Drosophila

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description: genus of insects

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She Has Her Mother's Laugh

by Carl Zimmer  · 29 May 2018

his story. Morgan kept rotting bananas in his lab at Columbia University in New York City in order to feed a species of fly called Drosophila melanogaster. He had begun studying them in 1907, hoping to catch one of de Vries’s species-creating mutations. But Morgan came to realize that

gained a lot of evidence in recent years: Meiosis lets evolution do its job better. Consider what meiosis does inside of one of Morgan’s Drosophila flies. Like other flies, it has a collection of traits—let’s say those traits include short wings, a strong immune response, and the ability

the discovery of flies with too many daughters. A Russian biologist named Sergey Gershenson went into a forest to trap a species of fly called Drosophila obscura. When he brought the flies back to the Institute of Experimental Biology in Moscow, he figured out how to keep them alive on a

lines he could study for inherited traits. There was something peculiar about two of the lines, Gershenson noticed. Typically, a batch of eggs produced by Drosophila obscura contains an even balance of males and females. But in two of Gershenson’s lines, the mothers tended to produce far more daughters than

about race came from other species, such as a little brown fly that lived on the west side of North America. * * * — The fly, known as Drosophila pseudoobscura, was studied by a Soviet émigré named Theodosius Dobzhansky. Dobzhansky spent his childhood catching butterflies and became a published expert on beetles at age

variations were spread out over the range of a wild species. He knew he couldn’t study Morgan’s favorite, Drosophila melanogaster. It was a garbage-feeding camp follower. Instead, Dobzhansky picked Drosophila pseuodoobscura, a truly wild animal that lived across a range stretching from Guatemala to British Columbia. Dobzhansky bought a

was committed to investigating his own scientific questions. What was most important to Lewontin was finding a new way to measure the genetic diversity in Drosophila pseudoobscura, Dobzhansky’s favorite fly. In his own work, Dobzhansky had only managed to get a crude measure of the fly’s genetic diversity. He

the proteins were the result of variations in the genes that encoded them. Lewontin and Hubby compared the weight of proteins in six populations of Drosophila pseudoobscura from Arizona, California, and Colombia. Looking at eighteen kinds of proteins, they found that 30 percent existed in different forms within a single population

for this so-called reform eugenics was a protégé of Thomas Hunt Morgan, the American-born biologist Hermann Muller. After Muller learned how to breed Drosophila flies in Morgan’s lab at Columbia, he went to the University of Texas, where he used X-rays in the 1920s to create new

about CRISPR, it sounded like a godsend. At the time, he was getting his PhD at the University of California, San Diego, studying genes in Drosophila and related flies. He tinkered with their genes and observed whether he could change how their embryos developed. But the best tools he could use

were clumsy and crude. In 2013, Gantz heard that researchers had figured out how to use CRISPR to alter a gene in Drosophila with easy precision. “It was one of the things I was waiting for,” Gantz told me when I visited him at his laboratory on a

about to discover a way to use CRISPR to alter heredity on a species-wide scale. Gantz decided to try out CRISPR by altering a Drosophila gene called yellow. It was, in a sense, an inherited choice. The yellow gene was discovered just over a century earlier in the lab of

earlier generations had learned how to make stone tools and how to plant barley. There’s even a website, called FlyTree—The Academic Genealogy of Drosophila Genetics, that chronicles this particular line of cultural inheritance. The entire tree begins, of course, with Thomas Hunt Morgan. It branches down to his many

yellow craft. He became Morgan’s scientific great-great-grandchild. To try out CRISPR, Gantz fashioned an RNA guide to alter the yellow gene in Drosophila embryos, introducing a mutation to make them golden. He added the molecules to the fly cells, let them develop into adults, and bred them together

the CRISPR molecules to see if he could use them on another species of fly he was studying for his PhD, called Megaselia scalaris. Unlike Drosophila melanogaster, it has a distinctively hunched thorax, which has earned it the common name of the humpbacked fly. It behaves differently, too, for which it

the way its maggots dig deep into the ground in search of food, sometimes traveling all the way down into buried caskets. Gantz tailored the Drosophila CRISPR molecules so that they would target the yellow gene in humpbacked flies. But when he used them on the flies, the experiment failed. “It

further into a population with every new generation. Under the right conditions, that might be a good thing. Instead of targeting the yellow gene in Drosophila, scientists could target genes in insects that destroy crops or spread disease. Other researchers had been searching for years for gene drives that might fight

unplanned changes he might unleash. Gantz devised a way to safely test the mutagenic chain reaction. He would attempt to edit the yellow gene in Drosophila. But he would prevent the flies from sneaking out of his lab by working in a secure room, housing the insects in shatterproof plastic vials

to someone else. “‘Yeah, do it’” was the consensus, Bier recalled. “‘Be careful, but do it.’” In October 2014, Gantz used CRISPR to modify some Drosophila larvae. If the molecules worked as he hoped, they would replace one copy of the yellow gene with a different stretch of DNA. That new

. James decided to take a crack at the problem. For his gene drive, he picked a piece of DNA called the P element. Carried by Drosophila flies, it spreads by occasionally getting its host cell to make a new copy of itself, which gets inserted at another spot in the fly

an hour and a half to visit James and plan out a new experiment. Plastic boxes and shatterproof tubes might be good enough to keep Drosophila in check, but for mosquitoes, they’d need much better security. James would need to run the experiment in the safety of his insectarium. As

1922. Abraham Myerson: Myerson 1925. “used his germplasm in orthodox fashion . . .”: Ibid., p. 78. “. . . any definite information about my great-great-grandfather . . .”: Ibid., p. 79. Drosophila melanogaster: See Endersby 2009; Schwartz 2008. many genes could influence a single trait: Morgan 1915. “It is of the utmost importance . . .”: See “Mendelism Up to

. “Somatic Copy Number Mosaicism in Human Skin Revealed by Induced Pluripotent Stem Cells.” Nature 492:438–42. Academic Family Tree. FlyTree—The Academic Genealogy of Drosophila Genetics. https://academictree.org/flytree/ (accessed May 10, 2017). Ackerman, Michael J. 2015. “Genetic Purgatory and the Cardiac Channelopathies: Exposing the Variants of Uncertain/unknown

Heritability Paradigm: A Dramatic Resurgence of the GIGO Syndrome in Genetics.” Human Heredity 79:1–4. Gershenson, S. 1928. “A New Sex-Ratio Abnormality in Drosophila obscura.” Genetics 13:488–507. Geserick, Gunther, and Ingo Wirth. 2012. “Genetic Kinship Investigation from Blood Groups to DNA Markers.” Transfusion Medicine and Hemotherapy 39

