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See detailComparative analysis of the genomic organization of Pax9 and its conserved physical association with Nkx2-9 in the human, mouse, and pufferfish genomes.
Santagati, F.; Gerber, J. K.; Blusch, J. H. et al

in Mammalian Genome : Official Journal of the International Mammalian Genome Society (2001), 12(3), 232-7

As a first step towards the identification of cis-regulatory elements of Pax9 by means of comparative genomics, we have analyzed genome regions encompassing the Pax9 gene in three vertebrate species ... [more ▼]

As a first step towards the identification of cis-regulatory elements of Pax9 by means of comparative genomics, we have analyzed genome regions encompassing the Pax9 gene in three vertebrate species, humans, mice (Mus musculus), and the Japanese pufferfish (Fugu rubripes). We show the genomic organization of Pax9 and its physical association with Nkx2-9 conserved in the three species. We discuss about possible implications of the conserved synteny between Pax9 and Nkx2-9 in a context of vertebrate evolution. This report also includes the first description of the primary structures of Fugu Pax9 and Nkx2-9. Furthermore, we report the identification of a novel upstream exon and putative transcription start sites in mouse Pax9. Our results suggest that transcription of Pax9 may be initiated at two alternative start sites and driven by TATA-less promoters. [less ▲]

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See detailPax1 and Pax9 synergistically regulate vertebral column development.
Peters, H.; Wilm, B.; Sakai, N. et al

in Development (1999), 126(23), 5399-408

The paralogous genes Pax1 and Pax9 constitute one group within the vertebrate Pax gene family. They encode closely related transcription factors and are expressed in similar patterns during mouse ... [more ▼]

The paralogous genes Pax1 and Pax9 constitute one group within the vertebrate Pax gene family. They encode closely related transcription factors and are expressed in similar patterns during mouse embryogenesis, suggesting that Pax1 and Pax9 act in similar developmental pathways. We have recently shown that mice homozygous for a defined Pax1 null allele exhibit morphological abnormalities of the axial skeleton, which is not affected in homozygous Pax9 mutants. To investigate a potential interaction of the two genes, we analysed Pax1/Pax9 double mutant mice. These mutants completely lack the medial derivatives of the sclerotomes, the vertebral bodies, intervertebral discs and the proximal parts of the ribs. This phenotype is much more severe than that of Pax1 single homozygous mutants. In contrast, the neural arches, which are derived from the lateral regions of the sclerotomes, are formed. The analysis of Pax9 expression in compound mutants indicates that both spatial expansion and upregulation of Pax9 expression account for its compensatory function during sclerotome development in the absence of Pax1. In Pax1/Pax9 double homozygous mutants, formation and anteroposterior polarity of sclerotomes, as well as induction of a chondrocyte-specific cell lineage, appear normal. However, instead of a segmental arrangement of vertebrae and intervertebral disc anlagen, a loose mesenchyme surrounding the notochord is formed. The gradual loss of Sox9 and Collagen II expression in this mesenchyme indicates that the sclerotomes are prevented from undergoing chondrogenesis. The first detectable defect is a low rate of cell proliferation in the ventromedial regions of the sclerotomes after sclerotome formation but before mesenchymal condensation normally occurs. At later stages, an increased number of cells undergoing apoptosis further reduces the area normally forming vertebrae and intervertebral discs. Our results reveal functional redundancy between Pax1 and Pax9 during vertebral column development and identify an early role of Pax1 and Pax9 in the control of cell proliferation during early sclerotome development. In addition, our data indicate that the development of medial and lateral elements of vertebrae is regulated by distinct genetic pathways. [less ▲]

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See detailTeeth. Where and how to make them.
Peters, H.; Balling, Rudi UL

in Trends in Genetics (1999), 15(2), 59-65

Organs have to develop at precisely determined sites to ensure functionality of the whole organism. Organogenesis is typically regulated by a series of interactions between morphologically distinct ... [more ▼]

Organs have to develop at precisely determined sites to ensure functionality of the whole organism. Organogenesis is typically regulated by a series of interactions between morphologically distinct tissues. The developing tooth of the mouse is an excellent model to study these processes and we are beginning to understand the networks regulating reciprocal tissue interactions at the molecular level. Synergistic and antagonistic effects of signaling molecules including FGFs and BMPs are recursively used to induce localized responses in the adjacent tissue layer (mesenchyme or epithelium). However, at different phases of odontogenesis these secreted growth factors have distinct effects and at the same time they are regulated by different upstream factors. The mesenchymal transcription factors Msx1 and Pax9 are initially regulated by epithelial FGFs and BMPs, but subsequently they function upstream of these signaling molecules. This cascade provides a molecular model by which reciprocal tissue interactions are controlled. [less ▲]

Detailed reference viewed: 99 (0 UL)
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See detailTargeted disruption of Pax1 defines its null phenotype and proves haploinsufficiency.
Wilm, B.; Dahl, E.; Peters, H. et al

in Proceedings of the National Academy of Sciences of the United States of America (1998), 95(15), 8692-7

The murine paired box-containing gene Pax1 is required for normal development of the vertebral column, the sternum, and the scapula. Previous studies have shown that three natural Pax1 mouse mutants, the ... [more ▼]

