The vertebrate tail: a gene playground for evolution

Abstract

The tail of all vertebrates, regardless of size and anatomical detail, derive from a post-anal extension of the embryo known as the tail bud. Formation, growth and differentiation of this structure are closely associated with the activity of a group of cells that derive from the axial progenitors that build the spinal cord and the muscle-skeletal case of the trunk. Gdf11 activity switches the development of these progenitors from a trunk to a tail bud mode by changing the regulatory network that controls their growth and differentiation potential. Recent work in the mouse indicates that the tail bud regulatory network relies on the interconnected activities of the Lin28/let-7 axis and the Hox13 genes. As this network is likely to be conserved in other mammals, it is possible that the final length and anatomical composition of the adult tail result from the balance between the progenitor-promoting and -repressing activities provided by those genes. This balance might also determine the functional characteristics of the adult tail. Particularly relevant is its regeneration potential, intimately linked to the spinal cord. In mammals, known for their complete inability to regenerate the tail, the spinal cord is removed from the embryonic tail at late stages of development through a Hox13-dependent mechanism. In contrast, the tail of salamanders and lizards keep a functional spinal cord that actively guides the tail's regeneration process. I will argue that the distinct molecular networks controlling tail bud development provided a collection of readily accessible gene networks that were co-opted and combined during evolution either to end the active life of those progenitors or to make them generate the wide diversity of tail shapes and sizes observed among vertebrates.

Sox2 and Canonical Wnt Signaling Interact to Activate a Developmental Checkpoint Coordinating Morphogenesis with Mesoderm Fate Acquisition

“…Here, we show that lowering the level of Wnt signaling can recapitulate the mouse Tbx6 ectopic spinal cord phenotype in zebrafish tbx16 mutants. One implication of this result is that the relative amount of Wnt signaling is higher in the zebrafish tailbud compared to the mouse, which may help explain the species-specific differences between NMP development (Martin and Kimelman, 2009;Steventon et al, 2016;Attardi et al, 2018;Mallo, 2020), including the phenotypic differences of the Tbx6 mouse mutant and the tbx16 single or tbx16/tbx6l and tbx16/msgn1 double zebrafish mutants (Chapman and Papaioannou, 1998;Fior et al, 2012;Yabe and Takada, 2012;Morrow et al, 2017).…”

Bioinformatics analysis of the expression of HOXC13 and its role in the prognosis of breast cancer

“…Each HOX gene contains a well-conserved DNA sequence, known as the homeobox (10). The unique expression pattern, including mutation, and dependent mechanism of the HOX genes regulates, to some extent, the embryonic development of vertebrates (11,12). When HOX protein expression is upregulated, it may lead to cancer (5).…”

Vertebral Formulae and Congenital Vertebral Anomalies in Guinea Pigs: A Retrospective Radiographic Study

“…This incomplete ossification of sacral bone can determine a different number of sacral vertebrae in the previously published text [11]. The number of Cd vertebrae varied in previously published literature from Cd 4 to Cd 7 compared to Cd 5-Cd 7 in our study, a variable number of Cd vertebra is common and is considered clinically irrelevant [10,12,32].…”