R. C. Lewontin. 1966. “A Molecular Approach to the Study of Genic Heterozygosity in Natural Populations. I. The Number of Alleles at Different Loci in Drosophila pseudoobscura.” Genetics 54:577–94. Hübler, Olaf. 2016. “Height and Wages.” In The Oxford Handbook of Economics and Human Biology. Edited by John Komlos and

. “An Inquiry into the Nature of the Skeletal Changes in Acromegaly.” Lancet 177:993–1002. Kelleher, Erin S. 2016. “Reexamining the P-Element Invasion of Drosophila melanogaster Through the Lens of PiRNA Silencing.” Genetics 203:1513–31. Kelsoe, John R., Edward I. Ginns, Janice A. Egeland, Daniela S. Gerhard, Alisa M

Slavery in Maryland. http://msa.maryland.gov/msa/intromsa/pdf/slavery_pamphlet.pdf. Mather, K., and T. Dobzhansky. 1939. “Morphological Differences Between the ‘Races’ of Drosophila pseudoobscura.” American Naturalist 73:5–25. Mathias, Rasika Ann, Margaret A. Taub, Christopher R. Gignoux, Wenqing Fu, Shaila Musharoff, Timothy D. O’Connor, Candelaria Vergara

, Yossi Kalifa, Liat Ravid, Zvulun Elazar, and Eli Arama. 2014. “Paternal Mitochondrial Destruction after Fertilization Is Mediated by a Common Endocytic and Autophagic Pathway in Drosophila.” Developmental Cell 29:305–20. Pollan, Michael. 2001. The Botany of Desire: A Plant’s-Eye View of the World. New York: Random House. Porter

Reviews of the Cambridge Philosophical Society 91:206–34. Sturtevant, A. H., and T. Dobzhansky. 1936. “Inversions in the Third Chromosome of Wild Races of Drosophila pseudoobscura, and Their Use in the Study of the History of the Species.” Proceedings of the National Academy of Sciences 22:448–50. Sudik, R

chimerism, 380–81, 386–91, 393, 398 and CRISPR mechanism, 143, 494, 523, 525, 552–54, 558, 573 and discovery of genes, 123–24 and Drosophila research, 98 and embryonic development, 328 and epigenetic inheritance, 472 and eukaryotes, 144 and fertilization process, 341, 542 and gene drives, 155, 473 and genetic

, 417–18 Crabbe, John, 301 Craven, Isabel, 72 Creger, William, 385 cretinism, 70, 306. See also feeblemindedness Crick, Francis, 124–25 CRISPR/Cas system and Drosophila research, 550–54 early research on, 488–91 and ethical issues of scientific advances, 542 and genetic vs. nongenetic heredity, 474 and human genome editing

), 125 Doudna, Jennifer, 488–90, 496–97, 523–27, 530, 561 Douglass, Frederick, 166, 197–98, 267 Down syndrome, 1–2, 386 Drake, Francis, 255 Drosophila research, 97–98, 147, 149, 153–54, 204–10, 550–55, 557 DSCF5 gene, 244 Du Bois, W. E. B., 202–4 Duchenne muscular dystrophy

and melanosomes, 229, 231 memes, 452–54 Mendel, Gregor background, 38–39 and Davenport’s research, 79–81 and discovery of genes, 132–33 and Drosophila research, 98–99 early plant experiments, 39–40, 46, 152–53 and embryonic development research, 329 and eugenics ideology, 84 and Fisher’s research, 334

, 131, 132 and chimerism, 392, 394–99 and CRISPR research, 490, 496, 531–32, 538–40, 542 and diagnosis of hereditary diseases, 133–34 and Drosophila research, 97–99, 499 and embryonic development, 331 and endosymbiosis, 410 and epigenetics, 438 and evolution of DNA-based life, 139 and fertility science, 504

, Dorothy, 158 Rawls, Lindsey, 572 recessive traits and mutations and causes of PKU, 117, 119, 122–23, 126, 129 and Davenport’s research, 79 and Drosophila research, 98 and genome sequencing, 184–85 and Germinal Choice program, 504 and Goddard’s research, 81 and height research, 262, 272 and isolation of

, 203 World War II, 101, 113, 121, 206, 296, 313, 375, 499 Wormeley, Agatha, 165 Wright, Robert, 134 X chromosomes and chimerism, 381, 393 and Drosophila research, 98, 153 fragile X mutation, 4–5 and genetic screening, 505 and genetic testing and counseling, 5 and Lyon’s research, 334–41 and

Yamanaka, Shinya, 543, 545–47 Yamnaya culture, 227–28 Yandruwandha people, 448–51, 454 Y chromosomes and chimerism, 380–81, 387–91, 393, 398 and Drosophila research, 98 and genetic screening, 505 and Lyon’s research, 334–35 and mosaicism, 355 and tracing lineages, 178–79, 190–92 Y-chromosome “Adam

The Ancestor's Tale: A Pilgrimage to the Dawn of Evolution

by Richard Dawkins  · 1 Jan 2004  · 734pp  · 244,010 words

faster life cycle than your own. Fruit flies and mice measure their generations in weeks and months, not decades as we do. In one experiment, Drosophila fruit flies were split into two 'lines'. One line was bred, over several generations, for a positive tendency to approach light. In each generation, the

have to wait for new mutations. But before this happens, a great deal of change can be achieved. Maize has a longer generation time than Drosophila. But in 1896 the Illinois State Agricultural Laboratory started breeding for oil content in maize seeds. A 'high line' was selected for increased oil content

, but that is presumably because it is hitting the floor of the graph: you can't have less oil than zero. This experiment, like the Drosophila one and like many others of the same type, brings home the potential power of selection to drive evolutionary change very fast indeed. Translate 90

generations of maize, or 20 generations of Drosophila, even 20 elephant generations, into real time, and you have something that is still negligible on the geological scale. One million years, which is too

the common ancestor (Concestor 26), which was probably an eye of some kind. The evidence is genetic, and it is persuasive. In the fruit fly Drosophila there is a gene called eyeless. Geneticists have the perverse habit of naming genes by what goes wrong when they mutate. The eyeless gene normally

be right, and that is the subject of this tale. That particular homeosis -- leg in place of antenna -- was later discovered in the fruit fly Drosophila and named antennapedia. Drosophila ('dew lover') has long been the geneticists' favourite animal. Embryology should never be confused with genetics, but recently

Drosophila has assumed a starring role in embryology as well as genetics, and this is a tale of embryology. Embryonic development is controlled by genes, but

under the control of the mother's genes, not the egg's own nuclear genes. For example, there is a gene called bicoid in the Drosophila mother's genotype, which expresses itself in the 'nurse' cells that make her eggs. The protein made by the bicoid gene is shipped into the

segments (T1, T2 and T3) are more obviously in a line, each bearing a pair of legs. T2 and T3 normally bear wings, but in Drosophila and other flies only T2 has wings.* The second pair of 'wings' is modified into halteres, small club-shaped organs on T3, which vibrate and

pair on each of the three thoracic segments. Behind the thoracic segments are a larger number of abdominal segments (11 in some insects, eight in Drosophila, depending on how you reckon the genitals at the rear end). Cells 'know' (in the sense already excused) which segment they are in, and they

