The independent emergence of similar features in phylogenetically non-allied groups of organisms has usually been explained as the result of similar selection pressures particular to specific environments. This explanation has been more or less helpful in elucidating convergent resemblances among organisms since the times of Darwin. Nevertheless, intensive research has brought new knowledge on the emergence of structural similarity among organisms, especially during the last two decades. We now have manifold evidence of the phenomena of evolutionary re-entries or re-evolution, which (...) happens when a particular character present in one organic taxon also appears in another taxon which does not share an immediate ancestry. This is not the re-appearance of the same character, but rather of a similar one. Here I propose a model of threefold origin of similar phenotypic features in unrelated organisms stemming from intrinsic, extrinsic and semiosic causation. It is suggested that neither externalist nor internalist explanations per se, nor any combination thereof, are sufficient to cover all the manifold instances of character re-evolution. There is also a special group of resemblances that consists of what is originated, shaped, and retained in evolution due to meaning attributed to them by particular organic subjects. These cases cannot be fully understood without inviting a biosemiotic approach. Integrating Uexkull’s theory of meaning with the recent evolutionary developmental perspective could complete our understanding of phenotypic re-evolution. (shrink)

The negative co‐variation of life‐history traits such as fecundity and lifespan across species suggests the existence of ubiquitous trade‐offs. Mechanistically, trade‐offs result from the need to differentially allocate limited resources to traits like reproduction versus self‐maintenance, with selection favoring the evolution of optimal allocation mechanism. Here I discuss the physiological (endocrine) mechanisms that underlie optimal allocation rules and how such rules evolve. The hormone testosterone may mediate life‐history trade‐offs due to its pleiotropic actions in male vertebrates. Conservation in the actions (...) of testosterone in vertebrates has prompted the ‘evolutionary constraint hypothesis,’ which assumes that testosterone signaling mechanisms and male traits evolve as a unit. This hypothesis implies that the actions of testosterone are similar across sexes and species, and only the levels of circulating testosterone concentrations change during evolution. In contrast, the ‘evolutionary potential hypothesis’ proposes that testosterone signaling mechanisms and male traits evolve independently. In the latter scenario, the linkage between hormone and traits itself can be shaped by selection, leading to variation in trade‐off functions. I will review recent case studies supporting the evolutionary potential hypothesis and suggest micro‐evolutionary experiments to unravel the mechanistic basis of life‐history evolution. BioEssays 29: 133–144, 2007. © 2007 Wiley Periodicals, Inc. (shrink)

Understanding how traits are integrated at the organismal level remains a fundamental problem at the interface of developmental and evolutionary biology. Hormones, regulatory signaling molecules that coordinate multiple developmental and physiological processes, are major determinants underlying phenotypic integration. The probably best example for this is the lipid-like juvenile hormone (JH) in insects. Here we review the manifold effects of JH, the most versatile animal hormone, with an emphasis on the fruit fly Drosophila melanogaster, an organism amenable to both genetics and (...) endocrinology. JH affects a remarkable number of processes and traits in Drosophila development and life history, including metamorphosis, behavior, reproduction, diapause, stress resistance and aging. While many molecular details underlying JH signaling remain unknown, we argue that studying “hormonal pleiotropy” offers intriguing insights into phenotypic integration and the mechanisms underlying life history evolution. In particular, we illustrate the role of JH as a key mediator of life history trade-offs. BioEssays 27:999–1010, 2005. © 2005 Wiley Periodicals, Inc. (shrink)