Introduction

Author(s):  
Timothy G. Barraclough

This chapter explains what the book is about and highlights the range of processes and questions to be considered. The central thesis is that species represent more than a unit of taxonomy, they are a model of how diversity is structured and how groups of organisms evolve. All organisms live in diverse communities with hundreds of other species. Knowledge of what species are, how they form, and the genetic and ecological interactions among them is therefore vital both for understanding where diversity comes from and for predicting contemporary and future evolution. It is time for evolutionary biology to embrace the diversity of life.

Author(s):  
Timothy G. Barraclough

‘Species’ are central to understanding the origin and dynamics of biological diversity; explaining why lineages split into multiple distinct species is one of the main goals of evolutionary biology. However, the existence of species is often taken for granted, and precisely what is meant by species and whether they really exist as a pattern of nature has rarely been modelled or critically tested. This novel book presents a synthetic overview of the evolutionary biology of species, describing what species are, how they form, the consequences of species boundaries and diversity for evolution, and patterns of species accumulation over time. The central thesis is that species represent more than just a unit of taxonomy; they are a model of how diversity is structured as well as how groups of related organisms evolve. The author adopts an intentionally broad approach to consider what species constitute, both theoretically and empirically, and how we detect them, drawing on a wealth of examples from microbes to multicellular organisms.


Author(s):  
Marc W. Cadotte ◽  
T. Jonathan Davies

This chapter reviews the history of the use of phylogenetics in ecology, beginning with a discussion of early attempts to classify the diversity of life and the development of evolutionary theory. In particular, it examines how early taxonomists, starting with Carl Linnaeus, have grouped species by similarity in their traits and how early ecologists and biologists such as Charles Darwin recognized the importance of relatedness in influencing ecological interactions and species distributions. The chapter proceeds by focusing on the introduction of the neutral theory of biodiversity into mainstream ecology and the development of the niche-based model of community assembly. It also considers how some ecologists questioned the relevance of phylogenetic corrections for ecology and concludes by analyzing the emergence of ecological phylogenetics or ecophylogenetics.


Author(s):  
Neo Martinez

Elucidating how an organism’s characteristics emerge from its DNA sequence has been one of the great triumphs of biology. This triumph has cumulated in sophisticated computational models that successfully predict how an organism’s detailed phenotype emerges from its specific genotype. Inspired by that effort’s vision and empowered by its methodologies, this Viewpoint describes a grand challenge to predict the biotic characteristics of an ecosystem, its metaphenome, from nucleic acid sequences of all the species in its community, its metagenome. Meeting this challenge would integrate rapidly advancing abilities of environmental nucleic acids (eDNA and eRNA) to identify organisms, their ecological interactions, and their evolutionary relationships with advances in mechanistic models of complex ecosystems. Addressing the challenge aims to help integrate ecology and evolutionary biology into a more unified and successfully predictive science that can better help describe and manage ecosystems and the services they provide to humanity.


2017 ◽  
Vol 7 (5) ◽  
pp. 20170015 ◽  
Author(s):  
Gerd B. Müller

Since the last major theoretical integration in evolutionary biology—the modern synthesis (MS) of the 1940s—the biosciences have made significant advances. The rise of molecular biology and evolutionary developmental biology, the recognition of ecological development, niche construction and multiple inheritance systems, the ‘-omics’ revolution and the science of systems biology, among other developments, have provided a wealth of new knowledge about the factors responsible for evolutionary change. Some of these results are in agreement with the standard theory and others reveal different properties of the evolutionary process. A renewed and extended theoretical synthesis, advocated by several authors in this issue, aims to unite pertinent concepts that emerge from the novel fields with elements of the standard theory. The resulting theoretical framework differs from the latter in its core logic and predictive capacities. Whereas the MS theory and its various amendments concentrate on genetic and adaptive variation in populations, the extended framework emphasizes the role of constructive processes, ecological interactions and systems dynamics in the evolution of organismal complexity as well as its social and cultural conditions. Single-level and unilinear causation is replaced by multilevel and reciprocal causation. Among other consequences, the extended framework overcomes many of the limitations of traditional gene-centric explanation and entails a revised understanding of the role of natural selection in the evolutionary process. All these features stimulate research into new areas of evolutionary biology.


2010 ◽  
Vol 365 (1537) ◽  
pp. 133-145 ◽  
Author(s):  
Simon Conway Morris

Evolutionary biology rejoices in the diversity of life, but this comes at a cost: other than working in the common framework of neo-Darwinian evolution, specialists in, for example, diatoms and mammals have little to say to each other. Accordingly, their research tends to track the particularities and peculiarities of a given group and seldom enquires whether there are any wider or deeper sets of explanations. Here, I present evidence in support of the heterodox idea that evolution might look to a general theory that does more than serve as a tautology (‘evolution explains evolution’). Specifically, I argue that far from its myriad of products being fortuitous and accidental, evolution is remarkably predictable. Thus, I urge a move away from the continuing obsession with Darwinian mechanisms, which are entirely uncontroversial. Rather, I emphasize why we should seek explanations for ubiquitous evolutionary convergence, as well as the emergence of complex integrated systems. At present, evolutionary theory seems to be akin to nineteenth-century physics, blissfully unaware of the imminent arrival of quantum mechanics and general relativity. Physics had its Newton, biology its Darwin: evolutionary biology now awaits its Einstein.


