scholarly journals Warning displays may function as honest signals of toxicity

2008 ◽  
Vol 276 (1658) ◽  
pp. 871-877 ◽  
Author(s):  
Jonathan D Blount ◽  
Michael P Speed ◽  
Graeme D Ruxton ◽  
Philip A Stephens

Many prey species use colourful ‘aposematic’ signalling to advertise the fact that they are toxic. Some recent studies have shown that the brightness of aposematic displays correlates positively with the strength of toxicity, suggesting that aposematic displays are a form of handicap signal, the conspicuousness of which reliably indicates the level of toxicity. The theoretical consensus in the literature is, however, at odds with this finding. It is commonly assumed that the most toxic prey should have less bright advertisements because they have better chances of surviving attacks and can therefore reduce the costs incurred by signalling. Using a novel theoretical model, we show that aposematic signals can indeed function as handicaps. To generate this prediction, we make a key assumption that the expression of bright displays and the storage of anti-predator toxins compete for resources within prey individuals. One shared currency is energy. However, competition for antioxidant molecules, which serve dual roles as pigments and in protecting prey against oxidative stress when they accumulate toxins, provides a specific candidate resource that could explain signal honesty. Thus, contrary to the prevailing theoretical orthodoxy, warning displays may in fact be honest signals of the level of (rather than simply the existence of) toxicity.

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 522 ◽  
Author(s):  
Wang ◽  
Xiao ◽  
Huang ◽  
Liu

In this study, cell death induced by the oxidant tert-butylhydroperoxide (tBH) was observed in U2OS cells; this phenotype was rescued by Syntaxin 17 (STX17) knockout (KO) but the mechanism is unknown. STX17 plays dual roles in autophagosome–lysosome fusion and mitochondrial fission. However, the contribution of the two functions of STX17 to apoptosis has not been extensively studied. Here, we sought to dissect the dual roles of STX17 in oxidative-stress-induced apoptosis by taking advantage of STX17 knockout cells and an autophagosome–lysosome fusion defective mutant of STX17. We generated STX17 knockout U2OS cells using the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) system and the STX17 knockout cells were reconstituted with wild-type STX17 and its autophagosome–lysosome fusion defective mutant. Autophagy was assessed by autophagic flux assay, Monomer red fluorescent protein (mRFP)–GFP–LC3 assay and protease protection assay. Golgi, endoplasmic reticulum (ER)/ER–Golgi intermediate compartment (ERGIC) and mitochondrial dynamics were examined by staining the different indicator proteins. Apoptosis was evaluated by caspase cleavage assay. The general reactive oxygen species (ROS) were detected by flow cytometry. In STX17 complete knockout cells, sealed autophagosomes were efficiently formed but their fusion with lysosomes was less defective. The fusion defect was rescued by wild-type STX17 but not the autophagosome–lysosome fusion defective mutant. No obvious defects in Golgi, ERGIC or ER dynamics were observed. Mitochondria were significantly elongated, supporting a role of STX17 in mitochondria fission and the elongation caused by STX17 KO was reversed by the autophagosome–lysosome fusion defective mutant. The clearance of protein aggregation was compromised, correlating with the autophagy defect but not with mitochondrial dynamics. This study revealed a mixed role of STX17 in autophagy, mitochondrial dynamics and oxidative stress response. STX17 knockout cells were highly resistant to oxidative stress, largely due to the function of STX17 in mitochondrial fission rather than autophagy.


2017 ◽  
Vol 372 (1724) ◽  
pp. 20160343 ◽  
Author(s):  
Ryan J. Weaver ◽  
Rebecca E. Koch ◽  
Geoffrey E. Hill

Many of the colour displays of animals are proposed to have evolved in response to female mate choice for honest signals of quality, but such honest signalling requires mechanisms to prevent cheating. The most widely accepted and cited mechanisms for ensuring signal honesty are based on the costly signalling hypothesis, which posits that costs associated with ornamentation prevent low-quality males from being highly ornamented. Alternatively, by the index hypothesis, honesty can be achieved via cost-free mechanisms if ornament production is causally linked to core physiological pathways. In this essay, we review how a costly signalling framework has shaped empirical research in mate choice for colourful male ornaments and emphasize that alternative interpretations are plausible under an index signalling framework. We discuss the challenges in both empirically testing and distinguishing between the two hypotheses, noting that they need not be mutually exclusive. Finally, we advocate for a comprehensive approach to studies of colour signals that includes the explicit consideration of cost-free mechanisms for honesty. This article is part of the themed issue ‘Animal coloration: production, perception, function and application’.


