An anachronism may be either intentional or unintentional. Intentional anachronisms may be introduced into a literary or artistic work to help a contemporary audience engage more readily with a historical period. Anachronism can also be used intentionally for purposes of rhetoric, propaganda, comedy, or shock. Unintentional anachronisms may occur when a writer, artist, or performer is unaware of differences in technology, terminology and language, customs and attitudes, or even fashions between different historical periods and eras.
Sir Walter Scott justified the use of anachronism in historical literature: "It is necessary, for exciting interest of any kind, that the subject assumed should be, as it were, translated into the manners as well as the language of the age we live in."[5] However, as fashions, conventions and technologies move on, such attempts to use anachronisms to engage an audience may have quite the reverse effect, as the details in question are increasingly recognized as belonging neither to the historical era being represented, nor to the present, but to the intervening period in which the artwork was created. "Nothing becomes obsolete like a period vision of an older period", writes Anthony Grafton; "Hearing a mother in a historical movie of the 1940s call out 'Ludwig! Ludwig van Beethoven! Come in and practice your piano now!' we are jerked from our suspension of disbelief by what was intended as a means of reinforcing it, and plunged directly into the American bourgeois world of the filmmaker."[6]
anachronism
Anachronisms abound in the works of Raphael[8] and Shakespeare,[9] as well as in those of less celebrated painters and playwrights of earlier times. Carol Meyers says that anachronisms in ancient texts can be used to better understand the stories by asking what the anachronism represents.[10] Repeated anachronisms and historical errors can become an accepted part of popular culture, such as the belief that Roman legionaries wore leather armor.[11]
Comedy fiction set in the past may use anachronism for humorous effect. Comedic anachronism can be used to make serious points about both historical and modern society, such as drawing parallels to political or social conventions.[12] The Flintstones, Hagar the Horrible, Histeria!, Time Squad, Mr. Peabody and Sherman (the movie and TV series), The Peabody's Improbable History segments from The Adventures of Rocky and Bullwinkle and Friends, Dinosaur Train, Dave the Barbarian, VeggieTales, History of the World, Part I, Robin Hood: Men in Tights, Blazing Saddles, Disney's Aladdin, Disney's Hercules, Disney's The Emperor's New Groove, Disney's Mickey, Donald, Goofy: The Three Musketeers, The Roman Holidays, the Shrek film series, Early Man, the Shake and Flick cartoon Raw Deal in Rome and Murdoch Mysteries are some of the movies and TV shows set in the past to include many anachronisms.
For example, many books, television shows, radio productions and films nominally set in the mid-21st century or later refer to the Soviet Union, to Saint Petersburg in Russia as Leningrad, to the continuing struggle between the Eastern and Western Blocs and to divided Germany and divided Berlin. Star Trek has suffered from future anachronisms; instead of "retconning" these errors, the 2009 film retained them for consistency with older franchises.[14]
Language anachronisms in novels and films are quite common, both intentional and unintentional.[17] Intentional anachronisms inform the audience more readily about a film set in the past. In this regard, language and pronunciation change so fast that most modern people (even many scholars) would find it difficult, or even impossible, to understand a film with dialogue in 15th-century English; thus, we willingly accept characters speaking an updated language, and modern slang and figures of speech are often used in these films.[18]
Unintentional anachronisms may occur even in what are intended as wholly objective and accurate records or representations of historic artifacts and artworks, because the perspectives of historical recorders are conditioned by the assumptions and practices of their own times, in a form of cultural bias. One example is the attribution of historically inaccurate beards to various medieval tomb effigies and figures in stained glass in records made by English antiquaries of the late 16th and early 17th centuries. Working in an age in which beards were in fashion and widespread, the antiquaries seem to have subconsciously projected the fashion back into an era in which they were rare.[19]
The extensive science fiction subgenre depicting time travel in effect consists of deliberate, consciously created anachronisms, letting people of one time meet and interact with those of another time. Covers of time-travel books often depict deliberate anachronisms of this kind. For example, the cover of Harry Turtledove's The Guns of the South (1992) features a portrait of Confederate General Robert E. Lee holding an AK-47 rifle.