' they are in segment 2. This brings us to the most wonderful part of the Fruit Fly's Tale. After they had been discovered in Drosophila, Hox genes started turning up all over the place: not only in other insects such as beetles, but in almost all other animals that have

the same order along chromosomes. Let's now turn to the mammal story, which has been most thoroughly worked out in the laboratory mouse -- that Drosophila of the mammal world. Mammals, like insects, have a segmented body plan, or at least a modular, repeated plan that affects the backbone and associated

we move from neck to tail. Blood vessels, nerves, muscle blocks, cartilage discs and ribs, where present, all follow the repetitive, modular plan. As with Drosophila the modules, though following the same general plan as each other, are different in detail. And like the insect division into head, thorax and abdomen

, vertebrae are grouped into cervical (neck), thoracic (upper back vertebrae with ribs), lumbar (lower back vertebrae without ribs) and caudal (tail). As in Drosophila, the cells, whether they are bone cells, muscle cells, cartilage cells or anything else, need to know which segment they are in. And as in

Drosophila, they know because of Hox genes -- Hox genes that recognisably correspond to particular Drosophila Hox genes -- although, unsurprisingly, given the immensity of time since Concestor 26, they are far from identical. Again

as in Drosophila, the Hox genes are arranged in the right order on the chromosome. Vertebrate modularity is very different from that of insects, and there is no

representative in 'slot' 7. When two, three or four versions of a Hox gene impinge upon one segment, their effects are combined. And, as with Drosophila, all mouse Hox genes exert their strongest effect in the first (most anterior) segment in their domain of influence, with a gradient of decreasing expression

downstream in more posterior segments. It gets better. With minor exceptions, each gene from the Drosophila array of eight Hox genes resembles its opposite number in the mouse series more than it resembles the other seven genes in the

Drosophila series. And they are in the same order along their respective chromosomes. Every one of the eight Drosophila genes has at least one representative in the mouse series of 13. The detailed gene-for

-gene coincidence between Drosophila and mouse can only indicate shared inheritance -- from Concestor 26, the grand progenitor of all the protostomes and all the deuterostomes. That means the vast

majority of animals are descended from an ancestor that had Hox genes arranged in the same linear order as we see in modern Drosophila and modern vertebrates. Think of it! Concestor 26 had Hox genes, and in the same order as ours. As I've already said, it doesn

interest to look for Hox genes in their modern descendants. Concestor 23 is the ancestor we share with amphioxus. Given that the more distantly related Drosophila has the same fore-and-aft series as mammals, it would be positively worrying if amphioxus didn't have it too. My colleague Peter Holland

body plan is mediated by (14) Hox genes, and yes, they are arranged in the right order along the chromosome. Unlike the mouse, but like Drosophila, there is only one series, not four parallel series. Presumably the entire cluster has been duplicated four times somewhere along the line leading from Concestor

that all these animals are descended from Concestor 26, and we already have good reason to think Concestor 26 had Hox genes, like its descendants Drosophila and mouse. Cnidarians, such as Hydra (they aren't due to join us until Rendezvous 28), are radially symmetrical -- they don't have an anterior

oral/aboral axis, but so far it isn't clear that this is so. Most cnidarians only have two Hox genes anyway, to pit against Drosophila's eight and amphioxus's fourteen. It is agreeable that one of these two genes resembles the anterior complex of

Drosophila, while the other resembles the posterior complex. Concestor 28, the one we share with them, presumably had the same. Then one of the two duplicated

Pox family is found in all animals. A particularly notable member of this family is Pax6, which corresponds to the gene known as ey in Drosophila. I've already mentioned that Pax6 is responsible for telling cells to make eyes. The same gene makes eyes in animals as different as

Drosophila and mouse, even though the eyes produced are radically different in the two animals. In a similar way to Hox genes, Pax6 doesn't tell

place to make an eye. A rather parallel example is the small family of genes called tinman. Again tinman genes are present in both Drosophila and mice. In Drosophila, tinman genes are responsible for telling cells to make a heart, and they normally express themselves in just the right place to make

a Drosophila heart. As we have by now come to expect, tinman genes are also involved in telling mouse cells to make a heart in the right

the hypha in a syncitium, meaning a tissue with many nuclei not divided into separate cells (we met other syncitia in the early development of Drosophila, and in Hadzi's theory of the origin of the Metazoa). Not all fungi have a thread-like mycelium. Some, such as yeasts, have reverted

.). Oxford University Press, Oxford. [124] HALDER, G., CAUAERTS, P., & GEHRING, W. J. (1995) Induction of ectopic eyes by targeted expression of the eyeless gene in Drosophila. Science 267:1788-1792. [125] HALLAM, A. & WIGNALL, P. B. (1997) Mass Extinctions and their Aftermath. Oxford University Press, Oxford. [126] HAMILTON, W. D. (2001

Life's Greatest Secret: The Race to Crack the Genetic Code

by Matthew Cobb  · 6 Jul 2015  · 608pp  · 150,324 words

in marine biology, investigating the development of pycnogonids or sea spiders, but he had recently begun studying evolution, using the tiny red-eyed vinegar fly, Drosophila.13 Morgan subjected his hapless insects to various environmental stresses – extreme temperatures, centrifugal force, altered lighting conditions – in the vain hope of causing a change

genes are made of; they were more interested in discovering what genes actually do. There was a potential link between these two approaches. As the Drosophila geneticist Jack Schultz put it in 1935, by studying the effects of genes it should be possible ‘to find out something about the nature of

gene’.34 One of the scientists who took Schultz’s suggestion very seriously was George Beadle, who had studied the genetics of eye colour in Drosophila in Morgan’s laboratory, alongside the Franco-Russian geneticist Boris Ephrussi. When Ephrussi returned to Paris, Beadle followed him to continue their work. Their objective

was to establish the biochemical basis of the mutations that changed the eye-colour of Drosophila flies. Beadle and Ephrussi’s experiments failed: the biochemistry of their system was too complicated, and they were unable to extract the relevant chemicals from

in. Currently, the largest known number of mRNAs that can be produced by a single gene is 38,016. These mRNAs are encoded by the Drosophila gene Dscam, which has four clusters of exons, each of which has twelve, forty-eight, thirty-three or two alternative splices.13 Many of the

first animal genome to be completed, in 1998, was that of the nematode worm, Caenorhabditis elegans, closely followed by that of the tiny vinegar fly, Drosophila melanogaster, in 2000. These projects provided vital information about two widely used laboratory organisms and were testing-grounds for different technical and commercial approaches to

genome sequencing. The C. elegans genome project, led by John Sulston, was entirely funded by public money, whereas the Drosophila genome was a joint effort between publicly funded researchers and a company called Celera Genomics, led by Craig Venter, a molecular biologist turned entrepreneur. Despite

the very different motivations of the public and private researchers, the Drosophila genome project was a success. In contrast, the Human Genome Project, which took place in parallel, was the focus of clashes of scientific and commercial

as of personality.40 The human genome contains around 3 billion base pairs, far more than that of C. elegans (100 million base pairs) or Drosophila (140 million base pairs). The size of the human genome and the large stretches of repetitive sequences it contains posed new difficulties that were exacerbated