2006 ◽  
Vol 274 (1611) ◽  
pp. 819-825 ◽  
Author(s):  
Carlos Alonso-Alvarez ◽  
Sophie Bertrand ◽  
Bruno Faivre ◽  
Olivier Chastel ◽  
Gabriele Sorci

Secondary sexual traits (SST) are usually thought to have evolved as honest signals of individual quality during mate choice. Honesty of SST is guaranteed by the cost of producing/maintaining them. In males, the expression of many SST is testosterone-dependent. The immunocompetence handicap hypothesis has been proposed as a possible mechanism ensuring honesty of SST on the basis that testosterone, in addition to its effect on sexual signals, also has an immunosuppressive effect. The immunocompetence handicap hypothesis has received mixed support. However, the cost of testosterone-based signalling is not limited to immunosuppression and might involve other physiological functions such as the antioxidant machinery. Here, we tested the hypothesis that testosterone depresses resistance to oxidative stress in a species with a testosterone-dependent sexual signal, the zebra finch. Male zebra finches received subcutaneous implants filled with flutamide (an anti-androgen) or testosterone, or kept empty (control). In agreement with the prediction, we found that red blood cell resistance to a free radical attack was the highest in males implanted with flutamide and the lowest in males implanted with testosterone. We also found that cell-mediated immune response was depressed in testosterone-treated birds, supporting the immunocompetence handicap hypothesis. The recent finding that red blood cell resistance to free radicals is negatively associated with mortality in this species suggests that benefits of sexual signalling might trade against the costs derived from oxidation.


2018 ◽  
Vol 21 (3) ◽  
pp. 317-341
Author(s):  
Wen-Chieh Wu ◽  
◽  
Yu-Chun Ma ◽  
Steven Bourassa ◽  
◽  
...  

In this paper, we examine whether Chinese folk customs and taboos have impacts on the home improvement decisions of Taiwanese homeowners. Based on traditional Chinese culture, we choose the Year of the Dragon and Widow Year as indicators of auspicious (fortune) and inauspicious (taboo) periods, respectively. With the use of a Heckman two-stage estimation approach, our empirical results provide evidence that traditional Chinese folk customs and taboos indeed have important roles in decisions on home improvement. We find that the likelihood that a homeowner will make home improvements is significantly reduced in the so-called taboo period. Moreover, we find that expenditures on home improvements increase in the so-called auspicious period, particularly in areas outside the capital city region. In addition to considering the impacts of folk customs on home improvement decisions, this paper contributes to the literature by establishing a theoretical model that reflects the fact that homeowners have dual roles as both consumers and suppliers of housing.


2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Shilin Luo ◽  
Kecheng Lei ◽  
Daxiong Xiang ◽  
Keqiang Ye

Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with a dismal prognosis, and the patients carrying EGFR-driven tumors with PTEN mutation do not respond to anti-EGFR therapy. The molecular mechanisms for this resistance remain unknown. Here, we show that PTEN induces the expression of NQO1, a flavoenzyme with dual roles in pro- and antitumorigenesis that decreases the formation of reactive oxygen species (ROS), which mediates the oxidative stress and GBM cell proliferation. NQO1 is reduced in EGFRvIII-overexpressed U87MG cells associated with low ROS, whereas NQO1 is highly escalated in PTEN stably expressed U87MG/EGFRvIII cells with high ROS. Interestingly, knockdown of NQO1 augments ROS and diminishes cell proliferation. Conversely, overexpression of NQO1 attenuates ROS and increases cell proliferation. By contrast, overexpression of PINK1, a PTEN-induced kinase 1, represses ROS and inhibits GBM cell proliferation. Therefore, our findings support that NQO1 displays a paradoxical role in mediating GBM growth in response to tumor suppressor PTEN.


