana-toxin-a, anatoxin-a(s) and saxitoxins plus the hepatotoxins; microcystins, nodularins and cylindrospermopsins. Confirmations of human deaths from cyanotoxins are limited to exposure through renal dialysis at a haemodialysis center in Caruaru, Brazil, in 1996. A major effort to compile all available information on toxic cyanobacteria including issues of human health, safe water practices, management, prevention and remediation have been published by the World Health Organization. This paper will review our current understanding of CTP's including their risk to human health.     

The Genetic Code: What Is It Good For? An Analysis of the Effects of Selection Pressures on Genetic Codes

How did the ``universal' genetic code arise? Several hypotheses have been put forward, and the code has been analyzed extensively by authors looking for clues to selection pressures that might have acted during its evolution. But this approach has been ineffective. Although an impressive number of properties has been attributed to the universal code, it has been impossible to determine whether selection on any of these properties was important in the code's evolution or whether the observed properties arose as a consequence of selection on some other characteristic. Therefore we turned the question around and asked, what would a genetic code look like if it had evolved in response to various different selection pressures? To address this question, we constructed a genetic algorithm. We found first that selecting on a particular measure yields codes that are similar to each other. Second, we found that the universal code is far from minimized with respect to the effects of mutations (or translation errors) on the amino acid compositions of proteins. Finally, we found that the codes that most closely resembled real codes were those generated by selecting on aspects of the code's structure, not those generated by selecting to minimize the effects of amino acid substitutions on proteins. This suggests that the universal genetic code has been selected for a particular structure—a structure that confers an important flexibility on the evolution of genes and proteins—and that the particular assignments of amino acids to codons are secondary. Received: 29 December 1998 / Accepted: 8 July 1999     

The Effects of Predator Evolution and Genetic Variation on Predator–Prey Population-Level Dynamics

This paper explores how predator evolution and the magnitude of predator genetic variation alter the population-level dynamics of predator–prey systems. We do this by analyzing a general eco-evolutionary predator–prey model using four methods: Method 1 identifies how eco-evolutionary feedbacks alter system stability in the fast and slow evolution limits; Method 2 identifies how the amount of standing predator genetic variation alters system stability; Method 3 identifies how the phase lags in predator–prey cycles depend on the amount of genetic variation; and Method 4 determines conditions for different cycle shapes in the fast and slow evolution limits using geometric singular perturbation theory. With these four methods, we identify the conditions under which predator evolution alters system stability and shapes of predator–prey cycles, and how those effect depend on the amount of genetic variation in the predator population. We discuss the advantages and disadvantages of each method and the relations between the four methods. This work shows how the four methods can be used in tandem to make general predictions about eco-evolutionary dynamics and feedbacks.     

Genetic Variation in Toxicant-Stressed Populations: An Evaluation of the “Genetic Erosion” Hypothesis

The question whether environmental pollution affects genetic diversity in natural populations remains unanswered to date despite the fact that genetic variation is one of the three pillars of biodiversity recognized in the Rio convention of 1993. The loss of genetic diversity in populations subjected to anthropogenic stress can be designated as “genetic erosion” and may be considered as a factor of concern in risk assessment of toxic chemicals. Theoretically there are four different ways in which toxicants can affect genetic variation: (i) by increasing mutation rates, (ii) by directional selection on tolerant genotypes, (iii) by causing bottleneck events, and (iv) by altering migration. This paper reviews studies that have documented genetic change in animal populations exposed to environmental pollution. In these studies, genetic variation is measured in a variety of ways: heritability of quantitative characters, heterozygosity of allozyme loci, haplotype diversity in mitochondrial DNA, and variability in RAPD fingerprints. Studies on cadmium tolerance of Collembola living in metal-contaminated soil suggest that strong directional selection pressure may decrease genetic variability of traits immediately linked to tolerance. Allozyme studies in fish have documented a similar decrease of genetic variation in populations living in strongly acidified waters. A correlation between RAPD-PCR-based genetic similarity and site contamination has been documented in crayfish. Overall, there is significant support for the genetic erosion hypothesis, but the issue cannot be considered settled. In most studies insufficient attention is given to factors such as population size, bottlenecks and mutation, which may influence genetic variability in addition to the toxicant selection regime. At the moment, there does not seem to be a sound scientific basis for incorporating genetic diversity measurements into risk assessment, despite the variety of easily applicable molecular techniques available. It is often not known what kind of variation is measured by these techniques (neutral or selectable) and how the markers are inherited. Given the importance of the issue, as stressed by the Rio Convention, a concentrated research effort is necessary to better define the question and find a general approach to evaluate its importance in ecological risk assessment.     

Genetic control of “natural” killer lymphocytes in the mouse

Spleens from normal young mice contain lymphocytes that can kill certain in vitro grown Moloney lymphoma lines in a⁵¹Cr-release cytotoxicity test. A lymphoid cell without detectable T- or B-cell markers was previously shown to be responsible. Killing activity shows a marked dependence on the genotype of the donor mouse. When tested against a YAC line of strain A origin maintained in vitro spleens of A, A.CA, and A.SW mice had low activity, whereas CBA, C3H, C57L, and C57Bl spleens were highly active. In semisyngeneic F₁ crosses with strain A as one parent, reactivity resembled the opposite parental strain. Thus, (A×CBA)F₁, (A×C3H)F₁, (A×C57L)F₁, and (A×C57Bl)F₁ were reactive, whereas A×A.CA showed no significant activity. Analysis of the reactivity in (A×C57Bl)F₁×A backcross mice suggests that multiple genes are involved. Preliminary linkage analysis suggests at least oneH-2 linked factor. Another gene appears to be linked to theB (black) locus.     