Celera colleagues enlisted computer scientists to develop algorithms for assembling the sequence, and they were able to prove the validity of their approach with the Drosophila genome. Despite hostility from many scientists around the world, Venter was probably right to argue that this method would make it possible to complete the

of the genome were amplified in bacteria to try and bridge the gap. This does not always work – some sections of the human and the Drosophila genomes have still not been joined up, fifteen years after the sequences were published. Despite the continuing clashes, the completion of the draft human genome

Ewan Birney set up a sweepstake inviting scientists to guess how many protein-encoding genes would be identified once the human genome was sequenced. The Drosophila genome, which had just been published, contained around 13,500 genes, and entrants in the sweepstake chose numbers between 26,000 and 140,000. The

the non-genetic transmission of information down the generations and the underlying mechanisms – one of my PhD students, Becky Lockyer, has recently studied them in Drosophila.17 The existence of intergenerational transmission of environmentally induced changes is now well established, and it is known that these effects can buffer populations of

– the proteins that package DNA. It is widely assumed that changes to histones are involved in gene regulation, but the evidence is unclear, and in Drosophila one kind of histone can be deleted completely without any effect on gene transcription.25 For the moment, there is no evidence that histone modifications

as it has been realised that the dangers are far less than was originally feared.37 In my own field, the study of behaviour in Drosophila, the introduction of DNA from other species into the fly’s genome has become widespread in order to mark and manipulate tissues, enabling us to

per cent of your DNA, whereas CTG is 4.1 per cent of your DNA. Broadly similar results are found for the mouse and for Drosophila, however in yeast CTA and CTG make up around 1.3 and 1.0 per cent of the DNA, respectively, whereas TTG is the most

species, and selection pressure to use one form of codon rather than another to avoid potential errors. Genome-wide analyses of codon bias in twelve Drosophila species have shown that codon bias can even extend across codons: the most frequent pairs of codons in these flies are XXG-CXX (so any

have different consequences in different contexts. The gene that got me interested in studying the effects of genes on behaviour, back in 1976, was a Drosophila gene called dunce that was identified in Seymour Benzer’s lab – flies with a mutation in this gene show defects in learning and memory.52

, J., One Plus One Equals One: Symbiosis and the Evolution of Complex Life, Oxford, Oxford University Press, 2014. Ashburner, M., Won for All: How the Drosophila Genome Was Sequenced, Cold Spring Harbor, Cold Spring Harbor Laboratory Press, 2006. Astbury, W. T., ‘X-ray studies of nucleic acids’, Symposia of the Society

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Crick’s final model 106–7, 107f The Double Helix, by Jim Watson 105, 108 Doudna, Jennifer 283–4 Dounce, Alexander 72, 116, 140, 214 Drosophila Beadle’s experiments on 9–10 codon bias in 294–5 Dscam gene 223 dunce gene 302 genetic engineering of 280 genome 231, 233 histone

and Virus: A Study of Macromolecular Pattern in Action, by Macfarlane Burnet 134–5, 139, 141, 146–7 Enzyme Cybernetics book project 159 Ephrussi, Boris Drosophila experiments 9–10 spoof letter on cybernetics 87–8, 88f, 111, 159 on whether DNA encodes amino acids 124–6, 128 Ephrussi-Taylor, Harriett 62

261 Timetree database 239 ‘Extrapolation, interpolation, and smoothing of stationary time series with engineering applications’ (Yellow Peril document) 24–5, 27, 30 eye colour in Drosophila 4, 9–10 F Farzadfard, Fahim 272 FASEB (Federation of American Societies for Experimental Biology) meetings 177, 179–80 Feedback Mechanisms and Circular Causal Systems

Longevity: To the Limits and Beyond (Research and Perspectives in Longevity)

by Jean-Marie Robine, James W. Vaupel, Bernard Jeune and Michel Allard  · 2 Jan 1997

mortality. Pop Index 55:613-643 Curtsinger JW, Fukui HH, Townsend D, Vaupel JW (1992) Demography of Genotypes: Failure of the Limited Lifespan Paradigm in Drosophila melanogaster. Science 258:461-463 Demeny P (1984) A perspective on long-term population growth. Pop Dev Rev 10: 103-126 Depoid F (1973) La

some of the ways in which life span has been increased in animal models. Routes to Increase Biological Life Span Artificial Selection In the fruitfly Drosophila melanogaster, life span has been increased by both indirect and direct selection procedures. Indirect selection has been carried out through selecting for late reproductive ability

constructed in which a particular function is altered in either an upward or downward direction. The value of this approach was clearly demonstrated with transgenic Drosophila melanogaster that were made to overexpress the antioxidant enzymes superoxide dismutase (SOD) and catalase (Orr and Sohal 1994). A resulting increase in life span was

-gene mutations and induced by thermal stress. Proc Natl Acad Sci USA 92:7540-7544 Luckinbill LS, Clare MJ (1985) Selection for life span in Drosophila melanogaster. Heredity 58:9-18 Masoro EJ (1992) Retardation of aging processes by nutritional means. Ann NY Acad Sci 673:29-35 Medawar PB (1952

unsolved problem of biology. London, H K Lewis. Orr WC, Sohal RS (1994) Extension of life-span by overexpression of superoxide dismutase and catalase in Drosophila melanogaster. Science 263:1128-1130 Partridge L, Barton NH (1993) Optimality, mutation and the evolution of ageing. Nature 362:305-311 Rose MR (1984) Laboratory

evolution of postponed senescence in Drosophila melanogaster. Evolution 38:1004-1010 Schachter F, Cohen D, Kirkwood TBL (1993) Prospects for the genetics of human longevity. Human Genet 91:519-526 Service

PM (1987) Physiological mechanisms of increased stress resistance in Drosophila melanogaster selected for postponed senescence. Physiol Zool 60:321- 326 Smith DWE (1994) The tails of survival curves. BioEssays 16:907-911 Weindruch R, Walford

