Detection vs selection: integration of genetic, epigenetic and environmental cues in fluctuating environments

ArticleThere are many inputs during development that influence an organism's fit to current or upcoming environments. These include genetic effects, transgenerational epigenetic influences, environmental cues and developmental noise, which are rarely investigated in the same formal framework. We study an analytically tractable evolutionary model, in which cues are integrated to determine mature phenotypes in fluctuating environments. Environmental cues received during development and by the mother as an adult act as detection-based (individually observed) cues. The mother's phenotype and a quantitative genetic effect act as selection-based cues (they correlate with environmental states after selection). We specify when such cues are complementary and tend to be used together, and when using the most informative cue will predominate. Thus, we extend recent analyses of the evolutionary implications of subsets of these effects by providing a general diagnosis of the conditions under which detection and selection-based influences on development are likely to evolve and coexist.This work was supported by a Leverhulme Trust International Network Grant to the four authors and by a grant from the Swedish Research Council (621-2010-5437) to O.L

Ecological genetic conflict: Genetic architecture can shift the balance between local adaptation and plasticity

This is the author accepted manuscript. The final version is available from University of Chicago Press via the DOI in this record.Genetic polymorphism can contribute to local adaptation in heterogeneous habitats, for instance as a single locus with alleles adapted to different habitats. Phenotypic plasticity can also contribute to trait variation across habitats, through developmental responses to habitat-specific cues. We show that the genetic architecture of genetically polymorphic and plasticity loci may influence the balance between local adaptation and phenotypic plasticity. These effects of genetic architecture are instances of ecological genetic conflict. A reduced effective migration rate for genes tightly linked to a genetic polymorphism provides an explanation for the effects, and they can occur both for a single trait and for a syndrome of co-adapted traits. Using individualbased simulations and numerical analysis, we investigate how among-habitat genetic polymorphism and phenotypic plasticity depend on genetic architecture. We also study the evolution of genetic architecture itself, in the form of rates of recombination between genetically polymorphic loci and plasticity loci. Our main result is that for plasticity genes that are unlinked to loci with between-habitat genetic polymorphism, the slope of a reaction norm is steeper in comparison with the slope favored by plasticity genes that are tightly linked to genes for local adaptation.This work was supported by grants from the Carl Trygger Foundation (CTS 15292) to OL and by a Leverhulme Trust International Network Grant to SRXD, PH, OL, and JMM

On the relevance of mitochondrial fusions for the accumulation of mitochondrial deletion mutants: A modelling study

The molecular mechanisms underlying the aging process are still unclear, but the clonal accumulation of mitochondrial deletion mutants is one of the prime candidates. An important question for the mitochondrial theory of aging is to discover how defective organelles might be selected at the expense of wild-type mitochondria. We propose that mitochondrial fission and fusion events are of critical importance for resolving this apparent contradiction. We show that the occurrence of fusions removes the problems associated with the idea that smaller DNA molecules accumulate because they replicate in a shorter time – the survival of the tiny (SOT) hypothesis. Furthermore, stochastic simulations of mitochondrial replication, mutation and degradation show that two important experimental findings, namely the overall low mosaic pattern of oxidative phosphorylation (OXPHOS) impaired cells in old organisms and the distribution of deletion sizes, can be reproduced and explained by this hypothesis. Finally, we make predictions that can be tested experimentally to further verify our explanation for the age-related accumulation of mitochondrial deletion mutants

Geometric Aspects of Ambrosetti-Prodi operators with Lipschitz nonlinearities

For Dirichlet boundary conditions on a bounded domain, what happens to the critical set of the Ambrosetti-Prodi operator if the nonlinearity is only a Lipschitz map? It turns out that many properties which hold in the smooth case are preserved, despite of the fact that the operator is not even differentiable at some points. In particular, a global Lyapunov-Schmidt decomposition of great convenience for numerical inversion is still available

Mech Ageing Dev

Mitochondrial morphology is regulated in many cultured eukaryotic cells by fusion and fission of mitochondria. A tightly controlled balance between fission and fusion events is required to ensure normal mitochondrial and cellular functions. During ageing, mitochondria are undergoing significant changes on the functional and morphological level. The effect of ageing on fusion and fission of mitochondria and consequences of altered fission and fusion activity are still unknown although theoretical models on ageing consider the significance of these processes. Human umbilical vein endothelial cells (HUVECs) have been established as a cell culture model to follow mitochondrial activity and dysfunction during the ageing process. Mitochondria of old and postmitotic HUVECs showed distinct alterations in overall morphology and fine structure, and furthermore, loss of mitochondrial membrane potential. In parallel, a decrease of intact mitochondrial DNA (mtDNA) was observed. Fission and fusion activity of mitochondria were quantified in living cells. Mitochondria of old HUVECs showed a significant and equal decrease of both fusion and fission activity indicating that these processes are sensitive to ageing and could contribute to the accumulation of damaged mitochondria during ageing

