Distinct Temporal Requirements for the Homeobox Gene Gsx2 in Specifying Striatal and Olfactory Bulb Neuronal Fates

Waclaw, Ronald R.; Wang, Bei; Pei, Zhenglei; Ehrman, Lisa A.; Campbell, Kenneth

doi:10.1016/j.neuron.2009.07.015

Cited by 124 publications

(248 citation statements)

References 65 publications

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“…We generated tetO-Gsx1-IRES-EGFP (IE) mice (described in SI Materials and Methods) to breed with Foxg1 tTA/+ mice (21) to drive the expression of Gsx1 throughout the developing telencephalon. In line with our previous experiments (17), we found that Foxg1 tTA/+ ; tetO-Gsx1-IE double transgenic (DT) embryos expressed EGFP throughout the telencephalon as early as E9.5.…”

Section: Resultssupporting

confidence: 90%

“…Indeed, Nkx2.1 expression in these embryos was never observed to be ectopic and was drastically reduced or missing (Fig. S3D), similar to that in Gsx2 DT embryos (17). Remarkably, in all Gsx1 DT embryos, Gsx2 expression was essentially lost ( (Fig.…”

Section: Resultssupporting

confidence: 60%

“…Unlike Gsx2 (3,17,18,20), Gsx1 protein has never been localized specifically in telencephalic progenitors due to lack of a wellcharacterized antibody. Thus, we obtained Gsx1-EGFP BAC transgenic mice from GENSAT (www.gensat.org) and characterized the EGFP-expressing cells using antibodies that recognize either Gsx2 (3) or Gsx1 and -2 (12) at various embryonic stages.…”

Section: Resultsmentioning

confidence: 99%

“…To address this issue, we used a gain-of-function approach using a binary transgenic system to conditionally express Gsx1 throughout the telencephalon, similar to the system our lab recently used to misexpress Gsx2 (17). We generated tetO-Gsx1-IRES-EGFP (IE) mice (described in SI Materials and Methods) to breed with Foxg1 tTA/+ mice (21) to drive the expression of Gsx1 throughout the developing telencephalon.…”

Section: Resultsmentioning

confidence: 99%

“…From embryonic day (E) 12.5 and onward, Gsx2 is expressed at a high level in progenitors of the dorsal LGE (dLGE) and relatively lower level in the ventral LGE (vLGE) and MGE progenitors, whereas Gsx1 is expressed mainly in the MGE and vLGE (4,10,(14)(15)(16)(17)(18). The graded Gsx2 expression pattern in LGE progenitors has recently been implicated in the distinct neuronal output of the dLGE versus the vLGE (17). In Gsx2 mutants, the expression of Gsx1 expands throughout the dorsal extent of the LGE (14,18).…”

mentioning

confidence: 99%

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Homeobox genes Gsx1 and Gsx2 differentially regulate telencephalic progenitor maturation

Pei¹,

Wang²,

Chen

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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105

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Homeobox genes Gsx1 and Gsx2 (formerly Gsh1 and Gsh2) are among the earliest transcription factors expressed in neuronal progenitors of the lateral ganglionic eminence (LGE) in the ventral telencephalon. Gsx2 is required for the early specification of LGE progenitor cells and recently has been shown to specify different LGE neuronal subtypes at distinct time points. In Gsx2 mutants, Gsx1 compensates, at least in part, for the loss of Gsx2 in the specification of LGE neuronal subtypes. Because no specific phenotype has been described in Gsx1 mutants, it is unclear what role this factor plays in the development of the ventral telencephalon. Here, we used a gain-of-function approach to express either Gsx1 or Gsx2 throughout the telencephalon and found that Gsx1 functions similarly to Gsx2 in the specification of LGE identity. However, our results show that Gsx1 and Gsx2 differentially regulate the maturation of LGE progenitors. Specifically, Gsx2 maintains LGE progenitors in an undifferentiated state, whereas Gsx1 promotes progenitor maturation and the acquisition of neuronal phenotypes, at least in part, through the down-regulation of Gsx2. These unique results indicate that the two closely related Gsx genes similarly regulate LGE patterning but oppositely control the balance between proliferation and differentiation in the neuronal progenitor pool.cell cycle kinetics | self-renewal