(1957) Pleiotropy, natural selection and the evolution of senescence. Evolution 11:398-411 Zwaan BJ, Bijlsma R, Hoekstra RF (1995) Direct selection on lifespan in Drosophila melanogaster. Evolution 49:649-659 Emergence of Centenarians and Super-centenarians B. Jeune and V. Kannisto • Abstract Until about 1950 centenarians were quite rare, and

. Finally, more recently, research has been carried out on the effect of a decrease in selection forces. Compared with the works carried out on animals, Drosophila Melanogaster or rodents, only a very few studies have been devoted recently to the longevity of the human species. For example, Pierre Philippe (1980) has

this interval (Sohal and Sohal 1991; Fig. 1 B). Mitochondrial H 2 0 2 production showed a similar age-related increase in the fruit fly, Drosophila melanogaster (Sohal et al. 1995a). Exposure of housefly mitochondria to experimental oxidative stress, in the form of 100 % O2 or 142 R.]. Mockett, R. S

et al. 1989a). Protein oxidative damage is most commonly measured as the level of carbonyl content. Carbonyl content increases as a function of age in Drosophila (Orr and Sohal 1994) and in gerbil brain, heart and testis (Sohal et al. 1995b). It increases exponentially in whole-body homogenates and flight muscle

mitochondrial 144 R.J. Mockett, R. S. Sohal DNA oxidative damage increase during aging in Musca, and 8-0HdG content increases steeply during aging of Drosophila (Sohal et al. 1995a). In summary, these results show that the age-related increase in oxidative stress is associated with increasing levels of oxidative molecular

60 80 100 b 10 20 30 40 50 60 70 Age (da}'s) Fig. lA. Survivorship curves for three groups of adult male transgenic Drosophila melanogaster overexpressing single extra copies of Cu-Zn SOD and catalase genes (groups A, B, and C). The control group has only the normal diploid

defenses and aging. The notable exception is the direct effects of Cu-Zn SOD and catalase co-overexpression on life spans and oxidative damage in Drosophila. It is possible that cooverexpression of these enzyme neutralizes a greater fraction of ROS before they gain access to certain compartments of the cell, thereby

have been generated and are currently being characterized. Glutathione peroxidase, which acts in tandem with MnSOD in mitochondria in some systems, has proven refractory in Drosophila. The flies do not contain detectable levels of endogenous glutathione peroxidase activity, and attempts to express the human enzyme were thwarted by the inability of

Drosophila to translate the unique selenocysteine codon at the active site. Recent reports of intramitochondrial catalase activity in rat heart (Radi et al. 1991) raise the

Dev. 29:63-69 Orr WC, Sohal RS (1992) The effects of catalase gene overexpression on life span and resistance to oxidative stress in transgenic Drosophila melanogaster. Arch. Biochem. Biophys. 297:35-41 Orr WC, Sohal RS (1993) The effects of Cu-Zn superoxide dismutase gene overexpression on life span and

resistance to oxidative stress in transgenic Drosophila melanogaster. Arch. Biochem. Biophys. 301 :34-40 Oxidative Stress May Be a Causal Factor in Senescence of Animals 153 Orr WC, Sohal RS (1994) Extension

of life-span by overexpression of superoxide dismutase and catalase in Drosophila melanogaster. Science 263:1128-1130 Pearl R (1928) The rate of living. Alfred A. Knopf, Inc., New York Radi R, Turrens JF, Chang LY, Bush

(1990 a) Effect of age on superoxide dis mutase, catalase, glutathione reductase, inorganic peroxides, TBA-reactive material, GSH/GSSG, NADPH/NADP+ and NADHI NAD+ in Drosophila melanogaster. Mech. Ageing Dev. 56:223-235 Sohal RS, Arnold LA, Sohal BH (1990b) Age-related changes in antioxidant enzymes and pro oxidant generation in

A, Agarwal S, Orr WC (1995a) Simultaneous overexpression of CU,Zn superoxide dismutase and catalase retards age related oxidative damage and increases metabolic potential in Drosophila melanogaster. J. BioI. Chern. 270:20224-20229 Sohal RS, Agarwal S, Sohal BH (1995 b) Oxidative stress and aging in Mongolian gerbil (Meriones unguiculatus). Mech

the primary focus of the efforts to identify gerontogenes: Saccharomyces cerevisiae (reviewed by Jazwinski 1996), C. elegans (reviewed by Lithgow 1996), and the fruit fly Drosophila melanogaster (reviewed by Fleming and Rose 1996). The focus on these species arises from two considerations: the desire to complete the research in a reasonable

in Caenorhabditis elegans: Chromosomal mapping of multiple noninteractive loci. Genetics 135: I 003 - 10 I 0 Fleming JE, Rose MR (1996) Genetics of aging in Drosophila. In: Rowe JW, Schneider EL (eds) Handbook of the biology of aging. 4th edn. Academic Press, New York, pp 74-93 Friedman DB, Johnson TE

stress. Proc Nat! Acad Sci USA 92:7540-7544 Luckinbill LS, Arking R, Clare MJ, Cirocco WC, Muck SA (1984) Selection for delayed senescence in Drosophila melanogaster. Evolution 38:996-1003 Martin GM, Austad SN, Johnson TE (1996) Genetic analysis of aging: Role of oxidative damage and environmental stresses. Nat Genetics

in gerontology. Bioessays 2:226-228 Identifying and Cloning Longevity-Determining Genes in the Nematode 163 Rose MR (1984) Laboratory evolution of postponed senescence in Drosophila melanogaster. Evolution 38:1004-1010 Shook D, Brooks A, Johnson TE (1996) Mapping quantitative trait loci specifying hermaphrodite survival or selffertility in the nematode Caenorhabditis

mono- and dizygous twins. Other Organisms Among the commonly used animal models for studies of aging are inbred fruit flies and nematodes. The fruit fly Drosophila, like other arthropods, also share with the cordates the developmental trait of statistical fluctuations of cell fate that are likely to lead to wide individual

These Strange New Minds: How AI Learned to Talk and What It Means

by Christopher Summerfield  · 11 Mar 2025  · 412pp  · 122,298 words

of fruit for a few days in summer, you may have noticed a swarm of tiny flies looping insistently above your blackening bananas. These are Drosophila melanogaster, an insect species that is much more popular in neuroscience laboratories than in the average kitchen. In the first few hours after hatching