Individual decision making and the evolutionary roots of institutions

Just as many aspects of individual decisions are sometimes called unconscious or automatic, we know that some institutions have evolved through unconscious, nondeliberative mechanisms. Their function can also be largely nondeliberative, as in the case of some institutions that may structure behavior without requiring any reflection on the part of the participants. On the other hand, political institutions exist for the purpose of bringing deliberative mechanisms to bear on institutions in the hope of changing them for the better. The immense project of building an integrated explanation of institutions from individual brains to nations-has only barely begun. In this chapter, we report on our discussions that attempted to sketch the mechanisms that connect individuals to large-scale institutions. We begin with a discussion of current thought on the design of individual decision making. If institutions regulate behavior, then presumably the mechanisms that have evolved to produce individual behavior will be relevant to the broader enterprise of integrating these two scales of explanation. Then we explore ways in which institutions may have evolved, both as a result of individual decision making and as a result of processes distinct from those that govern individual behavior. We approach this topic from two perspectives. Seen one way, unconscious psychological forces constrain the design of institutions, sometimes powerfully. Seen another way, unconscious population-level processes create functional institutional design that few social architects could conceive of with their individual deliberate faculties

Underappreciated features of cultural evolution.

Cultural evolution theory has long been inspired by evolutionary biology. Conceptual analogies between biological and cultural evolution have led to the adoption of a range of formal theoretical approaches from population dynamics and genetics. However, this has resulted in a research programme with a strong focus on cultural transmission. Here, we contrast biological with cultural evolution, and highlight aspects of cultural evolution that have not received sufficient attention previously. We outline possible implications for evolutionary dynamics and argue that not taking them into account will limit our understanding of cultural systems. We propose 12 key questions for future research, among which are calls to improve our understanding of the combinatorial properties of cultural innovation, and the role of development and life history in cultural dynamics. Finally, we discuss how this vibrant research field can make progress by embracing its multidisciplinary nature. This article is part of the theme issue 'Foundations of cultural evolution'

The evolution of social learning as phenotypic cue integration

This is the author accepted manuscript. The final version is available from the Royal Society via the DOI in this recordMost analyses of the origins of cultural evolution focus on when and where social learning prevails over individual learning, overlooking the fact that there are other developmental inputs that influence phenotypic fit to the selective environment. This raises the question how the presence of other cue ‘channels’ affects the scope for social learning. Here, we present a model that considers the simultaneous evolution of (i) multiple forms of social learning (involving vertical or horizontal learning based on either prestige or conformity biases) within the broader context of other evolving inputs on phenotype determination, including (ii) heritable epigenetic factors, (iii) individual learning, (iv) environmental and cascading maternal effects, (v) conservative bet-hedging and (vi) genetic cues.In fluctuating environments that are autocorrelated (and hence predictable), we find that social learning from members of the same generation (horizontal social learning) explains the large majority of phenotypic variation, whereas other cues are much less important. Moreover, social learning based on prestige biases typically prevails in positively autocorrelated environments, whereas conformity biases prevail in negatively autocorrelated environments. Only when environments are unpredictable or horizontal social learning is characterised by an intrinsically low information content, other cues such as conservative bet-hedging or vertical prestige biases prevail.Leverhulme TrustSwedish Research Counci

Quantitative proteomics identifies biomarkers to distinguish pulmonary from head and neck squamous cell carcinomas by immunohistochemistry

The differentiation between a pulmonary metastasis and a newly developed squamous cell carcinoma of the lung in patients with prior head and neck squamous cell carcinoma (HNSCC) is difficult due to a lack of biomarkers but is crucially important for the prognosis and therapy of the affected patient. By using high-resolution mass spectrometry in combination with stable isotope labelling by amino acids in cell culture, we identified 379 proteins that are differentially expressed in squamous cell carcinomas of the lung and the head and neck. Of those, CAV1, CAV2, LGALS1, LGALS7, CK19, and UGDH were tested by mmunohistochemistry on 194 tissue samples (98 lung and 96 HNSCCs). The combination of CAV1 and LGALS7 was able to distinguish the origin of the squamous cell carcinoma with high accuracy (area under the curve 0.876). This biomarker panel was tested on a cohort of 12 clinically classified lung tumours of unknown origin after HNSCC. Nine of those tumours were immunohistochemically classifiable