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Lack of the central nervous system- and neural crest-expressed forkhead gene Foxs1 affects motor function and body weight.

ABSTRACT: To gain insight into the expression pattern and functional importance of the forkhead transcription factor Foxs1, we constructed a Foxs1-beta-galactosidase reporter gene "knock-in" (Foxs1beta-gal/beta-gal) mouse, in which the wild-type (wt) Foxs1 allele has been inactivated and replaced by a beta-galactosidase reporter gene. Staining for beta-galactosidase activity reveals an expression pattern encompassing neural crest-derived cells, e.g., cranial and dorsal root ganglia as well as several other cell populations in the central nervous system (CNS), most prominently the internal granule layer of cerebellum. Other sites of expression include the lachrymal gland, outer nuclear layer of retina, enteric ganglion neurons, and a subset of thalamic and hypothalamic nuclei. In the CNS, blood vessel-associated smooth muscle cells and pericytes stain positive for Foxs1. Foxs1beta-gal/beta-gal mice perform significantly better (P < 0.01) on a rotating rod than do wt littermates. We have also noted a lower body weight gain (P < 0.05) in Foxs1beta-gal/lbeta-gal males on a high-fat diet, and we speculate that dorsomedial hypothalamic neurons, expressing Foxs1, could play a role in regulating body weight via regulation of sympathetic outflow. In support of this, we observed increased levels of uncoupling protein 1 mRNA in Foxs1beta-gal/beta-gal mice. This points toward a role for Foxs1 in the integration and processing of neuronal signals of importance for energy turnover and motor function.

SUBMITTER: Heglind M

PROVIDER: S-EPMC1157007 | biostudies-literature | 2005 Jul

REPOSITORIES: biostudies-literature

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Lack of the central nervous system- and neural crest-expressed forkhead gene Foxs1 affects motor function and body weight.

Heglind Mikael M Cederberg Anna A Aquino Jorge J Lucas Guilherme G Ernfors Patrik P Enerbäck Sven S

Molecular and cellular biology 20050701 13

To gain insight into the expression pattern and functional importance of the forkhead transcription factor Foxs1, we constructed a Foxs1-beta-galactosidase reporter gene "knock-in" (Foxs1beta-gal/beta-gal) mouse, in which the wild-type (wt) Foxs1 allele has been inactivated and replaced by a beta-galactosidase reporter gene. Staining for beta-galactosidase activity reveals an expression pattern encompassing neural crest-derived cells, e.g., cranial and dorsal root ganglia as well as several othe ...[more]

PMID: 15964817

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Project description:Acute central nervous system injuries are among the most common causes of disability worldwide, with widespread social and economic implications. Motor tract injury accounts for the majority of this disability; therefore, there is impetus to understand mechanisms underlying the pathophysiology of injury and subsequent reorganization of the motor tract that may lead to recovery. After acute central nervous system injury, there are changes in the microenvironment and structure of the motor tract. For example, ischemic stroke involves decreased local blood flow and tissue death from lack of oxygen and nutrients. Traumatic injury, in contrast, causes stretching and shearing injury to microstructures, including myelinated axons and their surrounding vessels. Both involve blood-brain barrier dysfunction, which is an important initial event. After acute central nervous system injury, motor tract reorganization occurs in the form of cortical remapping in the gray matter and axonal regeneration and rewiring in the white matter. Cortical remapping involves one cortical region taking on the role of another. cAMP-response-element binding protein is a key transcription factor that can enhance plasticity in the peri-infarct cortex. Axonal regeneration and rewiring depend on complex cell-cell interactions between axons, oligodendrocytes, and other cells. The RhoA/Rho-associated coiled-coil containing kinase signaling pathway plays a central role in axon growth/regeneration through interactions with myelin-derived axonal growth inhibitors and regulation of actin cytoskeletal dynamics. Oligodendrocytes and their precursors play a role in myelination, and neurons are involved through their voltage-gated calcium channels. Understanding the pathophysiology of injury and the biology of motor tract reorganization may allow the development of therapies to enhance recovery after acute central nervous system injury. These include targeted rehabilitation, novel pharmacotherapies, such as growth factors and axonal growth inhibitor blockade, and the implementation of neurotechnologies, such as central nervous system stimulators and robotics. The translation of these advances depends on careful alignment of preclinical studies and human clinical trials. As experimental data mount, the future is one of optimism.

Dataset Information

Lack of the central nervous system- and neural crest-expressed forkhead gene Foxs1 affects motor function and body weight.

Publications

Lack of the central nervous system- and neural crest-expressed forkhead gene Foxs1 affects motor function and body weight.

Similar Datasets

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