Skwim
Veteran Member
Background
Anatomical atavisms are closely related conceptually to vestigial structures. An atavism is the reappearance of a lost character specific to a remote evolutionary ancestor and not observed in the parents or recent ancestors of the organism displaying the atavistic character. Atavisms have several essential features: (1) presence in adult stages of life, (2) absence in parents or recent ancestors, and (3) extreme rarity in a population (Hall 1984). For developmental reasons, the occasional occurrence of atavisms is expected under common descent if structures or functions are gradually lost between ancestor and descendant lineages (Hall 1984; Hall 1995). Here we are primarily concerned with potential atavistic structures that are characteristic of taxa to which the organism displaying the structure does not belong. As a hypothetical example, if mutant horses occasionally displayed gills, this would be considered a potential atavism, since gills are diagnostic of taxa (e.g. fish) to which horses do not belong. As with vestigial structures, no organism can have an atavistic structure that was not previously found in one of its ancestors. Thus, for each species, the standard phylogenetic tree makes a huge number of predictions about atavisms that are allowed and those that are impossible for any given species.
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The Science
Humans are classified by taxonomists as apes; one of the defining derived characters of apes is the lack of an external tail. However, human embryos initially develop tails in development. At between four and five weeks of age, the normal human embryo has 10-12 developing tail vertebrae which extend beyond the anus and legs, accounting for more than 10% of the length of the embryo (Fallon and Simandl 1978; Moore and Persaud 1998, pp. 91-100; Nievelstein et al. 1993). The embryonic tail is composed of several complex tissues besides the developing vertebrae, including a secondary neural tube (spinal cord), a notochord, mesenchyme, and tail gut. By the eighth week of gestation, the sixth to twelfth vertebrae have disappeared via cell death, and the fifth and fourth tail vertebrae are still being reduced. Likewise, the associated tail tissues also undergo cell death and regress.
Using light and scanning electron microscopy, several detailed analyses of the embryonic human tail have shown that the dead and degenerating tail cells are ingested and digested by macrophages (macrophages are large white blood cells of the immune system which more normally ingest and destroy invading pathogens such as bacteria) (Fallon and Simandl 1978; Nievelstein et al. 1993; Sapunar et al. 2001; Saraga-Babic et al. 1994; Saraga-Babic et al. 2002). In adult humans, the tail is finally reduced to a small bone composed of just four fused vertebrae (the coccyx) which do not protrude from the back (Fallon and Simandl 1978; Sapunar et al. 2001) (see Figure 2.4.1).
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The true atavistic tail of humans results from incomplete regression of the most distal end of the normal embryonic tail found in the developing human fetus (see Figure 2.4.1 and the discussion below on the development of the normal human embryonic tail; Belzberg et al. 1991; Dao and Netsky 1984; Grange et al. 2001; Keith 1921). Though formally a malformation, the true human tail is usually benign in nature (Dubrow et al. 1988; Spiegelmann et al. 1985). The true human tail is characterized by a complex arrangement of adipose and connective tissue, central bundles of longitudinally arranged striated muscle in the core, blood vessels, nerve fibres, nerve ganglion cells, and specialized pressure sensing nerve organs (Vater-Pacini corpuscles). It is covered by normal skin, replete with hair follicles, sweat glands, and sebaceous glands (Dao and Netsky 1984; Dubrow et al. 1988; Spiegelmann et al. 1985). True human tails range in length from about one inch to over 5 inches long (on a newborn baby), and they can move via voluntary striped muscle contractions in response to various emotional states (Baruchin et al. 1983; Dao and Netsky 1984; Harrison 1901; Keith 1921; Lundberg et al. 1962).
Although human tails usually lack skeletal structures (some medical articles have claimed that true tails never have vertebrae), several human tails have also been found with cartilage and up to five, well-developed, articulating vertebrae (see Figure 2.2.3; Bar-Maor et al. 1980; Dao and Netsky 1984; Fara 1977; Sugumata et al. 1988). However, caudal vertebrae are not a necessary component of mammalian tails. Contrary to what is frequently reported in the medical literature, there is at least one known example of a primate tail that lacks vertebrae, as found in the rudimentary two-inch-long tail of Macaca sylvanus (the "Barbary ape") (Hill 1974, p. 616; Hooten 1947, p. 23).
True human tails are rarely inherited, though several familial cases are known (Dao and Netsky 1984; Ikpeze and Onuigbo 1999; Touraine 1955). In one case the tail has been inherited through at least three generations of females (Standfast 1992).
As with other atavistic structures, human tails are most likely the result of either a somatic mutation, a germline mutation, or an environmental influence that reactivates an underlying developmental pathway which has been retained, if only partially, in the human genome (Dao and Netsky 1984; Hall 1984; Hall 1995). In fact, the genes that control the development of tails in mice and other vertebrates have been identified (the Wnt-3a and Cdx1 genes; Greco et al. 1996; Prinos et al. 2001; Schubert et al. 2001; Shum et al. 1999; Takada et al. 1994). As predicted by common descent from the atavistic evidence, these tail genes have also been discovered in the human genome (Katoh 2002; Roelink et al. 1993).
