scholarly journals Insights into the genetic basis of predator‐induced response in Daphnia galeata

2020 ◽  
Vol 10 (23) ◽  
pp. 13095-13108
Author(s):  
Verena Tams ◽  
Jana Helene Nickel ◽  
Anne Ehring ◽  
Mathilde Cordellier

2018 ◽  
Author(s):  
Verena Tams ◽  
Jana Helene Nickel ◽  
Anne Ehring ◽  
Mathilde Cordellier

AbstractPhenotypic plastic responses allow organisms to rapidly adjust when facing environmental challenges - these responses comprise morphological, behavioral but also life-history changes. Alteration of life-history traits when exposed to predation risk have been reported often in the ecological and genomic model organism Daphnia. However, the molecular basis of this response is not well understood, especially in the context of fish predation. Here, we characterized the transcriptional profiles of two Daphnia galeata clonal lines with opposed life histories when exposed to fish kairomones. First, we conducted a differential gene expression, identifying a total of 125 candidate transcripts involved in the predator-induced response, uncovering substantial intra-specific variation. Second, we applied a gene co-expression network analysis to find clusters of tightly linked transcripts revealing the functional relations of transcripts underlying the predator-induced response. Our results showed that transcripts involved in remodeling of the cuticle, growth and digestion correlated with the response to environmental change in D. galeata. Furthermore, we used an orthology-based approach to gain functional information for transcripts lacking gene ontology (GO) information, as well as insights into the evolutionary conservation of transcripts. We could show that our candidate transcripts have orthologs in other Daphnia species but almost none in other arthropods. The unique combination of methods allowed us to identify candidate transcripts, their putative functions and evolutionary history associated with predator-induced responses in Daphnia. Our study opens up to the question as to whether the same molecular signature is associated fish kairomones-mediated life-history changes in other Daphnia species.





1996 ◽  
Vol 16 (02) ◽  
pp. 114-138 ◽  
Author(s):  
R. E. Scharf

SummarySpecific membrane glycoproteins (GP) expressed by the megakaryocyte-platelet system, including GPIa-lla, GPIb-V-IX, GPIIb-llla, and GPIV are involved in mediat-ing platelet adhesion to the subendothelial matrix. Among these glycoproteins, GPIIb-llla plays a pivotal role since platelet aggregation is exclusively mediated by this receptor and its interaction with soluble macromolecular proteins. Inherited defects of the GPIIb-llla or GPIb-V-IX receptor complexes are associated with bleeding disorders, known as Glanzmann's thrombasthenia, Bernard-Soulier syndrome, or platelet-type von Willebrand's disease, respectively. Using immuno-chemical and molecular biology techniques, rapid advances in our understanding of the molecular genetic basis of these disorders have been made during the last few years. Moreover, analyses of patients with congenital platelet membrane glycoprotein abnormalities have provided valuable insights into molecular mechanisms that are required for structural and functional integrity, normal biosynthesis of the glycoprotein complexes and coordinated membrane expression of their constituents. The present article reviews the current state of knowledge of the major membrane glycoproteins in health and disease. The spectrum of clinical bleeding manifestations and established diagnostic criteria for each of these dis-orders are summarized. In particular, the variety of molecular defects that have been identified so far and their genetic basis will be discussed.



Author(s):  
Deirdre O'Sullivan ◽  
Michael Moore ◽  
Susan Byrne ◽  
Andreas O. Reiff ◽  
Susanna Felsenstein

AbstractAcute disseminated encephalomyelitis in association with extensive longitudinal transverse myelitis is reported in a young child with positive anti-myelin oligodendrocyte glycoprotein (MOG) antibody with heterozygous NLRP3 missense mutations; p.(Arg488Lys) and p.(Ser159Ile). This case may well present an exceptional coincidence, but may describe a yet unrecognized feature of the spectrum of childhood onset cryopyrinopathies that contribute to the understanding of the genetic basis for anti-MOG antibody positive encephalomyelitis. Based on this observation, a larger scale study investigating the role of NLRP3 and other inflammasomes in this entity would provide important pathophysiological insights and potentially novel avenues for treatment.



Author(s):  
Lindsey Andrews ◽  
Jonathan M. Metzl

On 26 April 2013, the Wall Street Journal published an essay by neurocriminologist Adrian Raine promoting his newest book, The Anatomy of Violence: The Biological Roots of Crime. On the newspaper’s website, an image of a black-and-white brain scan overlaid with handcuffs headed the essay. Clicking ‘play’ turned the image into a video filled with three-dimensional brain illustrations and Raine’s claims that some brains are simply more biologically prone to violence than others. Rejecting what he describes as ‘the dominant model for understanding criminal behaviour in the twentieth century’ – a model based ‘almost exclusively on social and sociological’ explanations – Raine wrote that ‘the genetic basis of criminal behaviour is now well established’ through molecular and behavioural genetics.



Author(s):  
Terence D. Keel

The proliferation of studies declaring that there is a genetic basis to health disparities and behavioral differences across the so-called races has encouraged the opponents of social constructionism to assert a victory for scientific progress over political correctness. I am not concerned in this essay with providing a response to critics who believe races are expressions of innate genetic or biological differences. Instead, I am interested in how genetic research on human differences has divided social constructionists over whether the race concept in science can be used for social justice and redressing embodied forms of discrimination. On one side, there is the position that race is an inherently flawed concept and that its continued use by scientists, medical professionals, and even social activists keeps alive the notion that it has a biological basis. On the other side of this debate are those who maintain a social constructionist position yet argue that not all instances of race in science stem from discriminatory politics or the desire to prove that humans belong to discrete biological units that can then be classified as superior or inferior. I would like to shift this debate away from the question of whether race is real and move instead toward thinking about the intellectual commitments necessary for science to expose past legacies of discrimination.



2020 ◽  
Vol 75 (3) ◽  
pp. 204-213
Author(s):  
Varvara A. Ryabkova ◽  
Leonid P. Churilov ◽  
Yehuda Shoenfeld

The pathogenesis of autoimmune diseases is very complex and multi-factorial. The concept of Mosaics of Autoimmunity was introduced to the scientific community 30 years ago by Y. Shoenfeld and D.A. Isenberg, and since then new tiles to the puzzle are continuously added. This concept specifies general pathological ideas about the multifactorial threshold model for polygenic inheritance with a threshold effect by the action of a number of external causal factors as applied to the field of autoimmunology. Among the external factors that can excessively stimulate the immune system, contributing to the development of autoimmune reactions, researchers are particularly interested in chemical substances, which are widely used in pharmacology and medicine. In this review we highlight the autoimmune dynamics i.e. a multistep pathogenesis of autoimmune diseases and the subsequent development of lymphoma in some cases. In this context several issues are addressed namely, genetic basis of autoimmunity; environmental immunostimulatory risk factors; gene/environmental interaction; pre-clinical autoimmunity with the presence of autoantibodies; and the mechanisms, underlying lymphomagenesis in autoimmune pathology. We believe that understanding the common model of the pathogenesis of autoimmune diseases is the first step to their successful management.



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