Induction of neurogenin‐1 expression by sonic hedgehog: Its role in development of trigeminal sensory neurons

Ota, Masahiro; K, Ito

doi:10.1002/dvdy.10336

Cited by 31 publications

(26 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The alternative possibility that Shh may act on survival and/or proliferation of mesenchymal-neural CNCCs is unlikely because the latter scenario would have involved an increase in the total number of progenitors in the presence of Shh. The present findings, however, are in line with the possibility that Shh may regulate NCC survival, adhesion, and neuronal differentiation at various developmental stages, as shown in other experimental systems (30,32,33,(41)(42)(43).…”

Section: Discussionsupporting

confidence: 92%

Sonic Hedgehog promotes the development of multipotent neural crest progenitors endowed with both mesenchymal and neural potentials

Calloni

Glavieux-Pardanaud

Douarin

et al. 2007

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

View full text Add to dashboard Cite

In the vertebrate embryo, the cephalic neural crest cells (CNCCs) produce cells belonging to two main lineages: the neural [including neurons, glial cells of the peripheral nervous system (PNS), and melanocytes] and the mesenchymal (chondrocytes, osteoblasts, smooth muscle cells, and connective tissue cells), whereas the trunk NCCs (TNCCs) in amniotes yield only neural derivatives. Although multipotent cells have previously been evidenced by in vitro clonal analysis, the issue as to whether all of the mesenchymal and neural phenotypes can be derived from a unique NC stem cell has remained elusive. In the present work, we devised culture conditions that led us to identify a highly multipotent NCC endowed with both neural and mesenchymal potentials, which lies upstream of all the other NC progenitors known so far. We found that addition of recombinant Sonic Hedgehog (Shh) increased the number of CNCC progenitors yielding both mesenchymal and neural lineages and promoted the development of such precursors from the TNCC. Shh decreased the neural-restricted precursors without affecting the overall CNCC survival and proliferation. By showing a differential positive effect of Shh on the expression of mesenchymal phenotypes (i.e., chondrocytes and smooth muscle cells) by multipotent CNCCs, these results shed insights on the in vivo requirement of Shh for craniofacial morphogenesis. Together with evolutionary considerations, these data also suggest that the mesenchymal-neural precursor represents the ancestral form of the NC stem cell, which in extinct forms of vertebrates (the ostracoderms) was able to yield both the PNS and superficial skeleton.chondrogenesis ͉ clonal culture ͉ embryo ͉ quail ͉ stem cell

show abstract

Section: Discussionsupporting

confidence: 92%

Sonic Hedgehog promotes the development of multipotent neural crest progenitors endowed with both mesenchymal and neural potentials

Calloni

Glavieux-Pardanaud

Douarin

et al. 2007

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

View full text Add to dashboard Cite

show abstract

“…Determination of neuron and glia cell fates from NSCs during neural tube development depends on signalling molecules such as SHH and BMPs and their downstream transcription factors such as bHLH factors [35] and homeodomain factors [7]. Several lines of evidence suggest that Shh regulates the development of many neuronal cell types and oligodendrocytes by activating the expression of members of the bHLH factors such as Neurog1, Ascl1 and Olig1 [17,20,[36][37][38]. During neurodevelopment, the transient increase in the expression of Neurog1, Neurog2 and Ascl1 (the proneural bHLH factors) results in the initiation of neurogenesis [14,16,18].…”

Section: Discussionmentioning

confidence: 99%

High glucose alters the expression of genes involved in proliferation and cell-fate specification of embryonic neural stem cells

Tay

Ling

et al. 2006

Diabetologia

View full text Add to dashboard Cite

Aims/hypothesis: Maternal diabetes induces neural tube defects during embryogenesis. Since the neural tube is derived from neural stem cells (NSCs), it is hypothesised that in diabetic pregnancy neural tube defects result from altered expression of developmental control genes, leading to abnormal proliferation and cell-fate choice of NSCs. Materials and methods: Cell viability, proliferation index and apoptosis of NSCs and differentiated cells from mice exposed to physiological or high glucose concentration medium were examined by a tetrazolium salt assay, 5-bromo-2′-deoxyuridine incorporation, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling and immunocytochemistry. Expression of developmental genes, including sonic hedgehog (Shh), bone morphogenetic protein 4 (Bmp4), neurogenin 1/2 (Neurog1/2), achaete-scute complex-like 1 (Ascl1), oligodendrocyte transcription factor 1 (Olig1), oligodendrocyte lineage transcription factor 2 (Olig2), hairy and enhancer of split 1/5 (Hes1/5) and delta-like 1 (Dll1), was analysed by real-time RT-PCR. Proliferation index and neuronal specification in the forebrain of embryos at embryonic day 11.5 were examined histologically. Results: High glucose decreased the proliferation of NSCs and differentiated cells. The incidence of apoptosis was increased in NSCs treated with high glucose, but not in the differentiated cells. High glucose also accelerated neuronal and glial differentiation from NSCs. The decreased proliferation index and early differentiation of neurons were evident in the telencephalon of embryos derived from diabetic mice. Exposure to high glucose altered the mRNA expression levels of Shh, Bmp4, Neurog1/2, Ascl1, Hes1, Dll1 and Olig1 in NSCs and Shh, Dll1, Neurog1/2 and Hes5 in differentiated cells. Conclusions/interpretation: The changes in proliferation and differentiation of NSCs exposed to high glucose are associated with altered expression of genes that are involved in cell-cycle progression and cell-fate specification during neurulation. These changes may form the basis for the defective neural tube patterning observed in embryos of diabetic pregnancies.