In historical writing, the most common type of anachronism is the adoption of the political, social or cultural concerns and assumptions of one era to interpret or evaluate the events and actions of another. The anachronistic application of present-day perspectives to comment on the historical past is sometimes described as presentism. Empiricist historians, working in the traditions established by Leopold von Ranke in the 19th century, regard this as a great error, and a trap to be avoided.[20] Arthur Marwick has argued that "a grasp of the fact that past societies are very different from our own, and ... very difficult to get to know" is an essential and fundamental skill of the professional historian; and that "anachronism is still one of the most obvious faults when the unqualified (those expert in other disciplines, perhaps) attempt to do history".[21] Anachronism in academic writing is considered at best embarrassing, as in early-20th-century scholarship's use of translatio imperii, first formulated in the 12th century, to interpret 10th-century literature.[citation needed]
The use of anachronism in a rhetorical or hyperbolic sense is more complex. To refer to the Holy Roman Empire as the First Reich, for example, is technically inaccurate but may be a useful comparative exercise; the application of theory to works which predate Marxist, Feminist or Freudian subjectivities is considered an essential part of theoretical practice. In most cases, however, the practitioner will acknowledge or justify the use or context.[citation needed]
An anachronism is something that is out of place in terms of time or chronology. The word derives from chronos, the Greek word for "time," and ana-, a Greek prefix meaning "up," "back," or "again." In its earliest English use, anachronism referred to an error in the dating of something (as, for example, in etymology, when a word or use is mistakenly assumed to have arisen earlier than it did). Anachronisms were sometimes distinguished from parachronisms, chronological errors in which dates are set later than is correct. But parachronism did not stand the test of time. It is now a very rare word.
Going to a Renaissance Faire is always a good time. Not only do you have the ability to drink mead and watch knights joust in real time, but you can pat yourself on the back for being able to walk through an anachronism.
The Drosophila anachronism (ana) locus controls the proliferation of neuroblasts, neuronal stem cells that give rise to the central nervous system. In ana mutants, quiescent postembryonic central brain and optic lobe neuroblasts enter S phase precociously. ana encodes a novel secreted protein of 474 amino acids that is expressed not in the affected neuroblasts, but rather in a subclass of neighboring glial cells. These studies argue for an important role for glia in negatively regulating proliferation of neuronal precursor cells, thereby controlling the timing of postembryonic neurogenesis.
This Leverhulme Trust-funded project, running from 2016 to 2019, is undertaking the first systematic study of the concept of anachronism in Greco-Roman antiquity and of the role played by the idea of anachronism in the formation of the concept of antiquity itself.
