NPAS1 Represses the Generation of Specific Subtypes of Cortical Interneurons

Stanco, Amelia; Pla, Ramón; Vogt, Daniel; Chen, Yiran; Mandal, Shyamali; Walker, Jamie M.; Hunt, Reid; Lindtner, Susan; Erdman, Carolyn A.; Pieper, Andrew A.; Hamilton, Steven P.; Xu, Duan; Baraban, Scott C.; Rubenstein, John L.R.

doi:10.1016/j.neuron.2014.10.040

Cited by 66 publications

(64 citation statements)

References 56 publications

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“…At E17.5, Npas1 expression was reduced, a TF that marks SST + but not PV + interneurons (Fig. S3H,I) (Stanco et al, 2014). Therefore, at E12.5 Coup-TF2-sensitized mutants generated fewer immature interneurons expressing Sst, Lhx6 and Sox6.…”

Section: Resultsmentioning

confidence: 93%

“…By 17.5, mutants showed reduced expression of Npas1 (Fig. S3H,I), a TF that marks SST + and not PV + interneurons, and that positively regulates SST + interneuron numbers (Stanco et al, 2014). The dMGE has been proposed to be a major source of SST + interneurons (Flames et al, 2007;Wonders et al, 2008;Inan et al, 2012 (A,B) and Coup-TF2-sensitized mutant (A′,B′) coronal hemisections in two rostral-caudal planes (n=3 for each control and mutant).…”

Section: Discussionmentioning

confidence: 99%

“…We suggest that the SST + /PV + ratio should be measured in these individuals, as mutations in genes associated with neuropsychiatric disorders (NPAS3 and PTEN) alter the SST + /PV + ratio in mice with mutations of these genes (Vogt et al, 2015;Stanco et al, 2014). Moreover, circuit-level changes, such as gamma oscillations, which is a feature of schizophrenia, have been observed in PTEN mouse mutants (Stanco et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…For all immunohistochemistry on postnatal brains, staining was carried out on free-floating sections as described previously (Stanco et al, 2014). We performed all immunohistochemistry on n≥3 biological replicates for each control and mutant, except for Fig.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

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Coup-TF1 and Coup-TF2 control subtype and laminar identity of MGE-derived neocortical interneurons

Vogt

Lindtner

et al. 2017

Development

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Distinct cortical interneuron (CIN) subtypes have unique circuit functions; dysfunction in specific subtypes is implicated in neuropsychiatric disorders. Somatostatin-and parvalbuminexpressing (SST + and PV + ) interneurons are the two major subtypes generated by medial ganglionic eminence (MGE) progenitors. Spatial and temporal mechanisms governing their cellfate specification and differential integration into cortical layers are largely unknown. We provide evidence that Coup-TF1 and Coup-TF2 (Nr2f1 and Nr2f2) transcription factor expression in an arc-shaped progenitor domain within the MGE promotes time-dependent survival of this neuroepithelium and the time-dependent specification of layer V SST + CINs. Coup-TF1 and Coup-TF2 autonomously repress PV + fate in MGE progenitors, in part through directly driving Sox6 expression. These results have identified, in mouse, a transcriptional pathway that controls SST-PV fate.

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Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: In Situ Hybridizationmentioning

confidence: 99%

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Coup-TF1 and Coup-TF2 control subtype and laminar identity of MGE-derived neocortical interneurons

Vogt

Lindtner

et al. 2017

Development

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“…ST6GALNAC1 is known to be differentially regulated at key periods of neurodevelopment; Npas1 has already been described as an important mediator of neuron subtypes generation 49 in pre-natal brain development.…”

Section: Neurodevelopmentmentioning

confidence: 99%

Schizophrenia: neuroinflammation, neurodegeneration or neurodevelopment? A genetic overview

Polho¹,

Paula

2017

Rev. Med. (São Paulo)

