\u3ci\u3eVorticella\u3c/i\u3e: A Protozoan for Bio-Inspired Engineering

In this review, we introduce Vorticella as a model biological micromachine for microscale engineering systems. Vorticella has two motile organelles: the oral cilia of the zooid and the contractile spasmoneme in the stalk. The oral cilia beat periodically, generating a water flow that translates food particles toward the animal at speeds in the order of 0.1–1 mm/s. The ciliary flow of Vorticella has been characterized by experimental measurement and theoretical modeling, and tested for flow control and mixing in microfluidic systems. The spasmoneme contracts in a few milliseconds, coiling the stalk and moving the zooid at 15–90 mm/s. Because the spasmoneme generates tension in the order of 10–100 nN, powered by calcium ion binding, it serves as a model system for biomimetic actuators in microscale engineering systems. The spasmonemal contraction of Vorticella has been characterized by experimental measurement of its dynamics and energetics, and both live and extracted Vorticellae have been tested for moving microscale objects. We describe past work to elucidate the contraction mechanism of the spasmoneme, recognizing that past and continuing efforts will increase the possibilities of using the spasmoneme as a microscale actuator as well as leading towards bioinspired actuators mimicking the spasmoneme

Active colloids in complex fluids

We review recent work on active colloids or swimmers, such as self-propelled microorganisms, phoretic colloidal particles, and artificial micro-robotic systems, moving in fluid-like environments. These environments can be water-like and Newtonian but can frequently contain macromolecules, flexible polymers, soft cells, or hard particles, which impart complex, nonlinear rheological features to the fluid. While significant progress has been made on understanding how active colloids move and interact in Newtonian fluids, little is known on how active colloids behave in complex and non-Newtonian fluids. An emerging literature is starting to show how fluid rheology can dramatically change the gaits and speeds of individual swimmers. Simultaneously, a moving swimmer induces time dependent, three dimensional fluid flows, that can modify the medium (fluid) rheological properties. This two-way, non-linear coupling at microscopic scales has profound implications at meso- and macro-scales: steady state suspension properties, emergent collective behavior, and transport of passive tracer particles. Recent exciting theoretical results and current debate on quantifying these complex active fluids highlight the need for conceptually simple experiments to guide our understanding.Comment: 6 figure

Phenotypic plasticity from a predator perspective: empirical and theoretical investigations

Phenotypic plasticity is common in predator-prey interactions. Prey use inducible defenses to increase their chances of survival in periods of high predation risk. Predators, in turn, display inducible offenses (trophic polyphenisms) and adjust their phenotypes to the prevailing type of prey. In the past, inducible defenses have received considerably more attention than inducible offenses. Here, I point out three areas where taking a predator perspective can increase our understanding of phenotypic plasticity in predator-prey systems. In Part 1, I describe an inducible offense in the predatory ciliate Lembadion bullinum: Mean cell size in a genetically uniform Lembadion population increases with the size of the dominant prey species. This size polyphenism can be explained as the result of a trade-off: Large Lembadion are superior in feeding on large prey, whereas small Lembadion achieve higher division rates when small prey is available. Consequently, inducible predator offenses may evolve as adaptations to environments where important prey characteristics vary over space or time. In Part 2, I investigate the interplay of Lembadion's inducible offense with an inducible prey defense. Lembadion releases a kairomone (i.e. an infochemical) that induces defenses in several prey species. For example, in the herbivorous ciliate Euplotes octocarinatus, it triggers the production of protective lateral "wings". I show that Lembadion can reduce the effect of this defense by activating its inducible offense. This is one of the first known examples of reciprocal phenotypic plasticity in a predator-prey system. While the counter-reaction of Lembadion decreases the fitness of the prey, it could not be shown to significantly increase the fitness of Lembadion itself. Nevertheless, I discuss the hypothesis that phenotypic plasticity in both species is a result of (diffuse) coevolution. In Part 3, I further pursue the idea of coevolution and develop a mathematical model of a coevolving predator-prey pair which displays reciprocal phenotypic plasticity. In this model, the inducible offense is a truly effective counter-adaptation to the prey's defense. The model yields three main conclusions: First, the inducible prey defense can stabilize predator-prey population dynamics. The effect of the inducible counter-offense is less clear and depends on the relative magnitude of its costs and benefits. Second, the maintenance of phenotypic plasticity requires that both the defense and the offense are sufficiently strong. Third, preliminary results suggest that an inducible offense is favored over a constitutive (permanently expressed) one if and only if the model populations perform predator-prey cycles. This leads to the hypothesis that phenotypic plasticity may evolve as an adaptation to temporal heterogeneity created by the internal dynamics of predator-prey systemsZusammenfassung 3 Abstract 5 General Introduction: A predator perspective on phenotypic plasticity 7 Part 1. Trophic size polyphenism in Lembadion bullinum: costs and benefits of an inducible offense 9 1.1 Introduction 9 1.2 Material and methods 11 1.3 Results 16 1.4 Discussion 24 Part 2. Reciprocal phenotypic plasticity in a predator prey system: inducible offenses against inducible defenses? 30 2.1 Introduction 30 2.2 Material and methods 31 2.3 Results 36 2.4 Discussion 39 Part 3. Modeling a coevolving predator-prey system with reciprocal phenotypic plasticity 44 3.1 Introduction 44 3.2 The model 47 3.3 Results 61 3.4 Discussion 127 Conclusions 133 Acknowledgements 134 Danksagungen 135 Literature cited 136 Curriculum vitae 147 Lebenslauf 14