2008 ◽  
pp. 231-250 ◽  
Author(s):  
Tzipora Goldkorn ◽  
Elaine M. Khan
Keyword(s):  

2020 ◽  
Vol 60 (2) ◽  
pp. 497-508 ◽  
Author(s):  
Robbie S Wilson ◽  
Theodore P Pavlic ◽  
Rebecca Wheatley ◽  
Amanda C Niehaus ◽  
Ofir Levy

Synopsis Prey species often modify their foraging and reproductive behaviors to avoid encounters with predators; yet once they are detected, survival depends on out-running, out-maneuvering, or fighting off the predator. Though predation attempts involve at least two individuals—namely, a predator and its prey—studies of escape performance typically measure a single trait (e.g., sprint speed) in the prey species only. Here, we develop a theoretical model in which the likelihood of escape is determined by the prey animal’s tactics (i.e., path trajectory) and its acceleration, top speed, agility, and deceleration relative to the performance capabilities of a predator. The model shows that acceleration, top speed, and agility are all important determinants of escape performance, and because speed and agility are biomechanically related to size, smaller prey with higher agility should force larger predators to run along curved paths that do not allow them to use their superior speeds. Our simulations provide clear predictions for the path and speed a prey animal should choose when escaping from predators of different sizes (thus, biomechanical constraints) and could be used to explore the dynamics between predators and prey.


2019 ◽  
Author(s):  
Daniel J. Newhouse ◽  
Ben J. Vernasco

ABSTRACTSexually selected traits are hypothesized to be honest signals of individual quality due to the costs associated with their maintenance, development, and/or production. Testosterone, a sex steroid associated with the development and/or production of sexually selected traits, has been proposed to enforce the honesty of sexually selected traits via its immunosuppressive effects (i.e., the Immunocompetence Handicap Hypothesis) and/or by influencing an individual’s exposure/susceptibility to oxidative stress (i.e., the Oxidation Handicap Hypothesis). Previous work testing these hypotheses has primarily focused on physiological measurements of immunity or oxidative stress, but little is known about the molecular pathways by which testosterone could influence immunity and/or oxidative stress pathways. To further understand the transcriptomic consequences of experimentally elevated testosterone in the context of handicap hypotheses, we used previously published RNA-seq data from studies that measured the transcriptome of individuals treated with either a testosterone-filled or an empty (i.e., control) implant. Two studies encompassing three species of bird and three tissue types fit our selection criteria and we reanalyzed the data using weighted gene co-expression network analysis. Our results show that testosterone-treated individuals exhibited signatures of immunosuppression and we provide some evidence to suggest that the transcriptomic signature of immunosuppression is evolutionarily conserved between the three species. While our results provide no evidence to suggest testosterone mediates handicaps via pathways associated with oxidative stress, they do support the hypothesis that testosterone enforces the honesty of sexually-selected traits by influencing an individual’s immunocompetence. Overall, this study develops a framework for testing testosterone-mediated handicap hypotheses and provides guidelines for future integrative and comparative studies focused on the proximate mechanisms mediating sexually selected traits.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Charline Sophie Pinna ◽  
Maëlle Vilbert ◽  
Stephan Borensztajn ◽  
Willy Daney de Marcillac ◽  
Florence Piron-Prunier ◽  
...  

Müllerian mimicry is a positive interspecific interaction, whereby co-occurring defended prey species share a common aposematic signal. In Lepidoptera, aposematic species typically harbour conspicuous opaque wing colour patterns with convergent optical properties among co-mimetic species. Surprisingly, some aposematic mimetic species have partially transparent wings, raising the questions of whether optical properties of transparent patches are also convergent, and of how transparency is achieved. Here, we conducted a comparative study of wing optics, micro and nanostructures in neotropical mimetic clearwing Lepidoptera, using spectrophotometry and microscopy imaging. We show that transparency, as perceived by predators, is convergent among co-mimics in some mimicry rings. Underlying micro- and nanostructures are also sometimes convergent despite a large structural diversity. We reveal that while transparency is primarily produced by microstructure modifications, nanostructures largely influence light transmission, potentially enabling additional fine-tuning in transmission properties. This study shows that transparency might not only enable camouflage but can also be part of aposematic signals.


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