Evidence of genetic basis of zoophagy and nymphal developmental time in isogroup lines of the zoophytophagous mullein bug, Campylomma verbasci

BioControl ◽  
2016 ◽  
Vol 61 (4) ◽  
pp. 425-435 ◽  
Author(s):  
François Dumont ◽  
Eric Lucas ◽  
Denis Réale
Keyword(s):  
Genetic Basis ◽  
Developmental Time ◽  
Campylomma Verbasci

Genetic basis of extremely slow development in a population of Tribolium confusum

1985 ◽  
Vol 27 (6) ◽  
pp. 650-654
Author(s):  
Russel A. Riddle ◽  
Reneé Sykes ◽  
Linda J. Leffel ◽  
Peter S. Dawson
Keyword(s):  
Genetic Basis ◽  
Developmental Time ◽  
Pleiotropic Effect ◽  
Tribolium Confusum ◽  
Recessive Mutation ◽  
Pupal Weight ◽  
Laboratory Population ◽  
Slow Development ◽  
Autosomal Recessive Mutation ◽  
Phenotypic Shift

An extremely slow developing form of Tribolium confusum is described. The slow phenotype is caused by an autosomal recessive mutation, sl (slow). Expression of this allele on growth rate was not significantly altered by diet, although a pleiotropic effect on survival was diet dependent. The allele has become fixed in a laboratory population, producing a phenotypic shift in developmental time of 7.1 standard deviations. Pupal weight is reduced in homozygotes by about 15%. Allele frequency data suggest that fixation of the sl allele may have been the result of selection and not genetic drift. The mutation is discussed in relation to models of phenotypic evolution.Key words: Tribolium, phenotypic evolution, slow development.

scholarly journals Integration and the Developmental Genetics of Allometry

2019 ◽  
Vol 59 (5) ◽  
pp. 1369-1381 ◽  
Author(s):  
Benedikt Hallgrímsson ◽  
David C Katz ◽  
Jose D Aponte ◽  
Jacinda R Larson ◽  
Jay Devine ◽  
...  
Keyword(s):  
Genetic Basis ◽  
Developmental Time ◽  
Morphological Integration ◽  
Evolutionary Change ◽  
Developmental Genetics ◽  
Multiple Traits ◽  
Developmental Processes ◽  
Environmental Perturbations ◽  
Morphometric Analyses ◽  
Special Case

Abstract Allometry refers to the ways in which organismal shape is associated with size. It is a special case of integration, or the tendency for traits to covary, in that variation in size is ubiquitous and evolutionarily important. Allometric variation is so commonly observed that it is routinely removed from morphometric analyses or invoked as an explanation for evolutionary change. In this case, familiarity is mistaken for understanding because rarely do we know the mechanisms by which shape correlates with size or understand their significance. As with other forms of integration, allometric variation is generated by variation in developmental processes that affect multiple traits, resulting in patterns of covariation. Given this perspective, we can dissect the genetic and developmental determinants of allometric variation. Our work on the developmental and genetic basis for allometric variation in craniofacial shape in mice and humans has revealed that allometric variation is highly polygenic. Different measures of size are associated with distinct but overlapping patterns of allometric variation. These patterns converge in part on a common genetic basis. Finally, environmental modulation of size often generates variation along allometric trajectories, but the timing of genetic and environmental perturbations can produce deviations from allometric patterns when traits are differentially sensitive over developmental time. These results question the validity of viewing allometry as a singular phenomenon distinct from morphological integration more generally.

Molecular Basis and Clinical Aspects of Hereditary Megakaryocyte and Platelet Membrane Glycoprotein Disorders

1996 ◽  
Vol 16 (02) ◽  
pp. 114-138 ◽  
Author(s):  
R. E. Scharf
Keyword(s):  
Genetic Basis ◽  
Molecular Mechanisms ◽  
Molecular Genetic ◽  
Platelet Membrane ◽  
Clinical Aspects ◽  
Membrane Glycoprotein ◽  
Membrane Glycoproteins ◽  
Membrane Expression ◽  
Receptor Complexes ◽  
Platelet Membrane Glycoprotein

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.

Anti-Myelin Oligodendrocyte Glycoprotein Encephalomyelitis and Extensive Longitudinal Transverse Myelitis Associated with Compound Heterozygous NLRP3 Missense Mutations in a Young Child

2020 ◽  
Author(s):  
Deirdre O'Sullivan ◽  
Michael Moore ◽  
Susan Byrne ◽  
Andreas O. Reiff ◽  
Susanna Felsenstein
Keyword(s):  
Young Child ◽  
Genetic Basis ◽  
Transverse Myelitis ◽  
Acute Disseminated Encephalomyelitis ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Compound Heterozygous ◽  
Missense Mutations ◽  
Childhood Onset

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.

Reading the Image of Race: Neurocriminology, Medical Imaging Technologies and Literary Intervention

2018 ◽  
Author(s):  
Lindsey Andrews ◽  
Jonathan M. Metzl
Keyword(s):  
Twentieth Century ◽  
Wall Street Journal ◽  
Genetic Basis ◽  
Three Dimensional ◽  
Criminal Behaviour ◽  
Dominant Model ◽  
Wall Street ◽  
Behavioural Genetics ◽  
Black And White ◽  
Brain Scan

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.

Race on Both Sides of the Razor

2018 ◽  
Vol 5 (1) ◽  
Author(s):  
Terence D. Keel
Keyword(s):  
Social Constructionism ◽  
Political Correctness ◽  
Genetic Basis ◽  
Genetic Research ◽  
Scientific Progress ◽  
Social Constructionist ◽  
Behavioral Differences ◽  
Social Activists ◽  
Continued Use ◽  
Biological Differences

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.

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