Early ontogeny of catecholaminergic cell lineage in brain and peripheral neurons monitored by tyrosine hydroxylase-lacZ transgene

Son, Jin H.; Min, Nan; Joh, Tong H.

doi:10.1016/0169-328x(95)00255-q

Cited by 28 publications

(23 citation statements)

References 31 publications

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“…3B) (Son et al, 1996). In E10.5 Gata3 mutant embryos, Th expression is significantly weaker in both the SG and NT ( Fig.…”

Section: Tgmentioning

confidence: 85%

“…Previous reports documented the transient expression of Th and Dbh in the ventrolateral neural tube (NT) of mid-gestational embryos (E10.5-E13.5), indicative of the transient noradrenergic cell lineage in this region (Son et al, 1996;Teitelman et al, 1981). It was also reported that an hDBH promoter transgene faithfully recapitulated the transient NT expression at this stage .…”

Section: Research Articlementioning

confidence: 90%

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Gata3 participates in a complex transcriptional feedback network to regulate sympathoadrenal differentiation

et al. 2006

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Gata3 mutant mice expire of noradrenergic deficiency by embryonic day (E) 11 and can be rescued pharmacologically or, as shown here, by restoring Gata3 function specifically in sympathoadrenal (SA) lineages using the human DBH promoter to direct Gata3 transgenic expression. In Gata3-null embryos, there was significant impairment of SA differentiation and increased apoptosis in adrenal chromaffin cells and sympathetic neurons. Additionally, mRNA analyses of purified chromaffin cells from Gata3 mutants show that levels of Mash1, Hand2 and Phox2b (postulated upstream regulators of Gata3) as well as terminally differentiated SA lineage products (tyrosine hydroxylase, Th, and dopamine ␤-hydroxylase, Dbh) are markedly altered. However, SA lineage-specific restoration of Gata3 function in the Gata3 mutant background rescues the expression phenotypes of the downstream, as well as the putative upstream genes. These data not only underscore the hypothesis that Gata3 is essential for the differentiation and survival of SA cells, but also suggest that their differentiation is controlled by mutually reinforcing feedback transcriptional interactions between Gata3, Mash1, Hand2 and Phox2b in the SA lineage.

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“…3B) (Son et al, 1996). In E10.5 Gata3 mutant embryos, Th expression is significantly weaker in both the SG and NT ( Fig.…”

Section: Tgmentioning

confidence: 85%

Section: Research Articlementioning

confidence: 90%

Gata3 participates in a complex transcriptional feedback network to regulate sympathoadrenal differentiation

et al. 2006

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“…The resulting 11.7 kb of f usion gene was isolated from the plasmid vector by restriction digestion with HindIII. Transgenic mice were generated as described before (Min et al, 1994;Son et al, 1996b). Briefly, the 11.7 kb insert was purified by 0.8% agarose gel electrophoresis followed by electroelution, and subjected to cesium chloride gradient centrif ugation as previously described.…”

Section: Methodsmentioning

confidence: 99%

“…Previously, we have demonstrated that a 9.0 kb of 5Ј upstream promoter region of the rat TH gene can direct expression of lacZ reporter gene limited to DA neurons in both developing and adult transgenic mice (Min et al, 1994;Son et al, 1996b). Therefore, we first constructed the hybrid gene, TH9.0-SV40Tag-tsA58, consisting of 9.0 kb of 5Ј TH promoter region f used to the modulatable oncogene, SV40Tag-tsA58 ( Fig.…”

Section: The Conditional Immortalization Of Da Cells Of Embryonic Sn mentioning

confidence: 99%

Neuroprotection and Neuronal Differentiation Studies Using Substantia Nigra Dopaminergic Cells Derived from Transgenic Mouse Embryos

et al. 1999

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The major pathological lesion of Parkinson's disease (PD) is the selective cell death of dopaminergic (DA) neurons in substantia nigra (SN). Although the initial cause and subsequent molecular signaling mechanisms leading to DA cell death underlying the PD process remain elusive, brain-derived neurotrophic factor (BDNF) is thought to exert neuroprotective as well as neurotrophic roles for the survival and differentiation of DA neurons in SN. Addressing molecular mechanisms of BDNF action in both primary embryonic mesencephalic cultures and in vivo animal models has been technically difficult because DA neurons in SN are relatively rare and present with many heterogeneous cell populations in midbrain. We have developed and characterized a DA neuronal cell line of embryonic SN origin that is more accessible to molecular analysis and can be used as an in vitro model system for studying SN DA neurons. A clonal SN DA neuronal progenitor cell line SN4741, arrested at an early DA developmental stage, was established from transgenic mouse embryos containing the targeted expression of the thermolabile SV40Tag in SN DA neurons. The phenotypic and morphological differentiation of the SN4741 cells could be manipulated by environmental cues in vitro. Exogenous BDNF treatment produced significant neuroprotection against 1-methyl-4-phenylpyridinium, glutamate, and nitric oxide-induced neurotoxicity in the SN4741 cells. Simultaneous phosphorylation of receptor tyrosine kinase B accompanied the neuroprotection. This SN DA neuronal cell line provides a unique model system to circumvent the limitations associated with primary mesencephalic cultures for the elucidation of molecular mechanisms of BDNF action on DA neurons of the SN. Key words: neuroprotection; BDNF; substantia nigra; dopaminergic neuron; Parkinson's disease; transgenic mice; neuronal differentiation; conditional immortalizationThe neuropathological symptoms of Parkinson's disease (PD) result from the greater than normal selective degeneration of substantia nigra (SN) dopaminergic (DA) neurons during aging. In PD the initial cause or causes and molecular mechanisms leading to the DA cell death are unknown. Treatment to prevent DA cell loss in PD is not available. Because of the paucity of DA neurons and the presence of numerous other cell populations in SN, it has not been possible to definitively address the molecular mechanisms of both DA neuronal survival and differentiation. Thus, it is crucial to acquire an abundant source of homogeneous DA neurons in vitro for the molecular dissection of SN DA neurons. To generate a consistent and abundant source of SN DA neurons in vitro, several approaches, using developmental, anatomical, somatic, or genetic manipulations, have been investigated. First, Hynes et al. (1995) tried to recapitulate the ontogeny of SN DA neuronal differentiation in explant cultures. Sonic hedgehog can induce effectively DA neurons in rat embryonic forebrain /midbrain explant. But, to practically manipulate the DA neuronal differentiation in vitro...

