Coding Sequence and Expression Patterns of Mouse Chordin and Mapping of the Cognate MouseChrdand HumanCHRDGenes

Pappano, William N.; Scott, Ian C.; Clark, Timothy G.; Eddy, Roger L.; Shows, Thomas B.; Greenspan, Daniel S.

doi:10.1006/geno.1998.5474

Cited by 29 publications

(21 citation statements)

References 16 publications

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“…Chordin is a secreted extracellular antagonist of BMP signaling whose only known function is to bind BMP ligands and prevent them from interacting with their receptors (Piccolo et al, 1996). Chordin is expressed in many tissues throughout development, including the hippocampus (Pappano et al, 1998;Scott et al, 2000). We find that loss of chordin results in a presynaptic transmitter release defect that enhances short-and long-term synaptic plasticity in slice preparations.…”

Section: Introductionmentioning

confidence: 80%

“…A number of previous reports have shown expression of several BMP signaling pathway members in the adult hippocampus (Soderstrom et al, 1996;Pappano et al, 1998;Scott et al, 2000), but it is not clear whether this pathway is actually active in mature neurons because some important signaling pathway components that play a role in directing neurodevelopment are shut off after maturation of the CNS. Previous in situ hybridization results showed that the BMPRII receptor is expressed in the hippocampus.…”

Section: Expression Of Bmp Signaling Pathway Components In the Adult mentioning

confidence: 99%

“…Many components of the bone morphogenic protein (BMP) signaling pathway, a distinct subfamily within the TGF-␤s, are expressed in different parts of the mammalian adult brain, including the hippocampus (Soderstrom et al, 1996;Pappano et al, 1998;Scott et al, 2000). Despite this strong expression in the adult brain, their potential role in regulating postnatal neuronal plasticity in vertebrates has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

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Presynaptic Contributions of Chordin to Hippocampal Plasticity and Spatial Learning

Sun¹,

Thomas²,

Herder³

et al. 2007

J. Neurosci.

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Recently, several evolutionary conserved signaling pathways that play prominent roles in regulating early neurodevelopment have been found to regulate synaptic remodeling in the adult. To test whether adult neuronal expression of bone morphogenic protein (BMP) signaling components also plays a postnatal role in regulating neuronal plasticity, we modulated BMP signaling in mice both in vivo and in vitro by genetic removal of the BMP inhibitor chordin or by perfusing recombinant BMP signaling pathway components onto acute hippocampal slices. Chordin null mice exhibited a significant increase in presynaptic transmitter release from hippocampal neurons, resulting in enhanced paired-pulse facilitation and long-term potentiation. These mice also showed a decreased acquisition time in a water maze test along with less exploratory activity during Y-maze and open-field tests. Perfusion of BMP ligands onto hippocampal slices replicated the presynaptic phenotype of chordin null slices, but bath application of Noggin, another antagonist of BMP signaling pathway, significantly decrease the frequency of miniature EPSCs. These results demonstrate that the BMP signaling pathway contributes to synaptic plasticity and learning likely through a presynaptic mechanism.

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Section: Introductionmentioning

confidence: 80%

Section: Expression Of Bmp Signaling Pathway Components In the Adult mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Presynaptic Contributions of Chordin to Hippocampal Plasticity and Spatial Learning

Sun¹,

Thomas²,

Herder³

et al. 2007

J. Neurosci.

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“…24 In mice it is also thought to play a role in patterning of the early embryo, primarily in establishing the dorsoventral axis. 21 Targeted inactivation of chordin in mice leads to defects in ear, pharynx and cardiovascular organisation. 26 Mice that were double homozygous mutants for chordin and noggin had absent forebrain, eyes, nasal placodes and other facial structures, including agnathia.…”

Section: Discussionmentioning

confidence: 99%

“…Micro/Anophthalmia with deletion of 3q26?q28 A Male et al 810 tal protein known to be involved in dorsoventral patterning in the mouse. 21 …”

Section: Estimation Of Candidate Regionmentioning

confidence: 99%

Delineation of an estimated 6.7 MB candidate interval for an anophthalmia gene at 3q26.33-q28 and description of the syndrome associated with visible chromosome deletions of this region

et al. 2002

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Anophthalmia or microphthalmia occur in approximately one in 10 children who have severe visual impairment. These eye malformations are often of unknown aetiology, but can be inherited in autosomal dominant, recessive or X-linked forms, and can also occur in association with specific chromosome abnormalities. Four children are described in the medical literature with microphthalmia or anophthalmia in association with chromosome rearrangements involving distal 3q, suggesting the presence of a micro/anophthalmia gene in this region. We have identified two further patients with micro/anophthalmia and chromosome rearrangements involving 3q26?3q27 and identified a 6.7 MB common deleted region. Patient 1 had multiple abnormalities including bilateral anophthalmia, abnormalities of the first and second cranial nerves and partial absence of the corpus callosum. His karyotype was 46,XY,del(3)(q26.33q28). Patient 2 had right anophthalmia and left extreme microphthalmia. Her karyotype was 46,XX,del(3)(q26.33q28)t(3;7)(q28;q21.1). Both patients had intrauterine growth retardation (IUGR) and strikingly similar dysmorphic facies consisting of bossed forehead, downward-slanting palpebral fissures, grooved bridge of the nose, prominent low-set ears, small down-turned mouth and small mandible. We identified BAC clones mapping to distal 3q from the ENSEMBL and NCBI Entrez databases. These BAC clones were used as fluorescence in situ hybridisation (FISH) probes to identify the minimum deleted region common to both patients. This interval, between clones RPC11-134F2 and RPC11-132N15, was estimated to be 6.7 MB. We conclude that there is an anophthalmia locus within this interval. Candidate genes mapping to this region include Chordin and DVL3, a homologue of the Drosophila Dishevelled gene.

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Spatiotemporal expression patterns of mammalian chordin during postgastrulation embryogenesis and in postnatal brain

et al. 2000

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Coding Sequence and Expression Patterns of Mouse Chordin and Mapping of the Cognate MouseChrdand HumanCHRDGenes

Cited by 29 publications

References 16 publications

Presynaptic Contributions of Chordin to Hippocampal Plasticity and Spatial Learning

Presynaptic Contributions of Chordin to Hippocampal Plasticity and Spatial Learning

Delineation of an estimated 6.7 MB candidate interval for an anophthalmia gene at 3q26.33-q28 and description of the syndrome associated with visible chromosome deletions of this region

Spatiotemporal expression patterns of mammalian chordin during postgastrulation embryogenesis and in postnatal brain

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