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The Genetic Body
Published in Roger Cooter, John Pickstone, Medicine in the Twentieth Century, 2020
By the time Thomson wrote, Bateson had already coined the term ‘genetics,’ and Johannsen was shortly to offer the word ‘gene.’ The latter became the word of choice because “He had the wisdom to leave the gene undefined and to request that his simple term replace all those other terms that implied some specific structure or function.”12 Among those who adopted it was Thomas Hunt Morgan who was on the verge of making the fruit fly the model for classical genetics. Here was a rapidly reproducing organism with clearly identifiable traits which lent themselves to precise analysis. But humans were not like that. While Morgan and his disciples counted flies in bottles, drew up maps of genes, and built up the framework of classical genetics, studies of people were stronger on conviction than data. In Britain, the doctor-researcher Archibald Garrod provided a clear direction for studies of biochemical individuality with his landmark studies leading to the lectures published as Inborn Errors of Metabolism in 1909. But the rare disorders he discussed were of little interest to other doctors and his work was largely ignored until the microbial geneticists Beadle and Tatum established the “one gene — one enzyme hypothesis” thirty years later.13
A Brief History of Genetic Therapy: Gene Therapy, Antisense Technology, and Genomics
Published in Eric Wickstrom, Clinical Trials of Genetic Therapy with Antisense DNA and DNA Vectors, 2020
Notwithstanding the formal study and successful manipulation of genetics in nature, the actual genetic structure responsible for dictating the phenotype of organisms remained unknown. In other words, classical genetics was—and is—an indirect study of genetic forces.
Laboratory Studies
Published in Jacques Derek Charlwood, The Ecology of Malaria Vectors, 2019
In classical genetics, genes that fail to be transcribed or translated or to encode functional proteins segregate as recessive alleles relative to dominant alleles that encode a functional protein. Only individuals that inherit two copies of nonfunctional alleles will display the absence of gene function. Individuals with one (heterozygous) or two (homozygous) functional copies will display a normal phenotype.
Cataglyphis meets Drosophila
Published in Journal of Neurogenetics, 2020
At the beginning of the twentieth century William Morton Wheeler from Harvard University, then the world authority on the study of ants, their behavior and social interactions, referred to Drosophila as ‘that stupid little saprophyte’ (Grimaldi & Engel, 2005, p. 7). Had he lived hundred years later, his judgement would have been much more polite, and closer to the truth. He certainly would now agree with Gerald Rubin’s remark ‘that although other experimental animals may equal or even exceed Drosophila in the facility of a particular experimental area, only flies contain in one system the potential for the application of the tools of classical genetics, cytogenetics, molecular genetics, biochemistry, electrophysiology, cell cultures’ (Rubin, 1988, p. 1458), and as we currently may add, the potential of applying the increasing arsenal of neurogenetic tools including the expression of specific genes in specific cells, the ability to silence and activate such cells, and to in vivo monitor their neural activity by using optical recording techniques (Borst, 2009; Tomchik & Davis, 2013). Moreover, Wheeler would be excited about the many sophisticated learning paradigms to which fruit flies have meanwhile been subjected, and that, as a result of such investigations, his ‘little saprophyte’ and even its larval stages are now credited with as cognitive a capacity as foresight (Gerber & Hendel, 2006; Heisenberg, 2013).
Radiobiology in my life – Irma Mosse
Published in International Journal of Radiation Biology, 2022
The teaching of T.D. Lysenko was the main genetic theory in the Soviet Union in the time of 1948–1965. It was a political campaign, which rejected the theories of classical genetics, banned such research in the USSR and persecuted domestic ‘classical’ geneticists. Drosophila was a symbol of ‘bourgeois Weismannist-Morganist’ science. The topic of my PhD thesis was discussed at the Scientific Council in which there were many followers of Lysenko theory. They were against my investigations; however, N.V. Turbin, relying on his authority, insisted on the approval of the topic chosen for my study.
Molecular mechanisms governing axonal transport: a C. elegans perspective
Published in Journal of Neurogenetics, 2020
Amruta Vasudevan, Sandhya P. Koushika
Several C. elegans studies, employing a combination of classical genetics, molecular and biochemical approaches, helped identify various neuronal cell-type and cargo-specific regulators of the retrograde motor complex in vivo. The cyclin-dependent kinases PCT-1 and CDK-5 have been shown to act genetically upstream to components of the Dynein motor complex and inhibit Dynein by inactivating NUD-2 (C. elegans Nudel, a component of the Dynein complex) (Ou et al., 2010). CDK-5 has further been proposed to inhibit Dynein-dependent transport of DCVs into the dendrites of DB motor neurons (Goodwin et al., 2012). CDK-5, SYD-2 and SAD-1 have been proposed to inhibit Dynein-mediated transport of lysosomes into dendrites of C. elegans motor neurons (Edwards et al., 2015). Another study identified that the cargo adaptor UNC-16/JIP-3 forms a complex with neuronal Kinesin-1 and DLI-1 (Dynein Light Intermediate chain subunit), to regulate the subcellular distribution of DLI-1 to neuronal distal tips (Figure 2(a)), and consequently regulate the retrograde transport of synaptic vesicle proteins SNB-1, SNT-1, and APL-1 (human APP-like protein) (Arimoto et al., 2011). Tubulin mutations that increased the affinity of Dynein for microtubules caused Dynein-dependent mis-trafficking of synaptic vesicles to dendrites of C. elegans neurons (Hsu et al., 2014). C. elegans tauopathy models expressing mutated human Tau (microtubule associated protein) show reduced anterograde and retrograde transport velocities of synaptic vesicles (Butler et al., 2019). These mutations are proposed to perturb the direct interactions of Tau with Kinesins and components of the Dynein-Dynactin complex (Butler et al., 2019). In summary, C. elegans studies have contributed significantly to the identification of inhibitors of retrograde axonal transport in vivo and provided insights into the interaction of the retrograde motor complex with the axonal microtubule cytoskeleton.