EVOL V13.rar

EVOL V13.rar

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While RARs show a higher specificity towards retinoid compounds binding and are the main driver in retinoid-mediated patterning and teratogenicity [e.g. recently reviewed by 103], the role of RXRs is broader. One of the reasons is the molecular promiscuity of RXR. Type II nuclear receptors, characterized by forming heterodimers with RXR, govern the transcription of a large variety of target genes [104]. They are involved in the biological responses to many endogenous ligands, anthropogenic and natural chemicals and therapeutic drugs. The affected functions include lipid metabolism (peroxisome-proliferator activated receptor, PPAR), steroidogenesis, xenobiotic response (pregnane X receptor, PXR; constitutive androstane receptor, CAR), vitamin D receptor (VDR), liver functions (FXR, LXR), orphan nuclear receptors (Nurs), and thyroid hormone signalling (thyroid hormone receptor, TR [67]; Fig. 2) [7, 85, 88, 105,106,107]. Whilst the receptors TR, VDR, and RAR form non-permissive heterodimers, the others (Fig. 2) form permissive heterodimers with RXR, where the transcriptional activity is regulated by a ligand binding to one of the dimerization partners [85, 104, 106]. Dimerization is achieved via the asymmetrical so-called identity box - a small region within the ligand binding domain, which, in the case of RXRα, consists of 40 amino acids [108, 109]. This subdomain shows a very high degree of conservation. Especially, the two amino acids A416 and R421 have been shown crucial for dimerization of RXRα with RAR [108, 109]. The high conservation of the RXR identity box even across animal phyla underlines the evolutionary importance of RXR [110, 111].

The importance of co-evolution of nuclear receptors and overlapping cis-regulatory elements also becomes apparent at the intersection of RAR/RXR and ERα signalling pathways. RAR/RXR signalling has been demonstrated several times to antagonize ER binding to respective DNA target sequences [118,119,120,121]. Besides the therapeutic use of this observation particularly in ER-responsive breast cancer [121], ERs play a critical role in organogenesis and maturation processes that, thus, can be affected by dietary and environmental factors.

Been using that follower mod and its been working well so far. Its not a huge issue but I have noticed that my decidueye is invisible when following me. Everything else in the mod seems to work fine and it is a great mod imo. Its especially useful when my mons are handing me full restores and evolution stones in the early game.

The kingdom Bamfordvirae comprises the majority of the realm Varidnaviria and, according to the 2021 release of Virus Taxonomy by the International Committee on Taxonomy of Viruses, consists of the phyla Nucleocytoviricota and Preplasmiviricota. There are a number of fundamental unresolved issues related to the evolution of Bamfordvirae. These are questions concerning Bamfordvirae taxonomy include the branching order of Nucleocytoviricota and the question of the monophyly of Preplasmiviricota. Here, based on the analysis of individual core proteins phylogenies, supertree, concatenated trees, dendrograms, as well as superdendrogram, we refine the branching order of major groups within phylum Nucleocytoviricota using the rooting of the entire phylum on the cellular outgroups. This effort results in several major changes in Bamfordvirae phylogeny. In particular, we show that Nucleocytoviricota consists of two sister clades, consisting of Phycodnaviridae sensu lato on the one hand and Mimiviridae sensu lato, Iridoviridae/Ascoviridae, Marseilleviridae, pithoviruses including Cedratvirus, Solumvirus, Solivirus, and Orpheovirus, mininucleoviruses, Asfarviridae sensu lato, and Poxviridae on the other hand. According to our data, Asfarviridae sensu lato and Poxviridae have likely originated from within the class Megaviricetes. We give evidence for polyphyly of the phylum Preplasmiviricota and argue for a transfer of the families Lavidaviridae, Adintoviridae and Adenoviridae from the phylum Preplasmiviricota in to the phylum Nucleocytoviricota. We also argue for the origin of the Nucleocytoviricota from small prokaryotic viruses and give arguments against the origin of Nucleocytoviricota from the Adintoviridae/Polinton-like viruses. Thus, our work, by clarifying the phylogenetic relationships within the Bamfordvirae kingdom, provides a solid basis for studying the evolutionary relationships of this kingdom with a vast diversity of supposedly related viruses outside of Bamfordvirae, including Helvetiavirae (Varidnaviria).

Both empirical and modeling approaches have employed the concept of a cost of plasticity as a cornerstone of arguments about why organisms are not infinitely and ideally plastic: the underlying assumption behind these arguments has been that organisms with an enhanced capacity to exhibit plasticity must pay a price in fitness (van Tienderen, 1991; Moran, 1992). This led to the expectation that costs or limits should be readily detectable. Dozens of investigations have explicitly looked for costs of plasticity, and many more have invoked them. Detection of costs of plasticity, however, has been infrequent (see meta-analyses by van Kleunen and Fischer, 2005; van Buskirk and Steiner, 2009). In the findings of van Buskirk and Steiner (2009), of 536 tests they report 262 positive coefficients and 262 negative coefficients, with 12 zeroes. This balanced distribution is fully consistent with the results of the regression of a random variable against fitness. Relative to the expectation from a truly random pattern, the van Buskirk and Steiner results do show a surplus of significant results (20% in each direction). However, this might derive from a combination of (a) under-reporting of non-significant findings, (b) type I error (suggested by their evidence for a higher likelihood of significance with small sample sizes) and (c) accumulation of significant results due to replicated analyses on genetically correlated traits. Furthermore, investigation of the typical two-environment tests for costs has revealed flaws in the analytical framework (Auld et al., 2010; Roff, 2011). The lack of conformation of results to predictions has prompted us to take a fresh look at both the conceptual framework and the empirical approaches to evaluating constraints on the evolution of plasticity and highlight promising areas of investigation.