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Section: Resultssupporting

confidence: 90%

Section: Resultssupporting

confidence: 60%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Homeobox genes Gsx1 and Gsx2 differentially regulate telencephalic progenitor maturation

Pei¹,

Wang²,

Chen

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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105

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Transcriptional Regulation of Olfactory Bulb Neurogenesis

Díaz-Guerra

Pignatelli

Nieto‐Estévez

et al. 2013

The Anatomical Record

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The neurons in the olfactory bulb originate from molecularly defined and spatially distinct proliferative regions. Glutamatergic projection neurons are generated during the embryonic period in the local ventricular zone of the olfactory bulb, a territory in the dorsal telencephalon in which the transcription factor Pax6 is expressed. Some cells in this zone also express Tbr1, a marker of glutamatergic neurons. By contrast, embryonic olfactory bulb interneurons are derived from Gsx2 expressing cells in the dorsal lateral ganglionic eminence of the ventral telencephalon, and from progenitors outside the dorsal lateral ganglionic eminence, including the olfactory bulb neuroepithelium. Postnatally, interneurons arise from the subventricular zone of the lateral ventricle, although the rostral migratory stream and the olfactory bulb also appear to serve as a source of neurons. Transcription factors are crucial to generate all classes of neurons and glia in the olfactory bulb, both during development and adulthood. In this article, we discuss and propose models on how the spatial and temporal regulation of transcription factor expression controls the self-renewal, proliferation and cell fate of neural stem cells and progenitors, which finally leads to the generation of distinct functional subtypes of neurons in the developing and adult olfactory bulb. Anat Rec, 296:1364Rec, 296: -1382Rec, 296: , 2013. V C 2013 Wiley Periodicals, Inc.Key words: olfactory bulb; neurogenesis; transcription factor; neural stem cells; proliferation; differentiation

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Loss of Gsx1 and Gsx2 function rescues distinct phenotypes in Dlx1/2 mutants

Wang

Long

Flandin

et al. 2013

J of Comparative Neurology

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Mice lacking the Dlx1 and Dlx2 homeobox genes (Dlx1/2 mutants) have severe deficits in subpallial differentiation, including overexpression of the Gsx1 and Gsx2 homeobox genes. To investigate whether Gsx overexpression contributes to the Dlx1/2 mutant phenotypes, we made compound loss-of-function mutants. Eliminating Gsx2 function from the Dlx1/2 mutants rescued the increased expression of Ascl1 and Hes5 (Notch signaling mediators) and Olig2 (oligodendrogenesis mediator). In addition, Dlx1/2;Gsx2 mutants, like Dlx1/2;Ascl1 mutants, exacerbated the Gsx2 and Dlx1/2 patterning and differentiation phenotypes, particularly in the lateral ganglionic eminence (LGE) caudal ganglionic eminence (CGE), and septum, including loss of GAD1 expression. On the other hand, eliminating Gsx1 function from the Dlx1/2 mutants (Dlx1/2;Gsx1 mutants) did not severely exacerbate their phenotype; on the contrary, it resulted in a partial rescue of medial ganglionic eminence (MGE) properties, including interneuron migration to the cortex. Thus, despite their redundant properties, Gsx1 and -2 have distinct interactions with Dlx1 and -2. Gsx2 interaction is strongest in the LGE, CGE, and septum, whereas the Gsx1 interaction is strongest in the MGE. From these studies, and earlier studies, we present a model of the transcriptional network that regulates early steps of subcortical development. J. Comp. Neurol. 521:1561–1584, 2013. © 2012 Wiley Periodicals, Inc.

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Distinct Temporal Requirements for the Homeobox Gene Gsx2 in Specifying Striatal and Olfactory Bulb Neuronal Fates

Cited by 124 publications

References 65 publications

Homeobox genes Gsx1 and Gsx2 differentially regulate telencephalic progenitor maturation

Homeobox genes Gsx1 and Gsx2 differentially regulate telencephalic progenitor maturation

Transcriptional Regulation of Olfactory Bulb Neurogenesis

Loss of Gsx1 and Gsx2 function rescues distinct phenotypes in Dlx1/2 mutants

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