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Schizophrenia is a devastating mental illness and its etiology is still largely unknown. Several gene mapping studies suggest that schizophrenia is a complex disorder, with a cumulative impact of variable genetic effects coupled with environmental factors. There is evidence that schizophrenia could be a neurodegenerative, neuroinflammatory or neurodevelopmental disorder. Neuropsychological data indicate neurocognitive functions are relatively stable over time after illness onset, whereas morphological data indicate a degenerative process; potential roles of neuroinflammation in the etiology of psychiatric diseases including schizophrenia have also been suggested. Recent research indicates genetic overlap between schizophrenia and syndromes in which psychopathology manifests in childhood and that are often grouped together as 'neurodevelopmental disorders'. These findings challenge the etiological basis of current diagnostic categories and, together with evidence for frequent comorbidity, suggest that we should view the functional psychoses as members of a group that result in part from a combination of genetic and environmental effects on brain development and that are associated with specific and general impairments of cognitive function. The objective was to perform a systematic literature review of articles on genetics of schizophrenia relating to neurodegeneration, neuroinflammation and neurodevelopment. After proper filter, we included 40 studies and reviewed each finding and its relevance to the hypotheses. We can conclude that the evidence points to schizophrenia as a neurodevelopmental disease with the direct presence of factors related to neuroinflammation and neurodegeneration.Keywords: Schizophrenia/genetics; Neurodevelopmental disorders/ genetics; Pantothenate kinase-associated neurodegeneration/ genetics; Neurogenetic inflammation/genetics; Genetics.RESUMO: Esquizofrenia é uma doença mental debilitante e sua etiologia é, em sua maior parte, desconhecida. Alguns estudos de mapeamento genético sugerem que esquizofrenia é uma doença complexa, com impacto acumulativo de fatores genéticos variáveis associados a fatores ambientais. Há evidência de que a esquizofrenia poderia ser uma doença neurodegenerativa, neuroinflamatória ou do neurodesenvolvimento. Dados neuropsicológicos indicam que funções cognitivas são relativamente estáveis no decorrer do tempo após o início da doença, enquanto dados morfológicos indicam processos degenerativos; papéis importantes da neuroinflamação na etiologia de doenças psiquiátricas, incluindo esquizofrenia, também foram sugeridos. Pesquisas recentes indicam sobreposição entre esquizofrenia e síndromes cuja fisiopatologia se manifesta na infância e são em geral agrupadas como "doenças do neurodesenvolvimento". Estes achados desafiam a base etiológica das categorias atuais de diagnóstico e, juntamente com a evidência de comorbidade frequente, sugerem que devemos ver as psicoses como membros do grupo que resulta em parte da combinação de efeitos genéticos e ambientai...

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Phenotypic expression of 19q13.32 microdeletions: Report of a new patient and review of the literature

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Cunto

Pellegrin

et al. 2017

American J of Med Genetics Pt A

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The phenotypic manifestations of microdeletions in the 19q13.32 region are still poorly known. In this paper we report a patient who presented with hypotonia, developmental delay, facial dysmorphism, micrognathia, kyphoscoliosis, and buried penis. Chromosomal microarray revealed an interstitial 327 kb de novo microdeletion in the 19q13.32 region comprising eight genes (ARGHAP35, NPAS1, TMEM160, ZC3H4, SAE1, BBC3, MIR3190, and MIR3191). Previously reported cases of microdeletions in the 19q13.32 region were reviewed and compared to our patient, highlighting the common features of a possible 19q13.32 microdeletion syndrome.

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NPAS1 Represses the Generation of Specific Subtypes of Cortical Interneurons

Cited by 66 publications

References 56 publications

Coup-TF1 and Coup-TF2 control subtype and laminar identity of MGE-derived neocortical interneurons

Coup-TF1 and Coup-TF2 control subtype and laminar identity of MGE-derived neocortical interneurons

Schizophrenia: neuroinflammation, neurodegeneration or neurodevelopment? A genetic overview

Phenotypic expression of 19q13.32 microdeletions: Report of a new patient and review of the literature

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