Phenotypic plasticity from a predator perspective: empirical and theoretical investigations

Phenotypic plasticity is common in predator-prey interactions. Prey use inducible defenses to increase their chances of survival in periods of high predation risk. Predators, in turn, display inducible offenses (trophic polyphenisms) and adjust their phenotypes to the prevailing type of prey. In the past, inducible defenses have received considerably more attention than inducible offenses. Here, I point out three areas where taking a predator perspective can increase our understanding of phenotypic plasticity in predator-prey systems. In Part 1, I describe an inducible offense in the predatory ciliate Lembadion bullinum: Mean cell size in a genetically uniform Lembadion population increases with the size of the dominant prey species. This size polyphenism can be explained as the result of a trade-off: Large Lembadion are superior in feeding on large prey, whereas small Lembadion achieve higher division rates when small prey is available. Consequently, inducible predator offenses may evolve as adaptations to environments where important prey characteristics vary over space or time. In Part 2, I investigate the interplay of Lembadion's inducible offense with an inducible prey defense. Lembadion releases a kairomone (i.e. an infochemical) that induces defenses in several prey species. For example, in the herbivorous ciliate Euplotes octocarinatus, it triggers the production of protective lateral "wings". I show that Lembadion can reduce the effect of this defense by activating its inducible offense. This is one of the first known examples of reciprocal phenotypic plasticity in a predator-prey system. While the counter-reaction of Lembadion decreases the fitness of the prey, it could not be shown to significantly increase the fitness of Lembadion itself. Nevertheless, I discuss the hypothesis that phenotypic plasticity in both species is a result of (diffuse) coevolution. In Part 3, I further pursue the idea of coevolution and develop a mathematical model of a coevolving predator-prey pair which displays reciprocal phenotypic plasticity. In this model, the inducible offense is a truly effective counter-adaptation to the prey's defense. The model yields three main conclusions: First, the inducible prey defense can stabilize predator-prey population dynamics. The effect of the inducible counter-offense is less clear and depends on the relative magnitude of its costs and benefits. Second, the maintenance of phenotypic plasticity requires that both the defense and the offense are sufficiently strong. Third, preliminary results suggest that an inducible offense is favored over a constitutive (permanently expressed) one if and only if the model populations perform predator-prey cycles. This leads to the hypothesis that phenotypic plasticity may evolve as an adaptation to temporal heterogeneity created by the internal dynamics of predator-prey systems.Phänotypische Plastizität ist in Räuber-Beute Beziehungen weit verbreitet. Beuteorganismen setzen induzierbare Verteidigungen ein, um ihre Überlebenschancen in Zeiten mit hohem Prädationsrisiko zu verbessern. Räuber können ihrerseits induzierbare Angriffsmechanismen (trophische Polyphänismen) besitzen und ihren Phänotyp an die vorherrschende Beute anpassen. Bisher haben induzierbare Verteidigungen