Newborn babies born with tails:
Primarily due to intense medical interest, humans are one of the best characterized species and many developmental anomalies are known. There are several human atavisms that reflect our common genetic heritage with other mammals. One of the most striking is the existence of the rare "true human tail" (also variously known as "coccygeal process", "coccygeal projection", "caudal appendage", and "vestigial tail"). More than 100 cases of human tails have been reported in the medical literature. Less than one third of the well-documented cases are what are medically known as "pseudo-tails" (Dao and Netsky 1984; Dubrow et al. 1988). Pseudo-tails are not true tails; they are simply lesions of various types coincidentally found in the caudal region of newborns, often associated with the spinal column, coccyx, and various malformations.
In contrast, 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). As discussed below in detail, the development of the normal human tail in the early embryo has been investigated extensively, and apoptosis (programmed cell death) plays a significant role in removing the tail of a human embryo after it has formed. 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.