Mutant mice with scrambled brains: understanding the signaling pathways that control cell positioning in the CNS

Rice, Dennis S.; Curran, Tom

doi:10.1101/gad.13.21.2758

Cited by 141 publications

(92 citation statements)

References 164 publications

(179 reference statements)

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“…These layer-specific neuronal phenotypes are sequentially generated in the ventricular zone (VZ) of the dorsal telencephalon, and postmitotic neurons migrate to their destinations within the cortical plate (CP), in which later-born neurons migrate over earlier-born deeper-layer neurons and occupy more superficial layers (Angenvine and Sidman, 1961;Rakic, 1974). Recent genetic studies have identified various molecules involved in these processes (Rice and Curran, 1999;Soriano and del Rio, 2005). For instance, reelin, a protein secreted from Cajal-Retzuis (CR) neurons, regulates the migration and positioning of postmitotic neurons.…”

Section: Introductionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Participates in Determination of Neuronal Laminar Fate in the Developing Mouse Cerebral Cortex

Fukumitsu¹,

Ohtsuka²,

Murai³

et al. 2006

J. Neurosci.

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Section: Introductionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Participates in Determination of Neuronal Laminar Fate in the Developing Mouse Cerebral Cortex

Fukumitsu¹,

Ohtsuka²,

Murai³

et al. 2006

J. Neurosci.

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“…In mammals, newly produced neurons leave their birthplace, migrate toward the cortical surface, and form cortical layers in an inside-out pattern with respect to their time of birth (Angevine and Sidman 1961;Rakic 1972). Recent genetic studies have identified large numbers of functional molecules involved in the migration/ positioning of neocortical neurons (for review, see Rice and Curran 1999).…”

mentioning

confidence: 99%

Brn-1 and Brn-2 share crucial roles in the production and positioning of mouse neocortical neurons

Sugitani¹,

Nakai²,

Minowa³

et al. 2002

Genes Dev.

234

244

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Formation of highly organized neocortical structure depends on the production and correct placement of the appropriate number and types of neurons. POU homeodomain proteins Brn-1 and Brn-2 are coexpressed in the developing neocortex, both in the late precursor cells and in the migrating neurons. Here we show that double disruption of both Brn-1 and Brn-2 genes in mice leads to abnormal formation of the neocortex with dramatically reduced production of layer IV-II neurons and defective migration of neurons unable to express mDab1. These data indicate that Brn-1 and Brn-2 share roles in the production and positioning of neocortical neuron development. Received January 22, 2002; revised version accepted May 23, 2002. The mature neocortex is organized into six cell layers, each of which contains neurons with similar morphologies, molecular properties, and projection patterns. The development of this neocortical structure depends on a highly ordered pattern of neuronal production and migration. Cortical neurons that comprise each layer are sequentially produced in the ventricular zone of the dorsal telencephalon (Angevine and Sidman 1961;Takahashi et al. 1999). Although the regulatory factors that function in this sequential production of a variety of layer-specific neurons have not been identified in mammals, in Drosophila the successive production of different types of cells from neuroblasts has been found to require a temporally stereotyped pattern of expression of a set of transcription factors including the Drosophila POU transcription factors Pdm1 and Pdm2 (Isshiki et al. 2001). In mammals, newly produced neurons leave their birthplace, migrate toward the cortical surface, and form cortical layers in an inside-out pattern with respect to their time of birth (Angevine and Sidman 1961;Rakic 1972). Recent genetic studies have identified large numbers of functional molecules involved in the migration/ positioning of neocortical neurons (for review, see Rice and Curran 1999).Brn-1 and Brn-2, members of the mammalian class III POU transcription factor family, are prominently expressed in the embryonic brain, including the neocortex (He et al. 1989). Each single mutant, however, shows abnormalities only in limited brain regions. In Brn-2 mutant neonates, neuronal loss was observed only in the hypothalamic supraoptic and paraventricular nuclei, where Brn-1 is not expressed (Nakai et al. 1995;Schonemann et al. 1995). In Brn-1 mutants, remarkable changes in brain morphology were observed only in the hippocampus, where Brn-2 expression is barely detectable (data not shown). In the neocortex, where both Brn-1 and Brn-2 are expressed, no overt developmental defects were seen in either single mutant. These observations suggest functional complementation between Brn-1 and Brn-2 in neocortical development. Results and DiscussionTo explore their possible overlapping functions in neocortical development, we generated Brn-1/Brn-2 double homozygous mutants by intercrossing double heterozygotes that were healthy and fertile, wi...

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“…In mice, different mutations of genes involved in the reelin pathway led to phenotypes similar to that of the reeler mice (eg, scrambler mice, yotari mice or knock-out of mDab1 or cdk5). 23,25,26 Indeed, reelin is known to be part of a complex pathway (for review see 19,23 ) leading to phosphorylation of the microtubule-stabilizing protein tau 27 and the expression of reelin is regulated by transcription factors such as homeoprotein 28 and brain-derived neurotrophic factor (BDNF). 29 Therefore, the absence of association seen in this study does not discard the hypothesis that reelin and/or other genes in this pathway are involved in the pathophysiology of autism.…”

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confidence: 99%

“…In addition, a form of lissencephaly was found linked to a mutation of the reelin gene in one pedigree. 22 Reelin is the defective protein in the different strains of reeler mice, whose phenotype is characterized by severe ataxia and major anomalies of the lamination in the cortex, hippocampus and cerebellum (for review, see 19,23 ). The pattern of these anomalies resembles some of the anomalies seen in autism.…”

mentioning

confidence: 99%

Absence of association between a polymorphic GGC repeat in the 5′ untranslated region of the reelin gene and autism

et al. 2002

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Autism is a complex neurodevelopmental disorder with severe cognitive and communication disabilities, that has a strong genetic predisposition. 1 Reelin, a protein involved in neuronal migration during development, is encoded by a gene located on 7q22, 2 within the candidate region on 7q showing increased allele sharing in previous genome scans. [3][4][5][6][7][8] A case/control and familybased association study recently reported a positive association between a trinucleotide repeat polymorphism (GGC) located in the 5Ј untranslated region (UTR) of the reelin gene and autism. 9 We performed a transmission disequilibrium test (TDT) analysis of the 5ЈUTR polymorphism in 167 families including 218 affected subjects (117 trios and 50 affected sib pairs) and found no evidence of linkage/association. Our results do not support previous findings and suggest that this GGC polymorphism of the reelin gene is unlikely to be a major susceptibility factor in autism and/or genetic heterogeneity.

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Mutant mice with scrambled brains: understanding the signaling pathways that control cell positioning in the CNS

Cited by 141 publications

References 164 publications

Brain-Derived Neurotrophic Factor Participates in Determination of Neuronal Laminar Fate in the Developing Mouse Cerebral Cortex

Brain-Derived Neurotrophic Factor Participates in Determination of Neuronal Laminar Fate in the Developing Mouse Cerebral Cortex

Brn-1 and Brn-2 share crucial roles in the production and positioning of mouse neocortical neurons

Absence of association between a polymorphic GGC repeat in the 5′ untranslated region of the reelin gene and autism

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