NeuroD is required for differentiation of the granule cells in the cerebellum and hippocampus

Miyata, Takaki; Maeda, Tomoko; Lee, Jacqueline E.

doi:10.1101/gad.13.13.1647

Cited by 503 publications

(492 citation statements)

References 23 publications

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“…Similar to the results of previous reports in Bax single null mice (Knudson et al, 1995), ND +/-Bax +/-and ND +/-Bax -/-did not generate any ectopic phenotype except male infertility. Most of the ND -/-Bax +/+ , ND -/-Bax +/-and ND -/-Bax -/-mice died within 3 days postpartum, suggesting that the disruption of Bax did not rescue the pancreatic cell death and resulting severe diabetes caused by the mutation of NeuroD (Miyata et al, 1999;Naya et al, 1995).…”

Section: Resultsmentioning

confidence: 99%

“…The Bcl-2 family protein Bax is required for neuronal death upon neurotrophin deprivation (Deckwerth et al, 1996). It has been suggested that the cell death of NeuroD null cerebellum, hippocampus and inner ear cells was mediated by apoptosis (Kim et al, 2001;Miyata et al, 1999). In the present study, it was examined whether the elimination of the Bax protein rescues cells from cell death.…”

Section: Introductionmentioning

confidence: 87%

“…Previously reported NeuroD null mice (ND -/-) (Miyata et al, 1999) and Bax null mice (Bax -/-) (Knud-son et al, 1995) were used in the experiments. The mice were maintained in a mixed C57BL/6J and 129/SvJ background.…”

Section: Micementioning

confidence: 99%

“…In vertebrate neurogenesis, the bHLH family is divided into cell fate determination factors and cell survival/differentiation factors (Ben-Arie et al, 1997;Fode et al, 1998;Ma et al, 1996). NeuroD expression is observed during the later stages of neurogenesis and is believed to regulate neuronal survival and maturation (Kim, 2012;Kim et al, 2001; Lee, 1997;Lee et al, 1995;Miyata et al, 1999). A series of molecular genetics studies revealed that NeuroD regulates differentiation in many neuronal tissues, including the hippocampus dentate gyrus (DG), the cerebellar granule cell layers and the developing inner ear neurons.…”

Section: Introductionmentioning

confidence: 99%

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NeuroD Regulates Neuronal Migration

Kim

2013

Molecules and Cells

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NeuroD is required for the survival of many subtypes of developing neurons in the vertebrate central nervous system. Because NeuroD-deficient neurons in the hippocampus, cerebellum, and inner ear die prematurely in the early stage of neurogenesis, the role of NeuroD during the later stages of neurogenesis of these cell subtypes is not well understood. In addition, the mechanism of NeuroDdeficient neuronal death has not been investigated. It was hypothesized that NeuroD-dependent neuronal death occurs through a Bax-dependent apoptotic pathway. Based on this hypothesis, this study attempted to rescue neuronal cell death by deleting the Bax gene in NeuroD null mice to investigate the role of NeuroD in surviving neurons. The NeuroD and Bax double null mice displayed a decrease in the number of apoptotic cells in the hippocampus and the cerebellum and the rescue of vestibulocochlear ganglion (VCG) neurons that failed to migrate and innervate. In addition, at E13.5, the NeuroD -/-Bax -/-VCG neurons failed to express TrkB and TrkC, which are known to be essential for the survival of those neurons. These data suggest that neuronal death in NeuroD null mice is mediated by Bax-dependent apoptosis and that NeuroD is required for the migration of VCG neurons. Finally, these data show that TrkB and TrkC expression in E13.5 VCG neurons requires NeuroD and that TrkB and TrkC expression may be necessary for the normal migration and innervations of those neurons.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 87%

Section: Micementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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NeuroD Regulates Neuronal Migration

Kim

2013

Molecules and Cells

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“…Ngn1 or Ngn2 single knockout mice showed complementary loss of cranial sensory ganglia, whereas the Ngn1/2 double knockout mice lacked the spinal sensory ganglia as well as a majority of ventral spinal cord neurons, due to, as for Mash1, an early defect in neurogenesis [40,45,46]. NeuroD1 null mice have defects in the granule layers of the cerebellum and hippocampus, and in the inner ear sensory neurons because of a later function of NeuroD1 in neuronal differentiation [47,48]. Understanding the mechanism of how different neural bHLH factors integrate positional information into the process of neurogenesis will facilitate the generation of multiple types of neural cells from pluripotent stem cells in vitro.…”

Section: Discussionmentioning

confidence: 99%

Visualization of bHLH transcription factor interactions in living mammalian cell nuclei and developing chicken neural tube by FRET

et al. 2006

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Expression of neuroD/BETA2 in mitotic and postmitotic neuronal cells during the development of nervous system

et al. 2000

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NeuroD/BETA2, a basic helixloop-helix transcription factor, has been shown to play a role in tissue-specific differentiation of pancreatic and enteroendocrine cells. To gain further insight into the function of neuroD/ BETA2 in the nervous system development, we examined the expression pattern of neuroD/ BETA2 during embryonic and postnatal development by using in situ hybridization. Dynamic changes of neuroD/BETA2 expression in the central nervous system were observed during embryogenesis, especially in telencephalon, hippocampus, cerebellum, spinal cord, and olfactory epithelium. Moderate level of expression was also detected in developing pancreas in early embryogenesis. Although the neuroD/BETA2 expression in cerebellum and hippocampus increased over time, expression in cerebral cortex, spinal cord, as well as in fetal pancreas gradually decreased as embryogenesis proceeded. High level of the neuroD/BETA2 expression in developing cerebellum and hippocampus persisted throughout postnatal development and remained at a stable level in the adult brain. Interestingly, neuroD/BETA2 expression was detected not only in postmitotic but also in mitotic cells, as was evident in its expression in external granular layer of cerebellum and granule cells of the dentate gyrus during postnatal development. This observation suggests that neuroD/BETA2 may have a unique role in proliferation, differentiation, or both, of granule cells of cerebellum and dentate gyrus.

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NeuroD is required for differentiation of the granule cells in the cerebellum and hippocampus

Cited by 503 publications

References 23 publications

NeuroD Regulates Neuronal Migration

NeuroD Regulates Neuronal Migration

Visualization of bHLH transcription factor interactions in living mammalian cell nuclei and developing chicken neural tube by FRET

Expression of neuroD/BETA2 in mitotic and postmitotic neuronal cells during the development of nervous system

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