Cultural evolution and the variable phenotype

It is common in attempts to extend the theory of evolution to culture to generalize from the causal basis of biological evolution, so that evolutionary theory becomes the theory of copying processes. Generalizing from the formal dynamics of evolution allows greater leeway in what kinds of things cultural entities can be, if they are to evolve. By understanding the phenomenon of cultural transmission in terms of coordinated phenotypic variability, we can have a theory of cultural evolution which allows us to avoid the various difficulties with the elaboration of informational entities such as the cultural replicator, or meme. Such an account is a boon to the project of evolutionary epistemology since it confirms the presumption in favor of the general adaptiveness of culture, illuminating rather than obscuring the inherent intimacy of our relationship to (e.g.) our ideas.     

Origin of Sex Revisited

Why did sex ever arise in the first place? Why it does not disappear in view of the greater efficiency of asexuals? These are clearly two different questions, and we suggest here that the solution for the origin of sex does not necessarily come from theoretical considerations based on currently existing genetic systems. Thus, while we agree with a number of authors in that the emergence of sex (understood as the exchange of genetic material between genomes) is deeply rooted in the origin of life and happened during the very early stages in the transition from individual genes (`replicators') to bacteria-like cells (`reproducers'), we challenge the idea that recombinational repair was the major selective force for the emergence of sex. Taking the stochastic corrector model as a starting point, we provide arguments that question the putative costs of redundancy in primitive protocells. In addition, if genes that cause intragenomic conflict (i.e., parasites) are taken into account, it is certainly wrong to suggest that cellular fusion would be beneficial at the population level (although this strong claim needs some qualifications). However, when a continuous input of deleterious mutations that impair the fitness of the protocell as a whole is considered in the model (in the realistic range in which stable mutant distributions of quasi-species within compartments are established), there are circumstances when sex could be beneficial as a side effect of the dynamic equilibrium between cellular fusion-mutation-selection. The scenario we have explored numerically is fully consistent with the idea that the universal ancestor was not a discrete entity but an ensemble of proto-organisms that exchanged much genetic information.     

Acytota – associated kingdom of neglected life

There is a huge variety of RNA- and DNA-containing entities that multiply within and propagate between cells across all kingdoms of life, having no cells of their own. Apart from cellular organisms, these entities (viroids, plasmids, mobile elements and viruses among others) are the only ones with distinct genetic identities but which are not included in any traditional tree of life. We suggest to introduce or, rather, revive the distinct category of acellular organisms, Acytota, as an additional, undeservedly ignored full-fledged kingdom of life. Acytota are indispensable players in cellular life and its evolution. The six traditional kingdoms (Cytota) and Acytota together complete the classification of the biological world (Biota), leaving nothing beyond.     

High copy number plasmid vectors for use in lactic streptococci

Abstract A 3.8 kb DNA fragment from plasmid pBD64 which encoded chloramphenicol and kanamycin resistance genes, but had no replication region, was used as a replicator probe to select for the replication region of the cryptic lactic streptococcal plasmid pSH71 using Bacillus subtilis as host. Three of the resultant recombinant plasmids, pCK1, pCK17 and pCK21 are described. They are vectors in Streptococcus lactis and can be used to clone Bgl II-compatible fragments into their kanamycin resistance gene. All the plasmids have single sites for restriction endonucleases Ava I, Bam HI, Eco RI, Pvu II and Xba I, while plasmids pCK17 and pCK21 have single sites for Cla I.