The murine paired box-containing gene Pax1 is required for normal development of the vertebral column, the sternum, and the scapula. Previous studies have shown that three natural Pax1 mouse mutants, the undulated alleles, exhibit phenotypes of different severity in these skeletal elements. Nevertheless, these analyses have not clarified whether the semidominant Undulated short-tail (Uns) mutation, in which the complete Pax1 locus is deleted, represents a null allele. Moreover, the analyses of the classical undulated mutants did not allow a conclusion with respect to haploinsufficiency of Pax1. To address both questions we have created a Pax1 null allele in mice by gene targeting. Surprisingly, the phenotype of this defined mutation exhibits clear differences to that of Uns. This result strongly indicates the contribution of additional gene(s) to the Uns mutant phenotype. Furthermore, the phenotype of mice heterozygous for the null allele demonstrates that Pax1 is haploinsufficient in some though not all skeletal elements which express Pax1 during embryonic development. [less ▲]

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See detailPax genes and organogenesis: Pax9 meets tooth development.
Peters, H.; Neubuser, A.; Balling, Rudi UL

in European Journal of Oral Sciences (1998), 106 Suppl 1

Pax genes encode a family of transcription factors that play key roles during embryogenesis. They are required for the development of a variety of organs including the nervous and muscular system ... [more ▼]

Pax genes encode a family of transcription factors that play key roles during embryogenesis. They are required for the development of a variety of organs including the nervous and muscular system, skeleton, eye, ear, kidney, thymus, and pancreas. Whereas the developmental roles of many of the nine known Pax genes have been analyzed in great detail, a functional analysis of Pax9 has just begun. During mouse embryogenesis, Pax9 exhibits a highly specific expression pattern in derivatives of the foregut endoderm, somites, limb mesenchyme, midbrain, and the cephalic neural crest. In the mandibular arch mesenchyme, the expression of Pax9 marks the prospective sites of tooth development prior to any morphological signs of odontogenesis and is maintained in the developing tooth mesenchyme thereafter. To understand the function of Pax9 during mouse embryogenesis, we recently have created a null allele by gene targeting. Preliminary analyses show that Pax9 is essential for the formation of teeth, and we conclude that Pax9 is required for tooth development to proceed beyond the bud stage. Here, we briefly summarize our current knowledge about Pax genes and introduce Pax9 to the growing family of factors which are involved in tooth development. [less ▲]

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See detailPax9-deficient mice lack pharyngeal pouch derivatives and teeth and exhibit craniofacial and limb abnormalities.
Peters, H.; Neubuser, A.; Kratochwil, K. et al

in Genes & Development (1998), 12(17), 2735-47

Pax genes have been shown to play important roles in mammalian development and organogenesis. Pax9, a member of this transcription factor family, is expressed in somites, pharyngeal pouches, mesenchyme ... [more ▼]

Pax genes have been shown to play important roles in mammalian development and organogenesis. Pax9, a member of this transcription factor family, is expressed in somites, pharyngeal pouches, mesenchyme involved in craniofacial, tooth, and limb development, as well as other sites during mouse embryogenesis. To analyze its function in vivo, we generated Pax9 deficient mice and show that Pax9 is essential for the development of a variety of organs and skeletal elements. Homozygous Pax9-mutant mice die shortly after birth, most likely as a consequence of a cleft secondary palate. They lack a thymus, parathyroid glands, and ultimobranchial bodies, organs which are derived from the pharyngeal pouches. In all limbs, a supernumerary preaxial digit is formed, but the flexor of the hindlimb toes is missing. Furthermore, craniofacial and visceral skeletogenesis is disturbed, and all teeth are absent. In Pax9-deficient embryos tooth development is arrested at the bud stage. At this stage, Pax9 is required for the mesenchymal expression of Bmp4, Msx1, and Lef1, suggesting a role for Pax9 in the establishment of the inductive capacity of the tooth mesenchyme. In summary, our analysis shows that Pax9 is a key regulator during the development of a wide range of organ primordia. [less ▲]

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See detailAntagonistic interactions between FGF and BMP signaling pathways: a mechanism for positioning the sites of tooth formation.
Neubuser, A.; Peters, H.; Balling, Rudi UL et al

in Cell (1997), 90(2), 247-55

Vertebrate organogenesis is initiated at sites that are often morphologically indistinguishable from the surrounding region. Here we have identified Pax9 as a marker for prospective tooth mesenchyme prior ... [more ▼]

Vertebrate organogenesis is initiated at sites that are often morphologically indistinguishable from the surrounding region. Here we have identified Pax9 as a marker for prospective tooth mesenchyme prior to the first morphological manifestation of odontogenesis. We provide evidence that the sites of Pax9 expression in the mandibular arch are positioned by the combined activity of two signals, one (FGF8) that induces Pax9 expression and the other (BMP2 and BMP4) that prevents this induction. Thus it appears that the position of the teeth is determined by a combination of two different types of signaling molecules produced in wide but overlapping domains rather than by a single localized inducer. We suggest that a similar mechanism may be used for specifying the sites of development of other organs. [less ▲]

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See detailThe Genetics of Vertebral Column Development
Peters, H; Neubüser, A; Wallin, J et al

in Thiel; Klug (Eds.) Methods in Developmental Toxicology (1997)

Detailed reference viewed: 33 (0 UL)
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See detailIsolation of the Pax9 cDNA from adult human esophagus.
Peters, H.; Schuster, G.; Neubuser, A. et al

in Mammalian Genome : Official Journal of the International Mammalian Genome Society (1997), 8(1), 62-4

Detailed reference viewed: 86 (0 UL)