scholarly journals Sex Differences in 20-Hydroxyecdysone Hormone Levels Control Sexual Dimorphism in Bicyclus anynana Wing Patterns

2017 ◽  
Vol 35 (2) ◽  
pp. 465-472 ◽  
Author(s):  
Shivam Bhardwaj ◽  
Kathleen L Prudic ◽  
Ashley Bear ◽  
Mainak Dasgupta ◽  
Bethany R Wasik ◽  
...  
2017 ◽  
Author(s):  
Shivam Bhardwaj ◽  
Kathleen L Prudic ◽  
Ashley Bear ◽  
Mainak Das Gupta ◽  
Bethany R Wasik ◽  
...  

In contrast to the important role of hormones in the development of sexual dimorphic traits in vertebrates [1], the differentiation of these traits in insects is attributed exclusively to variation in cell-autonomous mechanisms controlled by members of the sex determination pathway [2], such as doublesex (dsx). Although hormones can shape the development of sexual traits in insects, and interact with dsx to create dimorphisms, variation in hormone levels are not known to cause dimorphism in these traits [3]. Here we show that butterflies use sex-specific differences in 20-hydroxyecdysone (20E) hormone titers to create sexually dimorphic wing ornaments, without the local involvement of dsx. Females of the dry season (DS) form ofBicyclus anynanadisplay a larger sexual ornament on their wings than males, whereas in the wet season (WS) form both sexes have similarly sized ornaments [4]. High levels of circulating 20E during larval development in DS females and WS forms cause proliferation of the cells fated to give rise to this wing ornament, and results in sexual dimorphism in the DS forms. This study advances our understanding of how the environment regulates sex-specific patterns of plasticity of sexual ornaments and conclusively shows that sex-specific variation in hormone titers can play a role in the development of secondary sexual traits in insects, just like they do in vertebrates.


2021 ◽  
Vol 22 (9) ◽  
pp. 4620
Author(s):  
Holly J. Woodward ◽  
Dongxing Zhu ◽  
Patrick W. F. Hadoke ◽  
Victoria E. MacRae

Sex differences in cardiovascular disease (CVD), including aortic stenosis, atherosclerosis and cardiovascular calcification, are well documented. High levels of testosterone, the primary male sex hormone, are associated with increased risk of cardiovascular calcification, whilst estrogen, the primary female sex hormone, is considered cardioprotective. Current understanding of sexual dimorphism in cardiovascular calcification is still very limited. This review assesses the evidence that the actions of sex hormones influence the development of cardiovascular calcification. We address the current question of whether sex hormones could play a role in the sexual dimorphism seen in cardiovascular calcification, by discussing potential mechanisms of actions of sex hormones and evidence in pre-clinical research. More advanced investigations and understanding of sex hormones in calcification could provide a better translational outcome for those suffering with cardiovascular calcification.


2021 ◽  
Vol 22 (15) ◽  
pp. 8111
Author(s):  
Kuang-Hsu Lien ◽  
Chao-Hui Yang

The triad of noise-generated, drug-induced, and age-related hearing loss is the major cause of acquired sensorineural hearing loss (ASNHL) in modern society. Although these three forms of hearing loss display similar underlying mechanisms, detailed studies have revealed the presence of sex differences in the auditory system both in human and animal models of ASNHL. However, the sexual dimorphism of hearing varies among noise-induced hearing loss (NIHL), ototoxicity, and age-related hearing loss (ARHL). Importantly, estrogen may play an essential role in modulating the pathophysiological mechanisms in the cochlea and several reports have shown that the effects of hormone replacement therapy on hearing loss are complex. This review will summarize the clinical features of sex differences in ASNHL, compare the animal investigations of cochlear sexual dimorphism in response to the three insults, and address how estrogen affects the auditory organ at molecular levels.


BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Basabi Bagchi ◽  
Quentin Corbel ◽  
Imroze Khan ◽  
Ellen Payne ◽  
Devshuvam Banerji ◽  
...  

Abstract Background Sexual dimorphism in immunity is believed to reflect sex differences in reproductive strategies and trade-offs between competing life history demands. Sexual selection can have major effects on mating rates and sex-specific costs of mating and may thereby influence sex differences in immunity as well as associated host–pathogen dynamics. Yet, experimental evidence linking the mating system to evolved sexual dimorphism in immunity are scarce and the direct effects of mating rate on immunity are not well established. Here, we use transcriptomic analyses, experimental evolution and phylogenetic comparative methods to study the association between the mating system and sexual dimorphism in immunity in seed beetles, where mating causes internal injuries in females. Results We demonstrate that female phenoloxidase (PO) activity, involved in wound healing and defence against parasitic infections, is elevated relative to males. This difference is accompanied by concomitant sex differences in the expression of genes in the prophenoloxidase activating cascade. We document substantial phenotypic plasticity in female PO activity in response to mating and show that experimental evolution under enforced monogamy (resulting in low remating rates and reduced sexual conflict relative to natural polygamy) rapidly decreases female (but not male) PO activity. Moreover, monogamous females had evolved increased tolerance to bacterial infection unrelated to mating, implying that female responses to costly mating may trade off with other aspects of immune defence, an hypothesis which broadly accords with the documented sex differences in gene expression. Finally, female (but not male) PO activity shows correlated evolution with the perceived harmfulness of male genitalia across 12 species of seed beetles, suggesting that sexual conflict has a significant influence on sexual dimorphisms in immunity in this group of insects. Conclusions Our study provides insights into the links between sexual conflict and sexual dimorphism in immunity and suggests that selection pressures moulded by mating interactions can lead to a sex-specific mosaic of immune responses with important implications for host–pathogen dynamics in sexually reproducing organisms.