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“…With the exception of the AP1/TRE and CRE sites (76), the roles of these proximal elements have not been documented in vivo. The production and analysis of transgenic mice have demonstrated that large parts of the rat TH promoter region are necessary to direct expression in the appropriate cells, but the elements responsible for cell-specific expression have not been mapped precisely (8,47,53,69,72). In contrast, in vitro studies have revealed the roles of several proximal elements, including the E-box/dyad, AP1/TRE, and CRE elements (37,41,42,75,86), octameric and heptameric (oct/hept) elements (18,86), SP1 (84), and the NBRE-like 1 motif (36).…”

mentioning

confidence: 99%

ZENON, a Novel POZ Kruppel-Like DNA Binding Protein Associated with Differentiation and/or Survival of Late Postmitotic Neurons

Kiefer

Chatail-Hermitte

Ravassard

et al. 2005

Molecular and Cellular Biology

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The rat tyrosine hydroxylase gene promoter contains an E-box/dyad motif and an octameric and heptameric element that may be recognized by classes of transcription factors highly expressed during nervous system development. In a one-hybrid genetic screen, we used these sites as targets to isolate cDNAs encoding new transcription factors present in the brain. We identified ZENON, a novel rat POZ protein that contains two clusters of Kruppel-like zinc fingers and that presents several features of a transcription factor. ZENON is found in nuclei following transient transfection with the cDNA. The N-terminal zinc finger cluster contains a DNA binding domain that interacts with the E box. Cotranfection experiments revealed that ZENON induces tyrosine hydroxylase promoter activity. Unlike other POZ proteins, the ZENON POZ domain is not required for either activation of transcription or self-association. In the embryonic neural tube, ZENON expression is restricted to neurons that have already achieved mitosis and are engaged in late stages of neuronal differentiation (late postmitotic neurons). ZENON neuronal expression persists in the adult brain; therefore, ZENON can be considered a marker of mature neurons. We propose that ZENON is involved in the maintenance of panneuronal features and/or in the survival of mature neurons.The two major cell types in the nervous system, neurons and glia, both comprise a large number of subtypes. The generation and maintenance of this phenotypic diversity require extracellular signals that are converted into tightly regulated transcriptional cascades. Many transcription factors involved in these cascades-often basic helix-loop-helix (bHLH), homeodomain, or zinc finger-containing proteins-remain to be identified. Description of these factors would help elucidate the molecular events leading to the differentiation of the various cell types in the nervous system.One way to identify these factors is to isolate novel proteins that interact with sequences promoting the neural expression of a highly developmentally regulated gene. A good candidate is the gene encoding tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis (44, 56). The expression of the TH gene is a common feature of all neurons and neuroendocrine cells that synthesize and release catecholamines (dopamine, norepinephrine, and epinephrine). These cells are extremely diverse in their functional, morphological, and anatomical properties and have different embryonic origins. Depending on their locations in the adult central nervous system (CNS) and peripheral nervous system (PNS), catecholaminergic cells originate from different parts of the neural tube and neural crest (6,73,74). In the embryonic neural tube, catecholaminergic cell groups arise from various neuromeres (64, 78), suggesting that a large number of extracellular signals and transcription factors govern the specification and maintenance of catecholaminergic identity.The production and functional analysis of knockout mice revealed the essen...

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Early ontogeny of catecholaminergic cell lineage in brain and peripheral neurons monitored by tyrosine hydroxylase-lacZ transgene

Cited by 28 publications

References 31 publications

Gata3 participates in a complex transcriptional feedback network to regulate sympathoadrenal differentiation

Gata3 participates in a complex transcriptional feedback network to regulate sympathoadrenal differentiation

Neuroprotection and Neuronal Differentiation Studies Using Substantia Nigra Dopaminergic Cells Derived from Transgenic Mouse Embryos

ZENON, a Novel POZ Kruppel-Like DNA Binding Protein Associated with Differentiation and/or Survival of Late Postmitotic Neurons

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