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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., Competing Interests: Authors declare that they have no competing interests., (© 2024 The Author(s).)

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., Competing Interests: The authors declare no competing interests., (© 2023.)

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., (© 2022 The Author(s).)

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., Competing Interests: No competing interests., (© 2020 The Author(s).)

Evolution is generally considered to be unpredictable because genetic variations are known to occur randomly. However, remarkable patterns of repeated convergent evolution are observed, for instance, loss of pigments by organisms living in caves. Analogous phenotypes appear in similar environments, sometimes in response to similar constraints. Alongside randomness, a certain evolutionary determinism also exists, for instance, the selection of particular phenotypes subjected to particular environmental constraints in the "evolutionary funnel." We pursue the idea that eco-evolutionary specialization is in some way determinist. The conceptual framework of phenotypic changes entailing specialization presented in this essay explains how evolution can be predicted. We also discuss how the predictability of evolution could be tested using the case of metabolic specialization through gene losses. We also put forward that microorganisms could be key models to test and possibly make headway evolutionary predictions and knowledge about evolution., (© 2020 The Author(s).)

It is not surprising that one of the most complex phenomena in nature is that of ageing. It does not only bear biological interest, but it is also associated with cultural, psychological, social and even philosophical issues. It is therefore to be expected that a great deal of research is being performed in order to study the evolution of ageing and, more specifically, the evolution of human ageing. Historical aspects of this evolution will be discussed. Evidence from a variety of sources shows that the human lifespan is increasing, and may well continue to increase to levels that are difficult to predict. In addition, the most important theories about ageing based on evolutionary principles will be examined. Examples are mutation accumulation, antagonistic pleiotropy and the disposable soma theory. Finally, a section about future evolution of human ageing, based upon newly emerging research, will shed some light and provide speculative-provocative ideas about the future of ageing in humans.

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.

The explanation for Vedanta offered by Bhakti Niskama Santa (BNS) 1 is valid from both scientific and philosophical grounds. It seems that the published critique of Gustavo Caetano-Anollés (GCA) 2 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 3 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 1 and thus also intends to clarify why the Caetano-Anollés critique is groundless.