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Summary: Expressed subtype of paralogous genes in functionally homologous cells sometimes show differences across species, the reasons for which have not been explained. The present study examined hypophysiotropic gonadotropin-releasing hormone (GnRH) neurons in vertebrates to investigate this mechanism. These neurons express either gnrh1 or gnrh3 paralogs, depending on the species, and apparent switching of the expressed paralogs in them occurred at least four times in vertebrate evolution. First, we found redundant expression of gnrh1 and gnrh3 in a single neuron in piranha and hypothesized that it may represent an ancestral GnRH system. Moreover, the gnrh1/gnrh3 enhancer of piranha induced reporter RFP/GFP co-expression in a single hypophysiotropic GnRH neuron in both zebrafish and medaka, whose GnRH neurons only express either gnrh3 or gnrh1. Thus, we propose that redundant expression of gnrh1/3 of relatively recent common ancestors may be the key to apparent switching of the paralog usage among present-day species.

The present paper attempts a comprehensive approach to the biological, cognitive, as well as cultural foundations of theory of mind development. A critical analysis and synthesis of contemporary research findings serves as a basis for revisiting key theoretical accounts regarding the nature and development of this valuable sociocognitive faculty. Are the findings best interpreted within frameworks which consider developmental change and individual differences in the domain-general cognitive abilities (executive functions) that may underlie performance on theory of mind tasks (processing account)? Or is it more fruitful to discuss the development of theory of mind based on domain-specific mechanisms or capacities: an innate, modular mechanism that is underpinned by neurological maturation (modularity theories), or an inborn capacity to form naïve, intuitive theories about the mind, which are then subject to conceptual change as a function of experience (theory theory account), or a mechanism that serves simulations of mental states and related attributions (simulation theories)? Where possible, biological and neurocognitive processes, and experiential influences are discussed in combination. A disentanglement of general cultural influences from more proximal, social or familial effects on theory of mind development is also attempted. The aim is to highlight the value of an integrative, interdisciplinary approach to its study: a biocultural perspective could essentially serve this purpose by shifting attention to the interplay of biological, cognitive, and environmental forces shaping the lifespan dynamics of human theory of mind.

Summary: Species diversity can vary dramatically across lineages due to differences in speciation and extinction rates. Here, we explore the effects of several plant traits on diversification, finding that most traits have opposing effects on diversification. For example, outcrossing may increase the efficacy of selection and adaptation but also decrease mate availability, two processes with contrasting effects on lineage persistence. Such opposing trait effects can manifest as differences in diversification rates that depend on ecological context, spatiotemporal scale, and associations with other traits. The complexity of pathways linking traits to diversification suggests that the mechanistic underpinnings behind their correlations may be difficult to interpret with any certainty, and context dependence means that the effects of specific traits on diversification are likely to differ across multiple lineages and timescales. This calls for taxonomically and context-controlled approaches to studies that correlate traits and diversification.

Summary: Drug resistance and metastasis—the major complications in cancer—both entail adaptation of cancer cells to stress, whether a drug or a lethal new environment. Intriguingly, these adaptive processes share similar features that cannot be explained by a pure Darwinian scheme, including dormancy, increased heterogeneity, and stress-induced plasticity. Here, we propose that learning theory offers a framework to explain these features and may shed light on these two intricate processes. In this framework, learning is performed at the single-cell level, by stress-driven exploratory trial-and-error. Such a process is not contingent on pre-existing pathways but on a random search for a state that diminishes the stress. We review underlying mechanisms that may support this search, and show by using a learning model that such exploratory learning is feasible in a high-dimensional system as the cell. At the population level, we view the tissue as a network of exploring agents that communicate, restraining cancer formation in health. In this view, disease results from the breakdown of homeostasis between cellular exploratory drive and tissue homeostasis.

The great advances of the last decades both in cognitive theories and in evolutionary biology have not yet fully merged. Most evolutionary hypotheses around the mind still rely on classical cognitivism, while most theories of cognition still look for adaptive explanations. We believe that the merging of novel cognitive theories into a pluralistic account can greatly improve our understanding of both what cognition is and how it evolved.

Summary: Cancers are the result of eco-evolutionary processes fueled by heritable phenotypic diversification and driven by environmentally dependent selection. Space represents a key growth-limiting ecological resource, the ability to explore this resource is likely under strong selection. Using agent-based modeling, we explored the interplay between phenotypic strategies centered on gaining access to new space through cell-extrinsic degradation of extracellular matrix barriers and the exploitation of this resource through maximizing cell proliferation. While cell proliferation is a cell-intrinsic property, newly accessed space represents a public good, which can benefit both producers and non-producers. We found that this interplay results in ecological succession, enabling emergence of large, heterogeneous, and highly proliferative populations. Even though in our simulations both remodeling and proliferation strategies were under strong positive selection, their interplay led to sub-clonal architecture that could be interpreted as evidence for neutral evolution, warranting cautious interpretation of inferences from sequencing of cancer genomes.

Matthew Rampley´s The Seductions of Darwin. Art, Evolution, Neuroscience presents a strong critique of evolutionary and neuroscientific approaches to art. The review critically analyses author´s positions, arguments and rhetoric, concluding that the book fails in its objective to examine the value of biological approaches for art history and thus contribute to bridging the divide between science and art.

The explanation for Vedanta offered by Bhakti Niskama Santa (BNS) is valid from both scientific and philosophical grounds. It seems that the published critique of Gustavo Caetano-Anollés (GCA) to Shanta's paper is purely emotional and does not have any valid scientific or philosophical justification. In his rebuttal to Caetano-Anollés's critique, Shanta highlighted how the concept of ‘Organic Whole’ in Vedanta is completely different than that of Creationist Movement and Intelligent Design. Thus Caetano-Anollé's attempt to equate Vedanta with Creationist Movement and Intelligent Design is merely superfluous. This article highlights the validity of the argument made by Bhakti Niskama Shanta and thus also intends to clarify why the Caetano-Anollés critique is groundless.

Abstract Direct tests of the random or non-random distribution of nucleotides on genomes have been devised to test the hypothesis of neutral, nearly-neutral or selective evolution. These tests are based on the direct base distribution and are independent of the functional (coding or non-coding) or structural (repeated or unique sequences) properties of the DNA. The first approach described the longitudinal distribution of bases in tandem repeats under the Bose–Einstein statistics. A huge deviation from randomness was found. A second approach was the study of the base distribution within dinucleotides whose bases were separated by 0, 1, 2… K nucleotides. Again an enormous difference from the random distribution was found with significances out of tables and programs. These test values were periodical and included the 16 dinucleotides. For example a high “positive” (more observed than expected dinucleotides) value, found in dinucleotides whose bases were separated by (3K + 2) sites, was preceded by two smaller “negative” (less observed than expected dinucleotides) values, whose bases were separated by (3K) or (3K + 1) sites. We examined mtDNAs, prokaryote genomes and some eukaryote chromosomes and found that the significant non-random interactions and periodicities were present up to 1000 or more sites of base separation and in human chromosome 21 until separations of more than 10 millions sites. Each nucleotide has its own significant value of its distance to neutrality; this yields 16 hierarchical significances. A three dimensional table with the number of sites of separation between the bases and the 16 significances (the third dimension is the dinucleotide, individual or taxon involved) gives directly an evolutionary state of the analyzed genome that can be used to obtain phylogenies. An example is provided.