Gene name - anachronism Synonyms - medullaless Cytological map position - 45A-45B Function - regulation of proliferation Keywords - glia
FlyBase ID:FBgn0011746 Genetic map position - NA Classification - secreted glycoprotein Cellular location - extracellular NCBI link: Entrez Gene anachronism orthologs: BiolitmineBIOLOGICAL OVERVIEW Glial cells are the often overlooked wallflowers of the neural family. They are, however, just as important as neurons. Glia protect, nourish and respond to neurons in a very intimate way. Without glia, neurons could not be neurons. anachronism illustrates, on a biochemical level, just how important glial cells are to neural development.Anachronism is a secreted glial glycoprotein that inhibits premature neuroblast proliferation. trol (terribly reduced optic lobes) acts downstream of ana to activate proliferation of quiescent neuroblasts in an ana-dependent pathway, possibly by inactivating or bypassing the ana repressor. Thus trol and ana are components of a novel developmental pathway, from glial cells to neurons via the secreted protein ANA, for the control of cell cycle activation in quiescent neuroblasts (Datta, 1995). This points to the important role of glia in negatively regulating proliferation of neuronal precursor cells, thereby controlling the timing of postembryonic neurogenesis (Ebens, 1993).Examination of lacZ expression from an ana enhancer trap line as well as detection of the Ana protein show that ana is also expressed in the larval antennal-maxillary complex (AMC) at all larval stages. As has been reported for the central nervous system, ana expression in the AMC appears to be confined to glial cells. Larval olfactory system function in ana mutants was assayed in a behavioral paradigm. When tested with the three different chemoattractants, third instar ana9 mutant larvae showed diminished olfactory response compared to controls. Examination of a second ana allele revealed aberrant olfactory response to ethyl acetate, demonstrating that more than one mutation in ana can give rise to abnormal larval olfactory behavior. Assays of early first instar ana9 mutant larvae revealed defective olfactory behavior, implying that the olfactory phenotype stems from early larval AMC and/or embryonic origins. This is consistent with proliferation analysis in the early larval AMC region that uncovered a significantly higher number of S-phase cells in ana9 mutants (Park, 1997).A mutation at the ana locus was originally identifiedby an insertion of a lacZ-containing P element that caused morphologic defects in the structure of the adult optic lobes. This is a strong hypomorph and possibly anull mutation by genetic criteria, although it shows variable expressivity of the adult morphologic abnormalities.The ana1 P element insertion expresses ß-galactosidase in the CNS in a pattern similar tothat seen by staining with an anti-Ana antibody. The cause of the aberrant optic lobe structure in ana mutants is due to precocious proliferation and differentiation of the optic lobe neuroblastsearly in larval life. The initiation of proliferation of the centraland thoracic neuroblasts is also premature in ana mutants. Molecular and biochemical analysis has revealed that ana encodes a novel glycoprotein secreted by glial cells neighboring neuroblasts thatbegin divisions prematurely in an ana mutant. These results led to the suggestion that ana encodes an inhibitor of premature neuroblast proliferation which acts to maintain quiescence of the optic lobe, central brain, and thoracic neuroblasts until the appropriate developmental stage (Park, 1997).Additional alleles of ana have been generated by imprecise excision of the P-element insertion comprising the ana1 mutation (Ebens, 1993). Of these, both ana8 and ana9 are deletion alleles with phenotypes statistically indistinguishable from ana1, suggesting that they are minimally strong hypomorphic alleles and possibly null alleles. All three of these mutant alleles are homozygous viable and show no gross morphologic abnormalities. Homozygous mutant adults do not live long after eclosion under crowded conditions in competition with wild-type siblings. Previous studies of ana expression focused on the embryonic and larval CNS, where ana appears to be expressed in glial cells as early as stage 14 in embryogenesis and continuing throughout larval development. However, no phenotype in ana mutants has been described earlier than the first premature division of the optic lobe neuroblasts (onbs) at approximately 8-10 h post-hatch. To ask if ana is required for the development or function of other organs, the pattern of ana expression was examined to identify other systems within the developing fruitfly that may require ana function (Park, 1997).The initial analysis of ana expression in other partsof the larva was carried out by monitoring ß-galactosidase activity produced from the P-element insertion in the