2012 ◽  
Vol 60 (2) ◽  
pp. 101 ◽  
Author(s):  
Thomas E. White ◽  
Joseph Macedonia ◽  
Debra Birch ◽  
Judith Dawes ◽  
Darrell J. Kemp

Structurally generated colours are at least as commonplace and varied components of animal signals as pigment colours, yet we know far less about the former, both in terms of the patterns and phenotypic variation and of their underlying correlates and causes. Many butterflies exhibit bright and iridescent colour signals that arise from a characteristic ‘ridge-lamellar’ scale surface nanoarchitecture. Although there are multiple axes of functional variation in these traits, few have been investigated. Here we present evidence that sexual dimorphism in the expression of a sexually homologous ridge-lamellar trait (iridescent ultraviolet) is mediated by sex differences in the density of lamellar-bearing scale ridges. This trait – ridge density – has also been causally related to iridescent signal variation in other coliadines (e.g. C. eurytheme), which suggests that it may offer a common basis to both intra- and intersexual differences in ultraviolet wing reflectance among these butterflies.


2021 ◽  
Vol 135 (24) ◽  
pp. 2691-2708
Author(s):  
Simon T. Bond ◽  
Anna C. Calkin ◽  
Brian G. Drew

Abstract The escalating prevalence of individuals becoming overweight and obese is a rapidly rising global health problem, placing an enormous burden on health and economic systems worldwide. Whilst obesity has well described lifestyle drivers, there is also a significant and poorly understood component that is regulated by genetics. Furthermore, there is clear evidence for sexual dimorphism in obesity, where overall risk, degree, subtype and potential complications arising from obesity all differ between males and females. The molecular mechanisms that dictate these sex differences remain mostly uncharacterised. Many studies have demonstrated that this dimorphism is unable to be solely explained by changes in hormones and their nuclear receptors alone, and instead manifests from coordinated and highly regulated gene networks, both during development and throughout life. As we acquire more knowledge in this area from approaches such as large-scale genomic association studies, the more we appreciate the true complexity and heterogeneity of obesity. Nevertheless, over the past two decades, researchers have made enormous progress in this field, and some consistent and robust mechanisms continue to be established. In this review, we will discuss some of the proposed mechanisms underlying sexual dimorphism in obesity, and discuss some of the key regulators that influence this phenomenon.


2014 ◽  
Vol 281 (1790) ◽  
pp. 20140333 ◽  
Author(s):  
Crystal M. Vincent ◽  
Darryl T. Gwynne

Sex differences in immunity are often observed, with males generally having a weaker immune system than females. However, recent data in a sex-role-reversed species in which females compete to mate with males suggest that sexually competitive females have a weaker immune response. These findings support the hypothesis that sexual dimorphism in immunity has evolved in response to sex-specific fitness returns of investment in traits such as parental investment and longevity, but the scarcity of data in sex-reversed species prevents us from drawing general conclusions. Using an insect species in which males make a large but variable parental investment in their offspring, we use two indicators of immunocompetence to test the hypothesis that sex-biased immunity is determined by differences in parental investment. We found that when the value of paternal investment was experimentally increased, male immune investment became relatively greater than that of females. Thus, in this system, in which the direction of sexual competition is plastic, the direction of sex-biased immunity is also plastic and appears to track relative parental investment.


Author(s):  
Shawna L. McMillin ◽  
Everett C. Minchew ◽  
Dawn A. Lowe ◽  
Espen E. Spangenburg

The importance of defining sex differences across various biological and physiological mechanisms is more pervasive now than it has been over the last 15-20 years. As the muscle biology field pushes to identify small molecules and interventions to prevent, attenuate or even reverse muscle wasting, we must consider the effect of sex as a biological variable. It should not be assumed that a therapeutic will affect males and females with equal efficacy or equivalent target affinities under conditions where muscle wasting is observed. With that said, it is not surprising to find that we have an unclear or even a poor understanding of the effects of sex or sex hormones on muscle wasting conditions. Although recent investigations are beginning to establish experimental approaches that will allow investigators to assess the impact of sex-specific hormones on muscle wasting, the field still has not established enough published scientific tools that will allow the field to rigorously address critical hypotheses. Thus, the purpose of this review is to assemble a current summary of knowledge in the area of sexual dimorphism driven by estrogens with an effort to provide insights to interested physiologists on necessary considerations when trying to assess models for potential sex differences in cellular and molecular mechanisms of muscle wasting.


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