, Drosophila go through a rapid series of larval stages, during which they look a bit like a squashed white gummy bear. In 2015, neuroscientists chopped the

brain of one unwitting six-hour-old larval Drosophila into thousands of wafer-thin slices, each of less than 4 nanometres (for comparison, an average human hair has a diameter of about 100,000

nanometres). Neuroscientists have known roughly how the brains of flies, mice, monkeys and humans are organized for decades, but this experiment with Drosophila was special. By studying the slices with an electron microscope – and after a lot of painstaking labour – a team of researchers was able to reconstruct

able to build a full reconstruction (or ‘connectome’) of the brain of an insect. Many behaviours that Drosophila exhibits are innately stamped into this network and thus utterly inflexible. For instance, in the wild Drosophila are exposed to various potential threats, such as being stung by parasitic wasps that inject them with

eggs (which, once hatched, devour their hapless host from within). To protect themselves, Drosophila larvae have evolved tailored escape behaviours. Ominous vibrations tend to produce a steady pulsatile ‘crawling’ away from the threat, whereas real stings will induce a

genetically modified so that their neurons fire when exposed to coloured light, and then zap the cells with a blue laser to cause the larval Drosophila to crawl or roll at the push of a button. It’s as if the fly brain works by storing a set of useful fixed

from the same shortcoming as other symbolic models – it is too brittle to deal with the messy reality of the real world. So how does Drosophila manage? The answer is that the strength of connections in the fruit-fly brain can adapt. In fact, like almost every other animal on Earth

able to learn – to adjust its behaviour with experience. This has been known since at least the 1970s, with early studies in which Drosophila were given the choice of flying down a blue or a yellow tunnel, and received an electric shock if they made the wrong choice (they

colour, by teaching male flies that red-eyed females tend to be more sexually receptive, whereas brown-eyed ones are generally less game.[*5] In Drosophila, learning doesn’t add or remove behaviours from the animal’s basic repertoire. You can’t teach it to fly backwards or dance the tango

a signal flowing between two neurons is followed by a positive outcome – such as sugar or sex – then this connection gets even stronger. So when Drosophila is rewarded with sucrose for extending its proboscis (the fruit-fly equivalent of sticking your tongue out) in response to banana oil, synapses linking cells

be better. Humans – who have reasoned deeply enough to build advanced civilization – have one of the largest brains in the animal kingdom.[*1] Whereas larval Drosophila have just over 3,000 neurons, the adult human brain clocks in at more than eighty billion, and a lower estimate of the number of

of a genetic mutation that allows recursive computation in our brains. This is an interesting idea, but not very plausible to most neuroscientists, because even Drosophila has a brain that is capable of recursive computation, but it isn’t all that good at producing sentences. Chomsky’s theory of phrase structure

, 149, 102601. Available at https://doi.org/10.1016/j.ijhcs.2021.102601. Spatz, H. Ch., Emanns, A., and Reichert, H. (1974), ‘Associative Learning of Drosophila melanogaster’, Nature, 248(5446), pp. 359–61. Available at https://doi.org/10.1038/248359a0. Sunstein, C. R. (2021), ‘Manipulation as Theft’. Preprint. SSRN Electronic

Is All You Need’. Preprint. arXiv. Available at http://arxiv.org/abs/1706.03762 (accessed 30 October 2020). Verzijden, M. N. et al. (2015), ‘Male Drosophila melanogaster Learn to Prefer an Arbitrary Trait Associated with Female Mating Status’, Current Zoology, 61(6), pp. 1036–42. Available at https://doi.org/10

, 24–5, 35–6 Borges, Jorge Luis: ‘The Library of Babel’, 184 Bostrom, Nick, 266, 321 brain computer and, 22, 144–7 consciousness and, 125 Drosophila, 33–4, 36–7, 47, 147 language and, 67, 74, 89, 92, 94, 95, 100–102, 111, 112, 115, 116 learning and, 160–62, 167

, 213 Foxes and Chickens problem, 26–7 fraud, AI-generated, 23, 189, 221, 226–7, 237, 301, 344, 345–6 Frontier AI, 242 fruit fly (Drosophila melanogaster), 33–4, 36–7, 47, 147 functional linguistic competence, 175–6 Future of Life Institute, 310, 312, 321 G Galileo, 67, 143, 152, 269

Climbing Mount Improbable

by Richard Dawkins and Lalla Ward  · 1 Jan 1996  · 309pp  · 101,190 words

begin, I need to apologize for a maddeningly silly convention adopted by geneticists over the naming of genes. The gene called eyeless in the fruitfly Drosophila actually makes eyes! (Wonderful, isn’t it?) The reason for this wantonly confusing piece of terminological contrariness is actually quite simple, and even rather interesting

part of the body. This is why livers are different from kidneys, even though both contain the same complete set of genes. In the adult Drosophila, ey usually expresses itself only in the head, which is why the eyes develop there. George Halder, Patrick Callaerts and Walter Gehring discovered an experimental

manipulation that led to ey’s being expressed in other parts of the body. By doctoring Drosophila larvae in cunning ways, they succeeded in making ey express itself in the antennae, the wings and the legs. Amazingly, the treated adult flies grew

Waldorf, working in the same Swiss laboratory, found that these particular mammal genes are almost identical, in their DNA sequences, to the ey gene in Drosophila. This means that the same, gene has come down from remote ancestors to modern animals as distant from each other as mammals and insects. Moreover

eyes. Remarkable fact number three is almost too startling. Halder, Callaerts and Gehring succeeded in introducing the mouse gene into Drosophila embryos. Mirabile dictu, the mouse gene induced ectopic eyes in Drosophila. Figure 5.29 (bottom) shows a small compound eye induced on the leg of a fruitfly by the mouse equivalent

is an insect compound eye that has been induced, not a mouse eye. The mouse gene has simply switched on the eyemaking developmental machinery of Drosophila. Genes with pretty much the same DNA sequence as ey have been found also in molluscs, marine worms called nemertines, and sea-squirts. Ey may

the statement that eyes evolve easily and at the drop of a hat remains unscathed. These experiments probably do mean that the common ancestor of Drosophila, mice, humans, sea-squirts and so on had eyes. The remote common ancestor had vision of some kind, and its eyes, whatever form they may

arthromorphs bred by artificial selection with an eye to their resemblance, however vague, to real arthropods. Figure 7.15 Homeotic mutations: (a) four-winged Drosophila. In normal Drosophila the second pair of wings is replaced by halteres, as in Figure 7.11; (b) normal (upper) and mutant (lower) silkworm caterpillars. Normally there

thoracic segments. The mutant has nine ‘thoracic’ segments. Figure 7.15 shows examples of so-called homeotic mutations in the fruitfly Drosophila and in the silkworm caterpillar. The normal Drosophila, like all flies, has only a single pair of wings. The second pair of wings is replaced by halteres as explained above

