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6 results for “nkx3.2”
OPT data from: A novel cis-regulatory element drives early expression of Nkx3.2 in the gnathostome primary jaw joint
<p><span>The acquisition of movable jaws was a major event during vertebrate evolution. The role of NK3 homeobox 2 (Nkx3.2) transcription factor in patterning the primary jaw joint of gnathostomes (jawed vertebrates) is well known, however, knowledge about its regulatory mechanism is lacking. In this study, we report a proximal enhancer element of <em>Nkx3.2</em> that is deeply conserved in most gnathostomes but undetectable in the jawless hagfish and lamprey. This enhancer is active in the developing jaw joint region of the zebrafish <em>Danio rerio</em>, and was thus designated as <em>jaw joint regulatory sequence 1</em> (JRS1). We further show that JRS1 enhancer sequences from a range of gnathostome species, including a chondrichthyan and mammals, have the same activity in the jaw joint as the native zebrafish enhancer, indicating a high degree of functional conservation despite the divergence of cartilaginous and bony fish lineages or the transition of the primary jaw joint into the middle ear of mammals. Finally, we show that deletion of JRS1 from the zebrafish genome using CRISPR/Cas9 results in a significant reduction of early gene expression of <em>Nkx3.2</em> and leads to transient jaw joint deformation and partial fusion. The emergence of this <em>Nkx3.2 </em>enhancer in early gnathostomes may have contributed to the origin and shaping of the articulating surfaces of vertebrate jaws.</span></p>
OPT data from: A novel cis-regulatory element drives early expression of Nkx3.2 in the gnathostome primary jaw joint
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nkx3.2 mutant zebrafish accommodate jaw joint loss through a phenocopy of the head shapes of Paleozoic jawless fish
The vertebrate jaw is a versatile feeding apparatus. To function, it requires a joint between the upper and lower jaws, so jaw joint defects are often highly disruptive and difficult to study. To describe the consequences of jaw-joint dysfunction, we engineered two independent null alleles of a single jaw-joint marker gene, <i>nkx3.2</i>, in zebrafish. These mutations caused zebrafish to become functionally jawless via fusion of the upper and lower jaw cartilages (ankylosis). Despite lacking jaw joints, <i>nkx3.2</i> mutants survived to adulthood and accommodated this defect by: a) remodeling their skulls; and b) altering their behavior from suction feeding to ram feeding. As a result, <i>nkx3.2</i> mutants developed skull shapes superficially similar to those observed in two lineages of ancient jawless vertebrates (anaspids and furcacaudiid thelodonts), including: a fixed open gape, reduced snout, and enlarged branchial region. However, no homology exists in individual skull elements between these taxa, and most of the modified elements in the mutant zebrafish occur outside known expression domains of <i>nkx3.2</i>. Therefore, we interpret the adult <i>nkx3.2</i> phenotype not as a reversal to an ancestral state, but as convergence due to similar functional requirements of feeding without moveable jaws. This remarkable convergence strongly suggests that jaw movements themselves dramatically influence the development of jawed vertebrate skulls. Thus, these mutants provide a unique model with which to: a) investigate adaptive responses to perturbation in skeletal development; b) re-evaluate evolutionarily inspired interpretations of phenocopies generated by gene knockdowns and knockouts; and c) gain insights into feeding mechanics of the extinct agnathans.
nkx3.2 mutant zebrafish accommodate jaw joint loss through a phenocopy of the head shapes of Paleozoic jawless fish
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Gene expression in pylorus stomach tissue in Bapx1 (Nkx3.2) deficient mice
GEO Series GSE13935. Mus musculus. 6 samples. Type: Expression profiling by array.
Single cell analysis of juvenile Nkx3.2 mutant zebrafish craniofacial skeleton
GEO Series GSE151354. Danio rerio. 2 samples. Type: Expression profiling by high throughput sequencing.
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