It is now known that down-regulation of the Wnt-3a gene induces apoptosis of tail cells during mouse development (Greco et al. 1996; Shum et al. 1999; Takada et al. 1994), and similar effects are observed in humans (Chan et al. 2002). Additionally, researchers have identified a mutant mouse that does not develop a tail, and this phenotype is due to a regulatory mutation that decreases the Wnt-3a gene dosage (Greco et al. 1996; Gruneberg and Wickramaratne 1974; Heston 1951). Thus, current evidence indicates that the genetic cause of tail loss in the evolution of apes was likely a simple regulatory mutation(s) that slightly decreased Wnt-3a gene dosage. Conversely, a mutation or environmental factor that increased dosage of the Wnt-3a gene would reduce apoptosis of the human tail during development and would result in its retention, as an atavism, in a newborn.
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Criticisms:
The existence of true human tails is unfortunately quite shocking for many religiously motivated anti-evolutionists, such as Duane Gish, who has written an often-quoted article entitled "Evolution and the human tail" (Gish 1983; see also Menton 1994; ReMine 1982). Solely based on the particulars of a single case study (Ledley 1982), these authors have erroneously concluded that atavistic human tails are "nothing more than anomalous malformations not traceable to any imaginary ancestral state" (Gish 1983). However, their arguments are clearly directed against pseudo-tails, not true tails. Gish claims these structures are not true tails for several reasons: (1) they lack vertebrae, (2) they are not inherited, and (3) the resemblance to tails is "highly superficial" and simply an "anomalous malformation". Menton further claims that (4) all true tails have muscles and can move, whereas human tails cannot. Each of these arguments are factually false, as explained above and as well-documented in the medical literature. Vertebrae and cartilage have occasionally been found in human tails. However, contrary to the claims of Gish, Menton, and ReMine, vertebrae are not a requirement for tails. M. sylvanus is a prime example of a primate whose fleshy tail lacks vertebrae (Hill 1974, p. 616; Hooten 1947, p. 23). Several cases are known where human tails have been inherited. Furthermore, we now know the genes responsible for the development of tails in mammals, and all humans have them. Inheritance of the tail structure per se is unnecessary since the developmental system has been inherited but is normally inactivated in humans. The "resemblance" to non-human tails is far from superficial, since all true human tails are complex structures composed of symmetrical layers of voluntary muscle, blood vessels, specialized nerves and sensing organs, and they can indeed move and contract.
source
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Anatomical atavisms are closely related conceptually to vestigial structures. An atavism is the reappearance of a lost character specific to a remote evolutionary ancestor and not observed in the parents or recent ancestors of the organism displaying the atavistic character. Atavisms have several essential features: (1) presence in adult stages of life, (2) absence in parents or recent ancestors, and (3) extreme rarity in a population (Hall 1984). For developmental reasons, the occasional occurrence of atavisms is expected under common descent if structures or functions are gradually lost between ancestor and descendant lineages (Hall 1984; Hall 1995). Here we are primarily concerned with potential atavistic structures that are characteristic of taxa to which the organism displaying the structure does not belong. As a hypothetical example, if mutant horses occasionally displayed gills, this would be considered a potential atavism, since gills are diagnostic of taxa (e.g. fish) to which horses do not belong. As with vestigial structures, no organism can have an atavistic structure that was not previously found in one of its ancestors. Thus, for each species, the standard phylogenetic tree makes a huge number of predictions about atavisms that are allowed and those that are impossible for any given species.
__________________________________
The Science
Humans are classified by taxonomists as apes; one of the defining derived characters of apes is the lack of an external tail. However, human embryos initially develop tails in development. At between four and five weeks of age, the normal human embryo has 10-12 developing tail vertebrae which extend beyond the anus and legs, accounting for more than 10% of the length of the embryo (Fallon and Simandl 1978; Moore and Persaud 1998, pp. 91-100; Nievelstein et al. 1993). The embryonic tail is composed of several complex tissues besides the developing vertebrae, including a secondary neural tube (spinal cord), a notochord, mesenchyme, and tail gut. By the eighth week of gestation, the sixth to twelfth vertebrae have disappeared via cell death, and the fifth and fourth tail vertebrae are still being reduced. Likewise, the associated tail tissues also undergo cell death and regress.
Using light and scanning electron microscopy, several detailed analyses of the embryonic human tail have shown that the dead and degenerating tail cells are ingested and digested by macrophages (macrophages are large white blood cells of the immune system which more normally ingest and destroy invading pathogens such as bacteria) (Fallon and Simandl 1978; Nievelstein et al. 1993; Sapunar et al. 2001; Saraga-Babic et al. 1994; Saraga-Babic et al. 2002). In adult humans, the tail is finally reduced to a small bone composed of just four fused vertebrae (the coccyx) which do not protrude from the back (Fallon and Simandl 1978; Sapunar et al. 2001) (see Figure 2.4.1).