deutlich mehr Aufmerksamkeit erhalten als induzierbare Angriffsmechanismen. In dieser Arbeit zeige ich drei Gebiete auf, in denen eine "Räuberperspektive" dazu beitragen kann, unser Verständnis von phänotypischer Plastizität in Räuber-Beute Systemen zu vergrößern. Im ersten Teil beschreibe ich einen induzierbaren Angriffsmechanismus bei dem räuberischen Ciliaten Lembadion bullinum: Die mittlere Zellgröße einer genetisch einheitlichen Lembadienpopulation nimmt mit der Größe der vorherrschenden Beuteart zu. Dieser Größenpolyphänismus kann als das Ergebnis eines Kompromisses zwischen den Kosten und Nutzen des induzierbaren Angriffsmechanismus (trade-off) erklärt werden. Große Lembadien sind überlegen, wenn es darum geht, große Beute zu überwältigen. Demgegenüber erreichen kleinen Lembadien bei Anwesenheit von kleiner Beute höhere Zellteilungsraten. Daher sollten induzierbare Angriffsmechanismen dann entstehen, wenn Räuber in einer veränderlichen Umwelt leben, in der wichtige Merkmale ihrer Beute räumlich oder zeitlich variieren. Im zweiten Teil untersuche ich das Zusammenspiel zwischen dem induzierbaren An-griffsmechanismus von Lembadion und einer induzierbaren Verteidigung. Lembadion gibt ein Kairomon (einen chemischen Botenstoff) ab, der Verteidigungen bei mehreren Beutearten induziert. Unter anderem löst er bei dem herbivoren Ciliaten Euplotes octocarinatus die Bildung seitlicher "Flügel" aus. Wie ich zeige, kann Lembadion die Wirkung dieser Verteidigung verringern, indem er seinen Angriffsmechanismus aktiviert. Dies ist eines der ersten bekannten Beispiele für reziproke phänotypische Plastizität in einem Räuber-Beute System. Die Gegenreaktion von Lembadion beeinträchtigt die Fitness der Beute, es konnte aber nicht nachgewiesen werden, dass sie die Fitness von Lembadion erhöht. Dennoch diskutiere ich die Hypothese, dass die phänotypische Plastizität in beiden Arten das Ergebnis von (diffuser) Coevolution zwischen Räuber und Beute ist. Im dritten Teil verfolge ich die obige Idee weiter und entwickle ein mathematisches Modell eines Räuber-Beute Systems, in dem Coevolution und reziproke phänotypische Plastizität vorkommen und in dem der induzierbare Angriffsmechanismus des Räubers eine unzweifelhaft wirksame Gegenanpassung gegen die induzierbare Verteidigung der Beute ist. Aus dem Modell ergeben sich drei wesentliche Schlussfolgerungen: Erstens kann die induzierbare Verteidigung der Beute die Populationsdynamik stabilisieren. Der Einfluss der Gegenanpassung des Räubers ist weniger eindeutig und hängt vom Verhältnis der Kosten und Nutzen des Angriffsmechanismus ab. Zweitens kann die phänotypische Plastizität nur dann aufrechterhalten werden, wenn sowohl die Verteidigung als auch der Angriffsmechanismus hinreichend effektiv sind. Drittens deuten vorläufige Ergebnisse darauf hin, dass ein induzierbarer Angriffsmechanismus gegenüber einem konstitutiven (d.h. permanent ausgebildeten) genau dann von Vorteil ist, wenn die Populationen im Modell Räuber-Beute-Zyklen vollführen. Daraus ergibt sich die Hypothese, dass phänotypische Plastizität als Anpassung an zeitliche Heterogenität entstehen kann, die auf der internen Dynamik von Räuber-Beute Systemen beruht

The emerging field of venom-microbiomics for exploring venom as a microenvironment, and the corresponding Initiative for Venom Associated Microbes and Parasites (iVAMP)