ana1 mutant allele. Larvae heterozygous for the ana1 P[lacZ] insertion were harvested atfirst, second, or third instar and crudely dissected to assay for ß-galactosidase activity. Staining was observed in the anterior larval tip at all three developmental stages. Fine dissections of the mouthhooks and anterior tip allowed more detailed examination of the ß-galactosidase staining pattern. In newly hatched first instar animals, ß-galactosidase staining was seen in virtually all the cells in the anterior lobe of the larvae. This ubiquitous staining resolved by 4 h after larval hatching into a bilaterally symmetric pattern of nuclei that remained consistent throughoutthe remainder of larval life. In this latter pattern the stained nuclei appear to form a cuplike structure around the antennal or dome organ and the maxillary organ in the anterior lobe. From each cuplike structure, a single strand of stained nuclei meanders posteriorly reaching approximatelyto the dorsal bridge and vertical plate of the mouth hooks. This staining pattern is highly reminiscent of the glial sheath that surrounds theantennal and maxillary organs, ganglia, and larval nerve (Park, 1997).The implied expression of ana in the anterior lobe was verified by staining with an anti-Ana monoclonal antibody. The ana1 mutation blocks secretion of the ana repressor, which then builds upin the cytoplasm of cells expressing ana. First instar larvae heterozygous for ana1 were dissected and stained for ß-galactosidase to mark the lacZ-expressing cells. The samples were then stained with the anti-Anaantibody to localize cells expressing ana. In all cases examined, the anti-Ana antibody staining appears to mark two nerve tracts adjacent to the curve of ß-galactosidase stained nuclei. To control for the possibility that the ana1 mutation had altered the pattern of ana expression in theanterior lobe, ana expression was also examined in wild-type animals at all three larval stages with the anti-Ana antibody. In all samples examined, the ana expression pattern in the anteriorlobe was similar to that seen in ana1mutant animals (Park, 1997).The ß-galactosidase staining pattern suggested thatana might be expressed in the glial sheath surroundingthe antennal and maxillary organs, antennaland maxillary ganglia, and larval antennal nerve. This possibility would be consistent with the pattern of expression previously described in the larval central nervous system (Ebens, 1993). To test this hypothesis, double labeling was done with ß-galactosidase and a cell type-specific marker. The enhancer trap lines 3-101 and 3-109 label distinct subsets of glial cells in the embryonic central nervous system. The pattern of lacZ expression for each enhancer trap line was analyzed in the anterior lobe of first, second, and third instar larvae. Line 3-101 showedno apparent lacZ expression in the anterior lobe atany stage of larval life. Line 3-109, however, expressed lacZ in a pattern very similarto that seen in ana1 mutant animals which carryan insertion of a lacZ-bearing P element at the analocus. This result suggests that the cells expressing ana in theanterior lobe are glial in nature. Because of the difficulty of obtaining reliableantibody penetration for double-labeling studies, further evidence of the glial identity of the ana expressingcells was obtained by analysis of the number of cells expressing lacZ in animals heterozygous for ana1 and 3-109. If ana1 and 3-109 result in ß-galactosidase expression in a similar but not overlappingset of cells, one would expect the double ana9 heterozygote to contain both sets of labeled cells (Park, 1997).This should result in a total number of labeled cells equivalent to the sum of the number of cells labeledin an ana1 heterozygote and a 3-109 animal. Alternatively,if ana1 and 3-109 label the same populationof cells, the double heterozygote should resultin the same number of labeled cells as ana1 or 3-109 animals. Cell counts of the number of labeledcells in ana1heterozygotes, 3-109 animals, andana1/+;+/3-109 transheterozygotes revealed thatapproximately the same number of cells were labeledin the transheterozygote as were by eitherana1or 3-109 alone (Park, 1997).The early onset of the larval olfactory phenotypecoupled with expression of ana in glial cells of larval AMC raised the question of whether ana also acts as a proliferation repressor in the AMC region. Therefore, 5-bromodeoxyuridine (BrdU) incorporationwas used to examine the relative numbers of S-phase cells in ana mutant and control AMCs early in first instar. A 2 h BrdU labeling of newlyhatched first instar larvae shows that ana9 mutantlarvae have a significantly higher number of BrdUstained cells in each side of the anterior lobe than do Oregon R or P[ana+];ana1 animals (Park, 1997).How might mutations in ana result in olfactory defects? In wild-type embryos the primordia of the AMC become visible in the epidermis by stage 