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Runx3 controls the axonal projection of proprioceptive dorsal root ganglion neurons

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TLDR
It is reported that Runx3-deficient (Runx3−/−) mice displayed severe motor discoordination and that few DRG neurons synthesized the proprioceptive neuronal marker parvalbumin and the data demonstrate that Run x3 is critical in regulating the axonal projections of a specific subpopulation of DRG neuron.
Abstract
Dorsal root ganglion (DRG) neurons specifically project axons to central and peripheral targets according to their sensory modality. The Runt-related genes Runx1 and Runx3 are expressed in DRG neuronal subpopulations, suggesting that they may regulate the trajectories of specific axons. Here we report that Runx3-deficient (Runx3(-/-)) mice displayed severe motor uncoordination and that few DRG neurons synthesized the proprioceptive neuronal marker parvalbumin. Proprioceptive afferent axons failed to project to their targets in the spinal cord as well as those in the muscle. NT-3-responsive Runx3(-/-) DRG neurons showed less neurite outgrowth in vitro. However, we found no changes in the fate specification of Runx3(-/-) DRG neurons or in the number of DRG neurons that expressed trkC. Our data demonstrate that Runx3 is critical in regulating the axonal projections of a specific subpopulation of DRG neurons.

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Journal ArticleDOI

Differential Requirements for Runx Proteins in CD4 Repression and Epigenetic Silencing during T Lymphocyte Development

TL;DR: It is shown here that binding sites for Runt domain transcription factors are essential for CD4 silencer function at both stages, and that different Runx family members are required to fulfill unique functions at each stage.
Journal ArticleDOI

Runx2 and Runx3 are essential for chondrocyte maturation, and Runx2 regulates limb growth through induction of Indian hedgehog

TL;DR: Investigation of the involvement of Runx3 in chondrocyte differentiation by generating Runx2-and-Runx3-deficient (Runx2(-/-)3(-/-)) mice found that chondrospermia differentiation was inhibited depending on the dosages of Run x2 and Runx4, and Run x3- deficient mice showed a complete absence of chond rocyte maturation.
Journal ArticleDOI

The runx genes: gain or loss of function in cancer

TL;DR: The RUNX genes have come to prominence recently because of their roles as essential regulators of cell fate in development and their paradoxical effects in cancer, in which they can function either as tumour-suppressor genes or dominant oncogenes according to context.
Journal ArticleDOI

TGF-β/BMP signaling and other molecular events: regulation of osteoblastogenesis and bone formation

TL;DR: Accumulating evidence indicates that Runx2 is the key integrator, whereas Hh is a possible modulator, miRNAs are regulators, and β-catenin is a mediator/regulator within the extensive intracellular network.
Journal ArticleDOI

Role and regulation of RUNX2 in osteogenesis.

TL;DR: The regulation of RUNX2 by factors commonly used during osteogenic studies will be discussed and the complexity of its regulation and its interactions within the osteoblast differentiation pathway are often overlooked.
References
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Journal ArticleDOI

Calbindin D-28k and parvalbumin in the rat nervous system

TL;DR: The distribution of structures stained with mono- and polyclonal antibodies to the calcium-binding proteins calbindin D-28k and parvalbumin in the nervous system of adult rats is described and it can be stated that cal bindin antibodies mainly label cells with thin, unmyelinated axons projecting in a diffuse manner.
Journal ArticleDOI

Functions of the neurotrophins during nervous system development: What the knockouts are teaching us

TL;DR: It is now apparent that regulation of neuronal function by the recently identified members of the neurotrophin family is far more complex than envisioned on the basis of work with NGF, particularly for neurons in the central nervous system (CNS).
Journal ArticleDOI

Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia

TL;DR: Transgenic mice are generated in which neurons overexpress the human BCL-2 protein under the control of the neuron-specific enolase (NSE) or phosphoglycerate kinase (PGK) promoters to gain insight into the possible role of bcl-2 during NOCD in vivo.
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