In this paper, we begin by addressing the distinction between costs of plasticity and costs of phenotype production, showing that these two types of costs are often conflated. We argue that costs of phenotype are more prevalent in many investigations of plasticity, and together with the environmental context may be a critical limit to the evolution of plasticity. We then refocus on examining constraints to the evolution of plasticity. In this discussion of constraints, we evaluate how costs of phenotypes might be offset, the potential influence of limits of plasticity, and offer discussion of promising research directions not previously evaluated in this context. In contrast to previous reviews distinguishing between costs of phenotype vs costs of plasticity, here we emphasize issues critical to evaluating potential costs of plasticity. We also draw attention to the importance of limits of plasticit y in our overall discussion of constraints. We follow Auld et al. (2010) in describing the limits to plasticity as trait based, where a plastic genotype produces a phenotype further away from the optimum for a particular environment than a non-plastic genotype. In addition, we offer a synthesis of novel and integrative approaches that move beyond classic quantitative genetics models and set new goals for inquiry in plasticity.

Although the importance of environmental heterogeneity is known, relative environmental frequencies are rarely estimated (although large-scale studies are emerging, for example, Fournier-Level et al., 2011). The relative frequency of each environment and the overall diversity of environments experienced (in space and time) will shape the speed and likelihood of the evolution of adaptive reaction norms (for example, Sultan and Spencer, 2002; Scheiner, 2013). Our understanding of the importance of environmental novelty or rarity dates back to initial models of the evolution of plasticity that suggest that rarity strongly influences evolution of plasticity (for example, Levins, 1968; Via and Lande, 1985). For populations that experience rare or novel environments, plastic responses can have two important effects: they may move populations closer to the new phenotypic optimum and they may uncover phenotypic variation (cryptic genetic variation), influencing both intensity and response to selection (Chevin et al., 2010; 2008). Each effect is fundamentally interesting and of particular contemporary importance in terms of predicting organismal responses to global change (Quintero and Wiens, 2013). Such conditions that favor plasticity are widely discussed and form a foundation for our discussion of constraints.

Under conditions in which plasticity is favored, an evolutionary response via phenotypic plasticity can be hindered by a lack of genetic variation (for example, through small population size or genetic drift), extensive gene flow and genetic correlation between genes for one trait and genes for plasticity of another trait. A lack of genetic variation or continued mixing can limit phenotypic evolution and evolution of plasticity (Schlichting and Pigliucci, 1998). What is novel in contemporary studies is that our knowledge of fine scale information on raw genetic variation and population genomic information is growing exponentially.

In the absence of continued environmental variation driving selection for plasticity, mutation accumulation and selection may erode plasticity (Maughan et al., 2007; Kvitek and Sherlock, 2013; Leiby and Marx, 2014). Selection that is not absent but relatively weak purifying or positive selection (relaxed selection) is also thought to be an important constraint in the evolution of plasticity (Snell-Rood et al., 2010). Relative to a specialist, a plastic generalist will experience less effective selection on developmental pathways specific to the range of environments they experience. When gene expression is specific to different environments (for example, Aubin-Horth and Renn, 2009), a specialist in one environment will purge deleterious mutations and fix beneficial mutations faster than a generalist, which experiences multiple environments (for example, Kawecki, 1994). The constraints imposed by relaxed selection are well established in the theoretical literature where specialists will often out-compete plastic generalists, but there are few data sets directly testing this idea. Genes specific to environmentally induced morphs in social insects and beetles show greater evolutionary divergence, consistent with weakened selection under conditions where the alternative morph is favored (Snell-Rood et al., 2011). Furthermore, some of these morph-specific genes show greater genetic variation, consistent with mutation accumulation due to less effective selection, although in some cases, strong sexual selection may offset this pattern (Kijimoto et al., 2014). Although there is strong theoretical evidence for relaxed selection on alternative developmental pathways, it is possible that the environment-specific gene expression assumed in these models is rare (for example, Snell-Rood et al., 2010) because of weakened selection on alternate developmental pathways. Emerging genomic data will clarify the mechanisms underlying plasticity and give insights to the degree of environment-specific expression and the likelihood of this weakened selection as a constraint on the evolution of plasticity. 59ce067264

https://www.rebeccasaracoffey.com/forum/design-forum/zeitgeist-moving-forward-2011