Misexpression of a bHLH gene,cNSCL1, results in abnormal brain development

Li, Chuanming; Yan, Run‐Tao; Wang, Shuzhen

doi:10.1002/(sici)1097-0177(199907)215:3<238::aid-aja6>3.0.co;2-f

Cited by 24 publications

(9 citation statements)

References 30 publications

(18 reference statements)

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“…The significance of these markers at boundary cells remains to be explored. This is especially intriguing since the roles of NSCL1 in other regions of the CNS are only partially understood (Chuan-Ming et al, 1999; Theodorakis et al, 2002) and since Brn3a is mostly considered as a marker for sensory neurons (Dykes et al, 2010; Lanier et al, 2007), and therefore its expression at boundary cells is surprising. Notably, MHB-derived FGF8 is known to either promote or inhibit differentiation of different types of neural progenitors at different DV parts of the midbrain and r1 (Alexandre et al, 2006; Basson et al, 2008; Brand et al, 1996; Canning et al, 2007; Crossley et al, 1996; Jukkola et al, 2006; Liu and Joyner, 2001; Mason et al, 2000; Raible and Brand, 2004; Saarimäki-Vire et al, 2007; Wassef and Joyner, 1997; Zervas et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Expression of hindbrain boundary markers is regulated by FGF3

Weisinger¹,

Kohl²,

Kayam³

et al. 2011

Biology Open

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SummaryCompartment boundaries act as organizing centers that segregate adjacent areas into domains of gene expression and regulation, and control their distinct fates via the secretion of signalling factors. During hindbrain development, a specialized cell-population forms boundaries between rhombomeres. These boundary cells demonstrate unique morphological properties and express multiple genes that differs them from intra-rhombomeric cells. Yet, little is known regarding the mechanisms that controls the expression or function of these boundary markers.Multiple components of the FGF signaling system, including ligands, receptors, downstream effectors as well as proteoglycans are shown to localize to boundary cells in the chick hindbrain. These patterns raise the possibility that FGF signaling plays a role in regulating boundary properties. We provide evidence to the role of FGF signaling, particularly the boundary-derived FGF3, in regulating the expression of multiple markers at hindbrain boundaries. These findings enable further characterization of the unique boundary-cell population, and expose a new function for FGFs as regulators of boundary-gene expression in the chick hindbrain.

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Section: Discussionmentioning

confidence: 99%

Expression of hindbrain boundary markers is regulated by FGF3

Weisinger¹,

Kohl²,

Kayam³

et al. 2011

Biology Open

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“…Replication-competent avian (RCAS) retroviruses expressing various genes were produced as previously described [neuroD and GFP (Yan and Wang, 1998); NCSL1 (Li et al, 1999a); ngn2 ; ath5 ; and ath5 and NSCL1 coexpression through an internal ribosomal entry site ]. To generate RCAS expressing RaxL, the coding region was first amplified by reverse transcription (RT)-PCR based on the published sequence (Chen and Cepko, 2002) and cloned into pGEMT (Promega, Madison, WI).…”

Section: Methodsmentioning

confidence: 99%

A Role ofath5in InducingneuroDand the Photoreceptor Pathway

Yan²,

Xie³

et al. 2004

J. Neurosci.

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Photoreceptors in the vertebrate retina are light-sensitive neurons, and their degeneration results in irreversible visual loss. Understanding how photoreceptor fate is determined is a prerequisite for developing photoreceptor replacement therapies. Previous studies identified two basic helix-loop-helix genes, neurogenin2 (ngn2) and neuroD, participating in a genetic pathway leading to photoreceptor genesis. Here we present experimental data suggesting that ath5, which is known for its critical role in retinal ganglion cell development, may also lead to photoreceptor production. In the developing retina, ath5 expression was detected in two zones of cells, and coexpression with neuroD was observed in the zone adjacent to young photoreceptor cells accumulating on the retinal pigment epithelial side. Retroviral-driven misexpression of ath5 in retinal cells increased the population of photoreceptor cells, as well as ganglion cells, in a developmental stage-dependent manner that is consistent with ath5 being involved in the development of multiple types of retinal neurons. Ectopic ath5 expression in cultures of non-neural retinal pigment epithelial cells elicited transdifferentiation into cells that expressed photoreceptor-specific genes and displayed photoreceptor-like morphologies. Gene expression analysis showed that ngn2 did not induce ath5, and ath5 did not induce ngn2, but both induced neuroD and RaxL. These data suggest a pathway of "ath5 3 neuroD 3 photoreceptor genes" separate from yet convergent with the ngn2 pathway.

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“…Four hours later, the eyes were fixed. Cryosections were subjected to in situ hybridization with antisense RNA probes against ngn2, followed by immunocytochemistry with a mAb against BrdUrd, as described (35).…”

Section: Methodsmentioning

confidence: 99%

neurogenin2 elicits the genesis of retinal neurons from cultures of nonneural cells

Yan

Wang

2001

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

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neurogenin2 (ngn2) encodes a basic helix-loop-helix transcription factor and plays an important role in neurogenesis from migratory neural crest cells. Its role in retinal development is poorly understood. We observed that in the developing chick retina, ngn2 was expressed in a subpopulation of proliferating progenitor cells. Ectopic expression of ngn2 in nonneural, retinal pigment epithelial cell culture triggered de novo generation of cells that expressed neural-specific markers and exhibited neuronal morphologies. Further molecular and morphological analyses showed that the main products of the induced neurogenesis were cells resembling young photoreceptor cells and cells resembling retinal ganglion cells. The generation of multiple cell types suggests that ngn2 induces various retinal pathways. Thus, unlike in the peripheral nervous system where ngn2 specifies one type of sensory neuron, ngn2 in the retina is likely involved in a common step leading to different cellular pathways. Our finding that ngn2 can instruct nonneural retinal pigment epithelial cells to differentiate toward retinal neurons demonstrates one possible way to induce de novo retinal neurogenesis.

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Misexpression of a bHLH gene,cNSCL1, results in abnormal brain development

Cited by 24 publications

References 30 publications

Expression of hindbrain boundary markers is regulated by FGF3

Expression of hindbrain boundary markers is regulated by FGF3

A Role ofath5in InducingneuroDand the Photoreceptor Pathway

neurogenin2 elicits the genesis of retinal neurons from cultures of nonneural cells

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