<i>Gata2</i>is a tissue-specific post-mitotic selector gene for midbrain GABAergic neurons

Kala, Kaia; Haugas, Maarja; Lilleväli, Kersti; Guimerà, Jordi; Wurst, Wolfgang; Salminen, Marjo; Partanen, Juha

doi:10.1242/dev.029900

Cited by 94 publications

(204 citation statements)

References 38 publications

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“…Gata2, Gata3 and their partners are expressed in regions of GABAergic neurogenesis in the posterior embryonic diencephalon As Gata2 is expressed in the GABAergic precursors in the midbrain (Kala et al, 2009), we postulated that it has similar cell-type specificity in the diencephalon. Therefore, we compared first the expression patterns of Gata2 and Gata3 and their putative co-factors, Tal1 and Tal2, with markers of GABAergic progenitors, Ascl1 and Helt, as well as to glutamic acid decarboxylase 1 (Gad1) in postmitotic GABAergic neurons.…”

Section: Resultsmentioning

confidence: 97%

“…As GABAergic-to-glutamatergic fate transformation takes place in midbrain neuronal precursors in the absence of Gata2 (Kala et al, 2009), we hypothesized that this would happen also in the developing diencephalon. Indeed, we detected ectopic expression of the glutamatergic neuron marker Slc17a6 in the putative GABAergic domain of P1 in E12.5 Foxg1 cre ; Gata2 F/F embryos (Fig.…”

Section: Gata2 Selects the Gabaergic Neurotransmitter Identity In P1mentioning

confidence: 99%

“…Furthermore, there are examples of transcription factors, putative 'terminal selector genes' (Hobert, 2008), which are often activated only in the postmitotic precursors and are important determinants of either GABAergic or glutamatergic identity in the spinal cord, cerebellum and telencephalon (Cheng et al, 2005;Glasgow et al, 2005;Hoshino et al, 2005;Rouaux and Arlotta, 2010). We showed previously that the zinc-finger transcription factor Gata2 is an essential postmitotic selector of the GABAergic neuron identity in the embryonic midbrain (Kala et al, 2009). Gata2 expression is induced when the midbrain GABAergic neuron precursors leave the cell cycle and differentiate.…”

Section: Introductionmentioning

confidence: 99%

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Transcriptional regulatory mechanisms underlying the GABAergic neuron fate in different diencephalic prosomeres

et al. 2012

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SUMMARYDiverse mechanisms regulate development of GABAergic neurons in different regions of the central nervous system. We have addressed the roles of a proneural gene, Ascl1, and a postmitotic selector gene, Gata2, in the differentiation of GABAergic neuron subpopulations in three diencephalic prosomeres: prethalamus (P3), thalamus (P2) and pretectum (P1). Although the different proliferative progenitor populations of GABAergic neurons commonly express Ascl1, they have distinct requirements for it in promotion of cell-cycle exit and GABAergic neuron identity. Subsequently, Gata2 is activated as postmitotic GABAergic precursors are born. In P1, Gata2 regulates the neurotransmitter identity by promoting GABAergic and inhibiting glutamatergic neuron differentiation. Interestingly, Gata2 defines instead the subtype of GABAergic neurons in the rostral thalamus (pTh-R), which is a subpopulation of P2. Without Gata2, the GABAergic precursors born in the pTh-R fail to activate subtype-specific markers, but start to express genes typical of GABAergic precursors in the neighbouring P3 domain. Thus, our results demonstrate diverse mechanisms regulating differentiation of GABAergic neuron subpopulations and suggest a role for Gata2 as a selector gene of both GABAergic neuron neurotransmitter and prosomere subtype identities in the developing diencephalon. Our results demonstrate for the first time that neuronal identities between distinct prosomeres can still be transformed in postmitotic neuronal precursors.

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Section: Resultsmentioning

confidence: 97%

Section: Gata2 Selects the Gabaergic Neurotransmitter Identity In P1mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Transcriptional regulatory mechanisms underlying the GABAergic neuron fate in different diencephalic prosomeres

et al. 2012

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“…These genes have complementary roles in the differentiation of the raphe cell identity. GATA2 governs the differentiation of the 5-HT and GABA raphe neurons in the rostral raphe (Craven et al, 2004;Kala et al, 2009), whereas GATA3 is involved in the differentiation of the caudal raphe 5-HT neurons (van Doorninck et al, 1999). GATA3 À/À mice die by E10 and have severely abnormal development (Pandolfi et al, 1995).…”

Section: Targeting the Development Of 5-ht Neurons In The Raphementioning

confidence: 99%

Genetic Models of Serotonin (5‐HT) Depletion: What do They Tell Us About the Developmental Role of 5‐HT?

Trowbridge¹,

Narboux-Nême²,

Gaspar³

2010

The Anatomical Record

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A large number of hyposerotonergic genetic models have been generated over the past few years. Serotonin (5-HT) depletion has been obtained via targeting of genes involved in 5-HT synthesis (Tph1 and Tph2), specification and determination of the 5-HT phenotype during development (GATA3, Pet1, and Lmx1b), and 5-HT storage or clearance (Vmat2 and SERT). Here we review these various models from a developmental perspective, beginning with a description of the sources of 5-HT during development. We then summarize the neurological and behavioral alterations that have been observed in the genetic hyposerotonergic models. Although these models appear to have normal brain development and do not exhibit any gross morphological defects, problems in somatic growth and physiological functions have been observed. Abnormal adult behavior is also seen, although whether it results from depletion of 5-HT during development or functional 5-HT deficiencies in adult life remains unclear. Evidence from these hyposerotonergic models suggests that the developing brain may not need 5-HT for the establishment of general organization and structure. However, central 5-HT appears to be necessary for postnatal body growth, maturation of respiratory and vegetative control, and possibly for the development of normal adult behavior. Anat Rec, 294:1615Rec, 294: -1623Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

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“…Development of serotonergic neurons in the rhombomere region 155 and organization of serotonergic dorsal raphe cells. 159…”

Section: Gata2 (Zfp) Serotonergic Neuronsmentioning

confidence: 99%

Transcription factors and neural stem cell self-renewal, growth and differentiation

Ahmed

Gan

Lam

et al. 2009

Cell Adhesion & Migration

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The central nervous system (CNS) is a large network of interconnecting and intercommunicating cells that form functional circuits. Disease and injury of the CNS are prominent features of the healthcare landscape. There is an urgent unmet need to generate therapeutic solutions for CNS disease/injury. To increase our understanding of the CNS we need to generate cellular models that are experimentally tractable. Neural stem cells (NSCs), cells that generate the CNS during embryonic development, have been identified and propagated in vitro. To develop NSCs as a cellular model for the CNS we need to understand more about their genetics and cell biology. In particular, we need to define the mechanisms of self-renewal, proliferation and differentiation-i.e. NSC behavior. The analysis of pluripotency of embryonic stem cells through mapping regulatory networks of transcription factors has proven to be a powerful approach to understanding embryonic development. Here, we discuss the role of transcription factors in NSC behavior.

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Gata2is a tissue-specific post-mitotic selector gene for midbrain GABAergic neurons

Cited by 94 publications

References 38 publications

Transcriptional regulatory mechanisms underlying the GABAergic neuron fate in different diencephalic prosomeres

Transcriptional regulatory mechanisms underlying the GABAergic neuron fate in different diencephalic prosomeres

Genetic Models of Serotonin (5‐HT) Depletion: What do They Tell Us About the Developmental Role of 5‐HT?

Transcription factors and neural stem cell self-renewal, growth and differentiation

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