. The picture shows a mutant Drosophila in which not only is there a second pair of wings instead of halteres, the entire second thoracic segment is reduplicated in substitution for the

the thoracic tagma have been duplicated, just as in the right-hand arthromorph of Figure 7.12. The most famous homeotic mutation is ‘antennapedia’ in Drosophila. fruitflies. Flies with this mutation have a normal-looking leg poking out of the socket where an antenna ought to be. The legproducing machinery has

a more foolhardy speculation. My suggestion is that Scyllarus may actually present an example in the wild of a homeotic mutation, analogous to antennapedia in Drosophila in the laboratory. Unlike antennapedia, this mutation has been incorporated into an actual evolutionary change in nature. My tentative conjecture is that an ancestral Scyllarid

.) Oxford: Oxford University Press. Halder, G., Callaerts, P., and Gehring, W. J. (1995) ‘Induction of ectopic eyes by targeted expression of the eyeless gene in Drosophila’. Science, 267, 1788–92. Hamilton, W. D. (1996) Narrow Roads of Gene Land: The collected papers of W. D. Hamilton, Vol. 1. Evolution of Social

As Gods: A Moral History of the Genetic Age

by Matthew Cobb  · 15 Nov 2022  · 772pp  · 150,109 words

DNA, the cloners – Stanley Cohen and Herb Boyer, along with Ron Davis and David Hogness, who had recently fused DNA from the geneticists’ friend, the Drosophila fly, with Cohen’s plasmid – were also invited to sign the document. The Berg letter was published with the imprimatur of the National Academy of

valid only in the United States). These cagey attitudes soon permeated fields where there were no immediate commercial stakes. I recall 1980s conference presentations in Drosophila neurobiology where researchers would flash up a laboriously obtained DNA sequence for a few seconds while some in the audience furiously tried to scribble it

finger and the DNA sequence it targeted was not easy to work out.7 Nevertheless, by 2003 these artificial enzymes had been used to get Drosophila cells to turn one version of a gene into another and had successfully targeted genes in human cells.8 The advent of programmable meganucleases held

out the ants’ olfactory receptors, the researchers revealed the unsuspected role of olfactory neurons in shaping the structure of the ant brain. Previously, studies in Drosophila had persuaded scientists that the olfactory parts of the insect brain were largely hard-wired because knocking out the fly’s olfactory receptors had no

effect on brain structure; the scrambled brains of the CRISPRed ants revealed that what is true in Drosophila is not necessarily true of all insects. There will be many similar instances in the future – by allowing scientists to investigate all sorts of organisms

provided an antidote. If the antidote component was not present, the insect died in the egg. In 2007, an artificial Medea system was built in Drosophila; within twelve generations, the construct had spread to every fly in the laboratory cages.11 One entomologist predicted that ‘in 5–10 years, fully functional

being created, almost by accident. In 2014, Valentino Gantz of the University of California San Diego was finishing his PhD on the development of the Drosophila wing; unable to create enough flies carrying two copies of the mutation he was studying, Gantz thought about using CRISPR to multiply the number of

it was supposed to cut and so it gradually declined in frequency. Similar results were observed by other researchers, studying two different gene drives in Drosophila. Their conclusion was gloomy for some but reassuring for others: The frequency of a CRISPR gene drive in two cages of mosquitoes over twenty-five

problems were revealed when genomic and experimental studies of natural populations of three different insects – flour beetles, African malaria mosquitoes and the invasive fruit pest Drosophila suzukii – all reported genetic variation in target sites that reduced drive efficiency and led to the appearance of resistance. As one group concluded: ‘standing genetic

different transgenic components and creating an organism in which only certain cells will perform a desired function under particular conditions. For example, in the fly Drosophila, which I have studied for over forty years, in the 1990s Andrea Brand and Norbert Perrimon developed a modular expression system involving two transgenes from

sequence); the Gal4 protein is a transcription factor – it acts like a switch on the UAS sequence, activating it.7 Researchers introduced Gal4 into the Drosophila genome repeatedly, and on some occasions the transgene randomly inserted itself into the promoter region of a gene that was expressed only in certain cells

application of these techniques. I can appreciate the attraction of simple, neat solutions – using the GAL4–UAS system to investigate the sense of smell in Drosophila maggots has brought me the same kind of joy in an elegant technique that Jon Beckwith and his colleagues felt with their experimental manipulation of

sugar/phosphate backbone and four bases: adenine, cytosine, guanine and thymine (A, C, G and T). The genetic material in all organisms and some viruses. Drosophila. A tiny fly used by geneticists since the beginning of the twentieth century. I have studied this insect for over forty years. E. coli. Escherichia

was the use of transposons or jumping genes. One kind of transposon (the P element) had recently been found to be invading wild populations of Drosophila, causing some strains to produce no viable offspring if they were crossed. Transposons were also used by molecular geneticists to delete or add DNA sequences

The Gene: An Intimate History

by Siddhartha Mukherjee  · 16 May 2016  · 824pp  · 218,333 words

winter evening in 1911, Sturtevant, then a twenty-year-old undergraduate student in Morgan’s lab, brought the available experimental data on the linkage of Drosophila (fruit fly) genes to his room and—neglecting his mathematics homework—spent the night constructing the first map of genes in flies. If A was

on a different chromosome. By the end of the evening, Sturtevant had sketched the first linear genetic map of half a dozen genes along a Drosophila chromosome. Sturtevant’s rudimentary genetic map would foreshadow the vast and elaborate efforts to map genes along the human genome in the 1990s. By using

might as well have left for the Galápagos. The decision to hunt for variation in wild flies proved critical. In a wild fly species named Drosophila pseudoobscura, for instance, Dobzhansky found multiple gene variants that influenced complex traits, such as life span, eye structure, bristle morphology, and wing size. The most

opened a vast genome conference at the Fontainebleau Hotel in Miami with its own strategic counterpunch: it had sequenced the genome of the fruit fly, Drosophila melanogaster. Working with the fruit fly geneticist Gerry Rubin and a team of geneticists from Berkeley and Europe, Venter’s team had assembled the fly

Kingdom, trans. J. B. Farmer and A. D. Darbishire (Chicago: Open Court, 1909). In the 1930s, Theodosius Dobzhansky: Robert E. Kohler, Lords of the Fly: Drosophila Genetics and the Experimental Life (Chicago: University of Chicago Press, 1994), “From Laboratory to Field: Evolutionary Genetics.” In September 1943, Dobzhansky: Th. Dobzhansky, “Genetics of

natural populations IX. Temporal changes in the composition of populations of Drosophila pseudoobscura,” Genetics 28, no. 2 (1943): 162. Dobzhansky could demonstrate it experimentally: Details of Dobzhansky’s experiments are sourced from Theodosius Dobzhansky, “Genetics of natural

populations XIV. A response of certain gene arrangements in the third chromosome of Drosophila pseudoobscura to natural selection,” Genetics 32, no. 2 (1947): 142; and S. Wright and T. Dobzhansky, “Genetics of natural populations; experimental reproduction of some of

the changes caused by natural selection in certain populations of Drosophila pseudoobscura,” Genetics 31 (March 1946): 125–56. Transformation If you prefer an “academic life”: H. J. Muller, “The call of biology,” AIBS Bulletin 3, no

a G’: The one-billionth nucleotide,” Nature 402, no. 6760 (1999): 331. it had sequenced the genome of the fruit fly: Declan Butler, “Venter’s Drosophila ‘success’ set to boost human genome efforts,” Nature 401, no. 6755 (1999): 729–30. In March 2000, Science published: “The