______________________________________
The true atavistic tail of humans results from incomplete regression of the most distal end of the normal embryonic tail found in the developing human fetus (see Figure 2.4.1 and the discussion below on the development of the normal human embryonic tail; Belzberg et al. 1991; Dao and Netsky 1984; Grange et al. 2001; Keith 1921). Though formally a malformation, the true human tail is usually benign in nature (Dubrow et al. 1988; Spiegelmann et al. 1985). The true human tail is characterized by a complex arrangement of adipose and connective tissue, central bundles of longitudinally arranged striated muscle in the core, blood vessels, nerve fibres, nerve ganglion cells, and specialized pressure sensing nerve organs (Vater-Pacini corpuscles). It is covered by normal skin, replete with hair follicles, sweat glands, and sebaceous glands (Dao and Netsky 1984; Dubrow et al. 1988; Spiegelmann et al. 1985). True human tails range in length from about one inch to over 5 inches long (on a newborn baby), and they can move via voluntary striped muscle contractions in response to various emotional states (Baruchin et al. 1983; Dao and Netsky 1984; Harrison 1901; Keith 1921; Lundberg et al. 1962).
Although human tails usually lack skeletal structures (some medical articles have claimed that true tails never have vertebrae), several human tails have also been found with cartilage and up to five, well-developed, articulating vertebrae (see Figure 2.2.3; Bar-Maor et al. 1980; Dao and Netsky 1984; Fara 1977; Sugumata et al. 1988). However, caudal vertebrae are not a necessary component of mammalian tails. Contrary to what is frequently reported in the medical literature, there is at least one known example of a primate tail that lacks vertebrae, as found in the rudimentary two-inch-long tail of Macaca sylvanus (the "Barbary ape") (Hill 1974, p. 616; Hooten 1947, p. 23).
True human tails are rarely inherited, though several familial cases are known (Dao and Netsky 1984; Ikpeze and Onuigbo 1999; Touraine 1955). In one case the tail has been inherited through at least three generations of females (Standfast 1992).
As with other atavistic structures, human tails are most likely the result of either a somatic mutation, a germline mutation, or an environmental influence that reactivates an underlying developmental pathway which has been retained, if only partially, in the human genome (Dao and Netsky 1984; Hall 1984; Hall 1995). In fact, the genes that control the development of tails in mice and other vertebrates have been identified (the Wnt-3a and Cdx1 genes; Greco et al. 1996; Prinos et al. 2001; Schubert et al. 2001; Shum et al. 1999; Takada et al. 1994). As predicted by common descent from the atavistic evidence, these tail genes have also been discovered in the human genome (Katoh 2002; Roelink et al. 1993).
It is now known that down-regulation of the Wnt-3a gene induces apoptosis of tail cells during mouse development (Greco et al. 1996; Shum et al. 1999; Takada et al. 1994), and similar effects are observed in humans (Chan et al. 2002). Additionally, researchers have identified a mutant mouse that does not develop a tail, and this phenotype is due to a regulatory mutation that decreases the Wnt-3a gene dosage (Greco et al. 1996; Gruneberg and Wickramaratne 1974; Heston 1951). Thus, current evidence indicates that the genetic cause of tail loss in the evolution of apes was likely a simple regulatory mutation(s) that slightly decreased Wnt-3a gene dosage. Conversely, a mutation or environmental factor that increased dosage of the Wnt-3a gene would reduce apoptosis of the human tail during development and would result in its retention, as an atavism, in a newborn.
_____________________
Criticisms:
The existence of true human tails is unfortunately quite shocking for many religiously motivated anti-evolutionists, such as Duane Gish, who has written an often-quoted article entitled "Evolution and the human tail" (Gish 1983; see also Menton 1994; ReMine 1982). Solely based on the particulars of a single case study (Ledley 1982), these authors have erroneously concluded that atavistic human tails are "nothing more than anomalous malformations not traceable to any imaginary ancestral state" (Gish 1983). However, their arguments are clearly directed against pseudo-tails, not true tails. Gish claims these structures are not true tails for several reasons: (1) they lack vertebrae, (2) they are not inherited, and (3) the resemblance to tails is "highly superficial" and simply an "anomalous malformation". Menton further claims that (4) all true tails have muscles and can move, whereas human tails cannot. Each of these arguments are factually false, as explained above and as well-documented in the medical literature. Vertebrae and cartilage have occasionally been found in human tails. However, contrary to the claims of Gish, Menton, and ReMine, vertebrae are not a requirement for tails. M. sylvanus is a prime example of a primate whose fleshy tail lacks vertebrae (Hill 1974, p. 616; Hooten 1947, p. 23). Several cases are known where human tails have been inherited. Furthermore, we now know the genes responsible for the development of tails in mammals, and all humans have them. Inheritance of the tail structure per se is unnecessary since the developmental system has been inherited but is normally inactivated in humans. The "resemblance" to non-human tails is far from superficial, since all true human tails are complex structures composed of symmetrical layers of voluntary muscle, blood vessels, specialized nerves and sensing organs, and they can indeed move and contract.
source
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