2017 ◽  
Author(s):  
Michael E Hochberg

One of the great challenges in ecology and evolutionary biology is to explain disease, whether caused by infectious agents such as parasites and pathogens, or by the deterioration or transformation of cellular behavior and function, a prime example of the latter being cancer. Decades of observation and research suggest that successfully treating disease requires insights into how the environment mediates the interactions between disease causing agents (DCAs) and diseased individuals. A major finding is that single factor, targeted therapies are not only likely to fail in controlling or eradicating many DCAs, but are also likely to select for resistance, reducing options for subsequent treatment attempts, and in cases of infectious DCAs, rendering therapeutic agents (e.g., antibiotics) obsolete. I argue that meeting the growing challenge of treating disease in agriculture and animal husbandry, in protected and domesticated species, wildlife, and in the human population will require a fundamental understanding of ecological interactions at sites of infection or disease. I discuss different ways in which components of such disease ecosystems mediate DCA and therapeutic dynamics and resistance evolution, and derive a very simple mathematical criterion for therapeutic success. I then touch on how fundamental insights as revealed by the processes of evolutionary rescue and competitive release can help understand why therapies succeed or fail. Finally, I present six “wedges” that can each contribute alone, or as part of multi-pronged approaches to successfully treating disease.


Author(s):  
Dan P. McAdams

“Primate” delves into evolutionary biology and primatology to unearth the psychological roots of human leadership as they apply to the case of President Donald J. Trump. In broad terms, evolved patterns of human leadership follow one of two forms. The older form, dominance leadership, traces back over 7 million years to our common ancestor with chimpanzees. The latter form, prestige leadership, traces back about 1 million years or so, reflecting our evolution as hunters and gatherers living in migrating groups. More than any president in American history, Trump personifies the pure dominance leader. The chapter documents the uncanny similarities between the behavior of alpha male chimpanzees and the leadership style of President Donald Trump. Dominance leaders rely upon force, bluffing, intimidation, and the power of their presence, whereas prestige leaders rely upon expertise and the promulgation of a narrative to justify authority. This characterization recalls the central thesis of the book: Donald Trump is a man without a story.


2017 ◽  
Vol 372 (1735) ◽  
pp. 20160431 ◽  
Author(s):  
Miguel A. Fortuna ◽  
Luis Zaman ◽  
Andreas Wagner ◽  
Jordi Bascompte

The origin of evolutionary innovations is a central problem in evolutionary biology. To what extent such innovations have adaptive or non-adaptive origins is hard to assess in real organisms. This limitation, however, can be overcome using digital organisms, i.e. self-replicating computer programs that mutate, evolve and coevolve within a user-defined computational environment. Here, we quantify the role of the non-adaptive origins of host resistance traits in determining the evolution of ecological interactions among host and parasite digital organisms. We find that host resistance traits arising spontaneously as exaptations increase the complexity of antagonistic host–parasite networks. Specifically, they lead to higher host phenotypic diversification, a larger number of ecological interactions and higher heterogeneity in interaction strengths. Given the potential of network architecture to affect network dynamics, such exaptations may increase the persistence of entire communities. Our in silico approach, therefore, may complement current theoretical advances aimed at disentangling the ecological and evolutionary mechanisms shaping species interaction networks. This article is part of the themed issue ‘Process and pattern in innovations from cells to societies’.


2017 ◽  
Author(s):  
Michael E Hochberg

One of the great challenges in ecology and evolutionary biology is to explain disease, whether caused by infectious agents such as parasites and pathogens, or by the deterioration or transformation of cellular behavior and function, a prime example of the latter being cancer. Decades of observation and research suggest that successfully treating disease requires insights into how the environment mediates the interactions between disease causing agents (DCAs) and diseased individuals. A major finding is that single factor, targeted therapies are not only likely to fail in controlling or eradicating many DCAs, but are also likely to select for resistance, reducing options for subsequent treatment attempts, and in cases of infectious DCAs, rendering therapeutic agents (e.g., antibiotics) obsolete. I argue that meeting the growing challenge of treating disease in agriculture and animal husbandry, in protected and domesticated species, wildlife, and in the human population will require a fundamental understanding of ecological interactions at sites of infection or disease. I discuss different ways in which components of such disease ecosystems mediate DCA and therapeutic dynamics and resistance evolution, and derive a very simple mathematical criterion for therapeutic success. I then touch on how fundamental insights as revealed by the processes of evolutionary rescue and competitive release can help understand why therapies succeed or fail. Finally, I present six “wedges” that can each contribute alone, or as part of multi-pronged approaches to successfully treating disease.


2017 ◽  
Vol 47 (2) ◽  
pp. 127-163
Author(s):  
Rachel Mason Dentinger

The field of “coevolutionary studies” is the origin of many evocative stories in evolutionary biology, as well as a demonstration of the value of studying the ecological interactions of whole organisms and populations. This field exploded after the publication of “Butterflies and Plants: A Study in Coevolution,” a 1964 paper co-authored by entomologist Paul Ehrlich and botanist Peter Raven. However, this paper argues that the foundation for “Butterflies and Plants” was laid in the previous decades, in the work of economic entomologists, crop-plant breeders, and insect physiologists. Using the work of an influential insect physiologist, Gottfried S. Fraenkel, this paper examines the prehistory of coevolutionary studies, showing that practical research on insect feeding in the 1940s and 1950s transformed plant chemicals into active biological molecules—causal forces modeled on hormones. Insect physiologists were the first to study the effects of these molecules on insects. Yet, rather than redefining insect-plant interactions in terms of reductionist molecular causation, they sought a more integrative explanation. Not only did these insect biologists see plants as active participants in their ecological and evolutionary landscapes, but they also came to see evolutionary history as the “raison d’être” of plant molecules and insect feeding behavior. This paper expands our understanding of the generative role that physiology and molecular methods played in the development of concepts and practices in evolutionary biology. Furthermore, it contributes to a growing literature that undermines the historical division between proximate and ultimate causation in biology.


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