Drosophila genome,” Science 287, no. 5461 (2000): 2105–364. Of the 289 human genes known to be: David N. Cooper, Human Gene Evolution (Oxford: BIOS Scientific

: Sinauer Associates, 2001), 262. “a man like me”: Marsh, William Blake, 56. “The lesson is that the complexity”: Quote from the director of the Berkeley Drosophila Genome Project, Gerry Rubin, in Robert Sanders, “UC Berkeley collaboration with Celera Genomics concludes with publication of nearly complete sequence of the genome of the

interventions in, 13, 458 therapeutic abortion based on prenatal test for, 267–68 variations among patients with, 275–76 Dozy, Andree, 280n Dreiser, Theodore, 117 Drosophila. See fruit flies Drysdale-Vickery, Alice, 73 Dulbecco, Renato, 203, 210 dwarfism, 77, 85, 138, 251, 265, 275, 482 Ebstein, Richard, 384–86 EcoR1 enzyme

How Not to Network a Nation: The Uneasy History of the Soviet Internet (Information Policy)

by Benjamin Peters  · 2 Jun 2016  · 518pp  · 107,836 words

many specific social purposes but basic research need not begin with any single goal in mind. Biologists, for example, run test on fruit flies—or Drosophila—not because they are particularly devoted to improving the life of fruit flies; they do so because fruit flies are convenient test subjects that reproduce

quickly and cheaply. Computer chess has been called “the drosophila of artificial intelligence” (Alexander Kronrod’s phrase, popularized by American computer scientist John McCarthy) because it is thought to stand in as an affordable test

How It Will Rise Again (Cambridge: MIT Press), 89–90. 42. Johnson, White King and Red Queen, chap. 6. 43. Nathan Engsmenger, “Is Chess the Drosophila of Artificial Intelligence?,” Social Studies of Science 42 (1) (2011): 5–30. See also John McCarthy, “Chess as the

Drosophila of AI,” accessed April 15, 2015, http://jmc.stanford.edu/articles/drosophila/drosophila.pdf. 44. E. M. Landis and I. M. Yaglom, “About Aleksandr Semenovich Kronrod,” Uspekhi Matematicheskikh Nauk 56 (5) (2001): 191–201

, 2003. Engsmenger, Nathan. The Computer Boys Take Over: Computers, Programmers, and the Politics of Technical Expertise. Cambridge: MIT Press, 2010. Engsmenger, Nathan. “Is Chess the Drosophila of Artificial Intelligence? A Social History of an Algorithm.” Social Studies of Science 42 (1) (2011): 5–30. Erickson, Paul, Judy L. Klein, Lorraine Dastone

, Liberty, and Automatic Machinery in Early Modern Europe. Baltimore: Johns Hopkins University Press, 1989. McCarthy, John. “Chess as the Drosophila of AI.” Accessed April 15, 2015, http://jmc.stanford.edu/articles/drosophila/drosophila.pdf. McCulloch, Warren S. “A Heterarchy of Values Determined by the Topology of Nervous Nets.” Bulletin of Mathematical Biophysics 7

Digital Computing Machines, 84, 108 Digital technologies, 104 Distributed networks, 55, 94, 96, 100, 120 Dnepr-2, 119 Dnieper computer series, 127 Donbass region, 154 Drosophila, 178 EASU (ekonomicheskaya avtomatizirovannaya sistema upravleniya). See Economic Automatic Management System (EASU) Economic Automatic Management System (EASU), 81, 86–87, 91, 103–104 Economic corruption

More Than You Know: Finding Financial Wisdom in Unconventional Places (Updated and Expanded)

by Michael J. Mauboussin  · 1 Jan 2006  · 348pp  · 83,490 words

crises. —Bill Gates, Fortune, 1998 Fruit Flies and Futility Geneticists and biologists love to work with Drosophila melanogaster, a common fruit fly, and have made it a staple of biological study. Indeed, insights from Drosophila research helped a trio of scientists win the 1995 Nobel prize in medicine. Thousands of researchers continue

to study the Drosophila to better understand various genetic and developmental issues. Drosophila is attractive to scientists because they understand its features and it is easy to handle. But the fly has another essential feature that

scientists covet: its life cycle. Drosophila go from embryo to death in about two weeks. This rapid rate of reproduction allows scientists to study hundreds of generations of the fly’s

development and mutations in a relatively short time. Drosophila’s fast evolution provides scientists with important clues about evolution in other species, which generally evolve at a relatively glacial pace.1 Why should businesspeople

care about Drosophila? A sound body of evidence now suggests that the average speed of evolution is accelerating in the business world. Just as scientists have learned a

companies may provide investors with some useful mental models for appreciating change at the slower evolving companies. The business world is going the way of Drosophila. 22 All the Right Moves How to Balance the Long Term with the Short Term Strategy in complex systems must resemble strategy in board games

. New York: Springer Verlag, 1997. ——. “A Multifractal Walk Down Wall Street.” Scientific American (February 1999): 70-73. Manning, Gerard. “A Quick and Simple Introduction to Drosophila melanogaster.” http://www.ceolas.org/fly/intro.html. Marquet, Pablo A., et al. “Lifespan, Reproduction, and Ecology: Scaling and Power-Laws in Ecological Systems.” Journal

; short-term.See also long term, management for Fooled by Randomness (Taleb) Fortune 50, Foster, Richard fractal systems French, Kenneth frequencies; magnitude vs. fruit flies (Drosophila melanogaster) fundamental analysis Galton, Francis gambling Gates, Bill Gazzaniga, Michael General Electric General Theory of Employment, The (Keynes) Gensler, Gary Gibrat’s law Gigerenzer, Gerd

The Clock Mirage: Our Myth of Measured Time

by Joseph Mazur  · 20 Apr 2020  · 283pp  · 85,906 words

Raw Data Is an Oxymoron

by Lisa Gitelman  · 25 Jan 2013

Deep Thinking: Where Machine Intelligence Ends and Human Creativity Begins

by Garry Kasparov  · 1 May 2017  · 331pp  · 104,366 words

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Denialism: How Irrational Thinking Hinders Scientific Progress, Harms the Planet, and Threatens Our Lives

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