13 of embryogenesis, and by early stage 14 the axons of theantennal organ have already grown along the larval antennal nerve into the subesophageal ganglion. Initial detection of ana expression in the embryonic CNSusing ß-galactosidase staining occurs at stages 14-16 (Ebens, 1993), after development of the larval antennal lobe and connectivity with the antennal organ. However, staining with the ana antibody has been observed in embryonic glial cells of CNS glial cells as early as stage 11. In addition, ana could be influencing early development through maternally supplied geneproducts although maternally supplied ana message or protein has not been described. Thus, it is possible that the larval olfactory phenotype may stem from an earlier embryonic CNS defect, or from abnormal development of the larval AMC during embryogenesis due to previously undetected expression of ana in the developing AMC. If ana is not required for the initial developmentof the larval olfactory system during embryogenesis, how might mutations in ana cause aberrant olfactory behavior? Lack of ana function in the larval CNS is known to result in premature proliferation of the central brain neuroblasts as early as first instar (Ebens, 1993). Mutations in ana result in supernumerary S-phase cells in the larval AMC area in newly hatched first instar and the organs they may contribute to are as yet unknown. It has been documented in vertebrate and mammaliansystems that the olfactory epithelium continues to add new neurons throughout much of the life of the system rather than only once during the initial development and assembly of the olfactory system. The same may hold true for the larval olfactory systemcentral nervous system in Drosophila. If this is true, and if ana function in glial cells of the AMC results in inhibition of neuroblastdivision as it does in the CNS, then mutations in ana may result in premature addition of cellsto the larval AMC and aberrant wiring of antennal ganglion or abnormal innervation of the larval antennal lobe. Interestingly enough, trials of ana9 and Oregon R adults with ethyl acetate at several concentrations in a T-maze choice paradigm revealed no significant olfactory phenotype (Park, 1997). Thus, ana is expressed by glial cells of the larval AMC and ana mutants show diminished olfactory sensitivity to several odorants. Evidence has been presented that the larval olfactory phenotype is probably not due to preture division of the larval CNS neuroblasts, but may be due to supernumerary S-phase cells in the earlyfirst instar AMC or lack of ana function in the embryo. Future studies will be aimed at determining whether the extra BrdU-labeled cells in the AMC areneuroblasts, and whether the progeny of those labeled cells are incorporated into the larval AMC. These investigations will enhance understanding of glial involvement in nervous system develment and function (Park, 1997).GENE STRUCTUREcDNA clone length - 2.4kbBases in 5' UTR - 230 Exons - fiveBases in 3' UTR - 764 PROTEIN STRUCTUREAmino Acids 474Structural DomainsThe protein has a high histidine concentration at the C-terminus. There are six potential N-linked glycosylation sites (Ebens, 1993). REGULATION Drosophila miR-124 regulates neuroblast proliferation through its target anachronismMicroRNAs (miRNAs) have been implicated as regulators of central nervous system (CNS) development and function. miR-124 is an evolutionarily ancient, CNS-specific miRNA. On the basis of the evolutionary conservation of its expression in the CNS, miR-124 is expected to have an ancient conserved function. Intriguingly, investigation of miR-124 function using antisense-mediated miRNA depletion has produced divergent and in some cases contradictory findings in a variety of model systems. This study investigated miR-124 function using a targeted knockout mutant and evidence is presented for a role during central brain neurogenesis in Drosophila. miR-124 activity in the larval neuroblast lineage is required to support normal levels of neuronal progenitor proliferation. anachronism (ana), which encodes a secreted inhibitor of neuroblast proliferation, was functionally identified as an important target of miR-124 acting in the neuroblast lineage. ana has previously been thought to be glial specific in its expression and to act from the cortex glia to control the exit of neuroblasts from quiescence into the proliferative phase that generates the neurons of the adult CNS during larval development. Evidence is provided that ana is expressed in miR-124-expressing neuroblast lineages and that ana activity must be limited by the action of miR-124 during neuronal progenitor proliferation. The possibility is discussed that the apparent divergence of function of miR-124 in different model systems might reflect functional divergence through target site evolution (Weng, 2012). 2ff7e9595c
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