Abstract
The Ventx family is one of the subfamilies of the ANTP (antennapedia) superfamily and belongs to the NK-like (NKL) subclass. Ventx is a homeobox transcription factor and has a DNA-interacting domain that is evolutionarily conserved throughout vertebrates. It has been extensively studied in Xenopus, zebrafish, and humans. The Ventx family contains transcriptional repressors widely involved in embryonic development and tumorigenesis in vertebrates. Several studies have documented that the Ventx family inhibited dorsal mesodermal formation, neural induction, and head formation in Xenopus and zebrafish. Moreover, Ventx2.2 showed functional similarities to Nanog and Barx1, leading to pluripotency and neural-crest migration in vertebrates. Among them, Ventx protein is an orthologue of the Ventx family in humans. Studies have demonstrated that human Ventx was strongly associated with myeloid-cell differentiation and acute myeloid leukemia. The therapeutic potential of Ventx family inhibition in combating cancer progression in humans is discussed. Additionally, we briefly discuss genome evolution, gene duplication, pseudo-allotetraploidy, and the homeobox family in Xenopus.
Highlights
Xenopus laevis is an established animal model for studying vertebrate development, neurobiology, immunology, cell biology, and toxicology [1,2]
Ventx family genes are clustered at chromosome 7 in Xenopus, though it has been identified as non-clustered in zebrafish (Chr13 and Chr10)
In Xenopus, the ectopic expression of Ventx family members attenuated the expression of organizer-specific genes, including goosecoid, chordin, noggin, and foxd4l1.1b; and the same occurred for zic3 in Xenopus embryos at St.11 [13,30,33–35,45–47]
Summary
Xenopus laevis is an established animal model for studying vertebrate development, neurobiology, immunology, cell biology, and toxicology [1,2]. In Xenopus, the ectopic expression of Ventx family members attenuated the expression of organizer-specific genes, including goosecoid (gsc), chordin, noggin, and foxd4l1.1b (an early neural marker); and the same occurred for zic (a neuroectodermal marker) in Xenopus embryos at St.11 [13,30,33–35,45–47] This attenuation caused the inhibition of dorsal mesoderm formation and neuroectodermal induction. Wu et al (2011) revealed that Ventx directly transactivated the tumor suppression pathways in a p53–p21 and p16ink4a-Rb (a molecular link protein between cell senescence and tumor suppression)-dependent manner, leading to cellular senescence [54] These studies suggested that the Ventx family plays multifaceted roles in hematopoietic cell differentiation and AML progression, tumor suppression, and apoptotic-pathway activation. We discuss the pseudo-tetraploidy, genome evolution, and gene duplication in Xenopus, Xenopus’s classes of the homeobox superfamily, and functional similarities of Ventx2.2 to Nanog and Barx
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