Erratum to: “Effects of Different Conservation Methods on the Genetic Stability of Potato Germplasm”

Russian Journal of Plant Physiology -     

The Effects of Water Stress on Photosystem Ⅱ in Wheat

The fluorescence yield at room temperature, the capacity of excitation energy distribution between photosystem Ⅰ and Ⅱ by Mg2+, variable fluorescence yield, variable fluorescence quenching rate and fluorescence complementary area were decreased under water stress. These indicated that photosystem Il was impaired. The inhibited variable fluorescence yield could be partly recovered by the addition of artificial electron donor DPC. Therefore, water stress inhibited not only the oxidizing site of photosystem Ⅱ but also impaired partly the reaction center of photosystem Ⅱ.     

The Uncertainty of “Fitness”: What Prevents Understanding of the Role of Genetic Exchange

The evolutionary development of highly organized species is attained through an increase in average survival of individuals, whereas the evolution of primitive species involves only an increase in fecundity (Zavadsky, 1968). However, in population genetics, survival (or ecological resistance) and fecundity are regarded as components of a single character, fitness. Employment of the notion of fitness, which lacks a strict definition, hinders understanding of the mechanism of progressive evolution as the process that enhances ecological resistance of organisms. The notion of fitness also hinders understanding the role of genetic exchange, since the primary advantage of genetic recombination and sexual reproduction apparently is producing of progeny with high ecological resistance rather than with high genetic diversity as such. Thus, the regular genetic exchange ensures restoration of the level of ecological resistance characteristic for the species, and on the macroevolutionary scale leads to the formation of new genomes and new species with high ecological resistance.     

The “Genetic Program”: Behind the Genesis of an Influential Metaphor

The metaphor of the “genetic program,” indicating the genome as a set of instructions required to build a phenotype, has been very influential in biology despite various criticisms over the years. This metaphor, first published in 1961, is thought to have been invented independently in two different articles, one by Ernst Mayr and the other by François Jacob and Jacques Monod. Here, after a detailed analysis of what both parties meant by “genetic program,” I show, using unpublished archives, the strong resemblance between the ideas of Mayr and Monod and suggest that their idea of genetic program probably shares a common origin. I explore the possibility that the two men met before 1961 and also exchanged their ideas through common friends and colleagues in the field of molecular biology. Based on unpublished correspondence of Jacob and Monod, I highlight the important events that influenced the preparation of their influential paper, which introduced the concept of the genetic program. Finally, I suggest that the genetic program metaphor may have preceded both papers and that it was probably used informally before 1961.     

What's in a Cause?: The Pragmatic Dimensions of Genetic Explanations

The paper argues for a pragmatic account of genetic explanation. This is to say that when a disease or other trait is termed genetic, the reasons for singling out genes as causes over other, also necessary, genetic and nongenetic conditions are not wholly theoretical but include pragmatic dimensions. Whether the explanation is the presence of a trait in an individual or differences in a trait among individuals, genetic explanations are context-dependent in three ways: they are relative to a causal background of genetic and nongenetic factors; they are relative to a population; and they are relative to the present state of knowledge. Criteria like causal priority, nonstandardness, and causal efficacy that purport to distinguish objectively between genetic causes and nongenetic conditions either incorporate pragmatic elements or fail for other reasons. When the pragmatic dimensions of genetic explanations are recognized, we come to understand the current phenomenon of geneticization to be a reflection of increased technological capacities to manipulate genes in the laboratory, and potentially the clinic, rather than theoretical progress in understanding how diseases and other traits arise. This calls into question the value of the search for theoretical definitions of designations like genetic disease or genetic susceptibility as directives for action.     

Genetic mining of the “dark matter” in fungal natural products

<正>Filamentous fungi are one of the major sources of natural products (NPs; which are also termed as secondary metabolites (SMs)) with diverse biological activities, which have been widely used in agriculture, industry, and pharmaceuticals. Fungi are the second largest species in nature, and their biodiversity implies genomic diversity, which, in turn,predicts the structural diversity of metabolites. In general,     

The strategy of “The strategy of model building in population biology”

In this essay, I argue for four related claims. First, Richard Levins’ classic “The Strategy of Model Building in Population Biology” was a statement and defense of theoretical population biology growing out of collaborations between Robert MacArthur, Richard Lewontin, E. O. Wilson, and others. Second, I argue that the essay served as a response to the rise of systems ecology especially as pioneered by Kenneth Watt. Third, the arguments offered by Levins against systems ecology and in favor of his own methodological program are best construed as “pragmatic”. Fourth, I consider limitations of Levins’ arguments given contemporary population biology.

The Sex Specific Genetic Variation of Energetics in Bank Voles,Consequences of Introgression?

Interaction between mitochondrial and nuclear genomes is expected to affect energetic phenotypes of traits linked to mitochondrial physiology, further influencing the fitness. A rodent, the bank vole (Myodes glareolus), has a population structure completely or partially introgressed with mitochondria from its relative, the red vole (M. r utilus). Females that carried either bank vole mitochondria or mitochondria from the introgressed species were repeatedly mated with males of both mtDNA types. We found that in males, but not in females, morpho-physiological phenotypes are affected by sire type, causing decreases in body mass (BM) and basal metabolic rate (BMR; including BM corrected, rBMR) in individuals sired by fathers carrying introgressed mitochondria. Higher effect sizes for the proportion of additive genetic variation (and 5.6, 1.9 and 3.6 times higher narrow sense heritability for BM, BMR and rBMR, respectively), and lower for proportion of environmental variation were detected in progeny of non-introgressed males. Our data indicate that co-adapted and possibly co-introgressed nuclear genes related to energetic physiology have an important role in adaptation to the northern conditions in bank voles, and that sex linked nuclear genes are a potential source for variation in basal metabolic rate.