scholarly journals Heterogeneous genetic basis of age at maturity in salmonid fishes

2021 ◽  
Vol 30 (6) ◽  
pp. 1435-1456
Author(s):  
Charles D. Waters ◽  
Anthony Clemento ◽  
Tutku Aykanat ◽  
John Carlos Garza ◽  
Kerry A. Naish ◽  
...  
1979 ◽  
Vol 17 (11-12) ◽  
pp. 1079-1091 ◽  
Author(s):  
F. M. Utter ◽  
F. W. Allendorf ◽  
B. May

Author(s):  
Charles D. Waters ◽  
Anthony Clemento ◽  
Tutku Aykanat ◽  
John Carlos Garza ◽  
Kerry A. Naish ◽  
...  

AbstractUnderstanding the genetic basis of repeated evolution of the same phenotype across taxa is a fundamental aim in evolutionary biology and has applications to conservation and management. However, the extent to which interspecific life-history trait polymorphisms share evolutionary pathways remains under-explored. We address this gap by studying the genetic basis of a key life-history trait, age at maturity, in four species of Pacific salmon (genus Oncorhynchus) that exhibit intra- and interspecific variation in this trait – Chinook Salmon, Coho Salmon, Sockeye Salmon, and Steelhead Trout. We tested for associations in all four species between age at maturity and two genome regions, six6 and vgll3, that are strongly associated with the same trait in Atlantic Salmon (Salmo salar). We also conducted a genome-wide association analysis in Steelhead to assess whether additional regions were associated with this trait. We found the genetic basis of age at maturity to be heterogeneous across salmonid species. Significant associations between six6 and age at maturity were observed in two of the four species, Sockeye and Steelhead, with the association in Steelhead being particularly strong in both sexes (p = 4.46×10−9 after adjusting for genomic inflation). However, no significant associations were detected between age at maturity and the vgll3 genome region in any of the species, despite its strong association with the same trait in Atlantic Salmon. We discuss possible explanations for the heterogeneous nature of the genetic architecture of this key life-history trait, as well as the implications of our findings for conservation and management.


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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