show abstract

“…This is consistent with the finding that Neurog1 is able to repress the transcription of ascl1, whereas Ascl1 is able to direct neuronal precursors toward a GABAergic fate (15). Interestingly, both genes are induced by the same signal, Shh (41)(42)(43) (Fig. S6).…”

Section: Discussionmentioning

confidence: 99%

Her6 regulates the neurogenetic gradient and neuronal identity in the thalamus

Scholpp

Delogu²,

Gilthorpe³

et al. 2009

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

View full text Add to dashboard Cite

During vertebrate brain development, the onset of neuronal differentiation is under strict temporal control. In the mammalian thalamus and other brain regions, neurogenesis is regulated also in a spatially progressive manner referred to as a neurogenetic gradient, the underlying mechanism of which is unknown. Here we describe the existence of a neurogenetic gradient in the zebrafish thalamus and show that the progression of neurogenesis is controlled by dynamic expression of the bHLH repressor her6. Members of the Hes/Her family are known to regulate proneural genes, such as Neurogenin and Ascl. Here we find that Her6 determines not only the onset of neurogenesis but also the identity of thalamic neurons, marked by proneural and neurotransmitter gene expression: loss of Her6 leads to premature Neurogenin1-mediated genesis of glutamatergic (excitatory) neurons, whereas maintenance of Her6 leads to Ascl1-mediated production of GABAergic (inhibitory) neurons. Thus, the presence or absence of a single upstream regulator of proneural gene expression, Her6, leads to the establishment of discrete neuronal domains in the thalamus.diencephalon ͉ Hes1 ͉ mash1 ͉ ngn1 ͉ zona limitans intrathalamica N eurogenesis in the developing vertebrate CNS is regulated with a high degree of temporal and spatial precision, with stereotypic patterns of neuronal differentiation and extensive neuronal migration (1, 2). Dynamic patterns of mitotically active neuronal precursors, known as 'neurogenetic gradients' (3) have been described in several brain regions, including the neocortex (4, 5), the dorsal midbrain colliculi (6), and the dopaminergic region of the ventral midbrain (7). In the mammalian diencephalon, in particular the thalamus (formerly known as dorsal thalamus), two main neurogenetic gradients have been described: from posterior to anterior and from lateral to medial (8,9). In rodents, all thalamic neurons are generated in about 6 days, and the orthogonal gradients of glutamatergic neurogenesis sweep across the boundaries of future nuclei. The underlying molecular mechanisms responsible for generating the neurogenetic gradients of the thalamus are unknown.The major constituent of the thalamus is a population of excitatory neurons generated in the caudal thalamus (cTh), whereas a minor population of inhibitory neurons is generated in the rostral thalamus (rTh). The latter is thought to give rise to the reticular nucleus and the ventral lateral geniculate nucleus, including the intergeniculate leaflet (10). During development, this rostro-caudal partitioning is seen in the expression domains of proneural basic helix-loop-helix (bHLH) genes: the achaete-scute-like complex genes (Ascl formerly known as Mash in mouse and Zash in zebrafish) mark the GABAergic rTh and the prethalamus (PTh) and the Neurogenin genes (Neurog, formerly known as Ngn) mark the glutamatergic cTh (2,11,12). Several lines of evidence show that these genes function as determinants of transmitter phenotype: in the mouse telencephalon, Neurog1/2 are required to ...

show abstract

Induction of neurogenin‐1 expression by sonic hedgehog: Its role in development of trigeminal sensory neurons

Cited by 31 publications

References 51 publications

Sonic Hedgehog promotes the development of multipotent neural crest progenitors endowed with both mesenchymal and neural potentials

Sonic Hedgehog promotes the development of multipotent neural crest progenitors endowed with both mesenchymal and neural potentials

High glucose alters the expression of genes involved in proliferation and cell-fate specification of embryonic neural stem cells

Her6 regulates the neurogenetic gradient and neuronal identity in the thalamus

Contact Info

Product

Resources

About