Venom is a known source of novel antimicrobial natural products. The substantial, increasing number of these discoveries have unintentionally culminated in the misconception that venom and venom-producing glands are largely sterile environments. Culture-dependent and -independent studies on the microbial communities in venom microenvironments reveal the presence of archaea, algae, bacteria, endoparasites, fungi, protozoa, and viruses. Venom-centric microbiome studies are relatively sparse to date and the adaptive advantages that venom-associated microbes might offer to their hosts, or that hosts might provide to venom-associated microbes, remain unknown. We highlight the potential for the discovery of venom-microbiomes within the adaptive landscape of venom systems. The considerable number of known, convergently evolved venomous animals juxtaposed with the comparatively few studies to identify microbial communities in venom provides new possibilities for both biodiversity and therapeutic discoveries. We present an evidence-based argument for integrating microbiology as part of venomics to which we refer to as venom-microbiomics. We also introduce iVAMP, the Initiative for Venom Associated Microbes and Parasites (https://ivamp-consortium.github.io/), as a growing consortium for interested parties to contribute and collaborate within this subdiscipline. Our consortium seeks to support diversity, inclusion and scientific collaboration among all researchers interested in this subdiscipline

Hypothesis of the basic biological sense of cancer revisited: a putative explanation of Peto's paradox

The conventional interpretation of cancer, summarized in the unified genetic theory of carcinogenesis, assumes that the malignant cell is the anatomical and physiological unit of cancer. This assumption means that any evolutionary increase in the number of cells (and thus body size) should lead to a higher tumor incidence since the population at risk is higher. However, the available data fail to support this prediction: most animals, in particular most mammals, exhibiting wide differences in body size and lifespan, from the mouse to the blue whale, display a roughly similar tumor incidence. This unexpected lack of correlation between body size, lifespan and cancer is usually called Peto?s paradox and it has intrigued theoretical oncologists for decades.In this essay, we attempt to offer a putative explanation of this paradox based on the notion that the unit at risk of carcinogenesis is actually the tissue or organ rather than the individual cell. In turn, this notion is based on a different interpretation of neoplastic diseases that we proposed some years ago and that has been called the hypothesis of the biological sense of cancer. This hypothesis was based on the observation that throughout the animal kingdom, cancer seems to arise only in organs and tissues (or parts of them) that have experienced a significant decrease in the regenerative ability, and this would occur when a critical proportion of their cells have partially or wholly lost that capacity. In such a case, if an organism or an organ were x times larger than another one, the probability that its regenerative capacity is critically diminished would be x times lower, because an x times greater number of cells would have to be affected to depress that capacity. This lower probability would balance the proportionally higher number of their cells that could be transformed and this would explain why the blue whale displays no greater risk of developing cancer than the mouse by unit of time. However, since big animals tend to live y times longer than small ones, it remains to explain why both animals may display a similar tumor incidence by lifespan. The concept of mass-specific basal metabolic rate (msBMR) can account for this problem since msBMR diminishes with body weight as much as lifespan increases meaning that the time for individual cells to get both the natural decline in regenerative ability and potential neoplastic mutations should be, in the big animal, y times slower than in the small one. This could explain why the tumor incidence in blue whales along their long lifespan may be not higher than that observed in mice along their short life.Fil: Bustuoabad, Oscar David. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Ruggiero, Raul Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentin

Predator-Prey Dynamics Driven by Feedback between Functionally Diverse Trophic Levels

Neglecting the naturally existing functional diversity of communities and the resulting potential to respond to altered conditions may strongly reduce the realism and predictive power of ecological models. We therefore propose and study a predator-prey model that describes mutual feedback via species shifts in both predator and prey, using a dynamic trait approach. Species compositions of the two trophic levels were described by mean functional traits—prey edibility and predator food-selectivity—and functional diversities by the variances. Altered edibility triggered shifts in food-selectivity so that consumers continuously respond to the present prey composition, and vice versa. This trait-mediated feedback mechanism resulted in a complex dynamic behavior with ongoing oscillations in the mean trait values, reflecting continuous reorganization of the trophic levels. The feedback was only possible if sufficient functional diversity was present in both trophic levels. Functional diversity was internally maintained on the prey level as no niche existed in our system, which was ideal under any composition of the predator level due to the trade-offs between edibility, growth and carrying capacity. The predators were only subject to one trade-off between food-selectivity and grazing ability and in the absence of immigration, one predator type became abundant, i.e., functional diversity declined to zero. In the lack of functional diversity the system showed the same dynamics as conventional models of predator-prey interactions ignoring the potential for shifts in species composition. This way, our study identified the crucial role of trade-offs and their shape in physiological and ecological traits for preserving diversity