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|Coordinate||79,454,595 bp (GRCm38)|
|Base Change||T ⇒ A (forward strand)|
|Gene Name||neurogenic differentiation 1|
|Synonym(s)||bHLHa3, BETA2, Neurod|
|Chromosomal Location||79,452,521-79,456,751 bp (-)|
|MGI Phenotype||Homozygotes for targeted null mutations exhibit neonatal diabetes, pancreatic enteroendocrine cell deficits, impaired hearing and balance, retinal degeneration, and seizures. Survival past birth is dependent on genetic background.|
|Amino Acid Change||Asparagine changed to Isoleucine|
|Institutional Source||Beutler Lab|
|Gene Model||predicted gene model for protein(s): [ENSMUSP00000040364]|
AA Change: N148I
|Predicted Effect||probably damaging
PolyPhen 2 Score 1.000 (Sensitivity: 0.00; Specificity: 1.00)
|Phenotypic Category||behavior/neurological, hearing/vestibular/ear|
|Alleles Listed at MGI|
|Mode of Inheritance||Autosomal Recessive|
|Local Stock||Live Mice|
|Last Updated||03/01/2017 12:00 PM by Anne Murray|
|Record Created||03/10/2016 2:33 PM by Jamie Russell|
The cruz phenotype was identified among G3 mice of the pedigree R3795, some of which showed hyperactivity and head tossing (Figure 1).
|Nature of Mutation|
Whole exome HiSeq sequencing of the G1 grandsire identified 37 mutations. The behavioral phenotypes were linked to a mutation in Neurod1: an A to T transversion at base pair 79,454,595 (v38) on chromosome 2, or base pair 2,042 in the GenBank genomic region NC_000068 encoding Neurod1. Linkage was found with a recessive model of inheritance (P = 0.001777), wherein three affected mice were homozygous for the variant allele, and 19 unaffected mice were either heterozygous (N = 17) or homozygous for the reference allele (N = 11); the genotyping of one unaffected mouse failed at all reads (Figure 2).
The mutation corresponds to residue 540 in the NM_010894 mRNA sequence in exon 2 of 2 total exons.
The mutated nucleotide is indicated in red. The mutation results in an asparagine (N) to isoleucine (I) substitution at position 148 (N148I) in the NeuroD protein, and is strongly predicted by PolyPhen-2 to be damaging (score = 1.000).
Neurod1 encodes NeuroD (alternatively, BETA2), a basic helix-loop-helix (bHLH) transcription factor. bHLH proteins have a DNA binding domain and a helix-loop-helix (HLH) domain (Figure 3). The bHLH transcription factors bind a specific E-box DNA sequence, CANNTG, in target genes through their DNA binding domain (1). bHLH transcription factors typically heterodimerize with other bHLH transcription factors (e.g., E12/E47) through interactions with their respective HLH domains (Figure 4) (2). In addition to the DNA binding domain and the HLH domain, NeuroD has a nuclear localization sequence at amino acids 87 to 93.
NeuroD activity is regulated by several factors. NeuroD is acetylated by p300-associated factor (PCAF) (3). NeuroD acetylation is proposed to regulate NeuroD-associated insulin gene regulation and other functions of NeuroD. NeuroD undergoes O-linked glycosylation upon exposure to glucose, which regulates the subcellular localization of NeuroD in pancreatic beta cells (4). GSK3β is proposed to phosphorylate NeuroD at Ser274, which may inhibit NeuroD activity (5;6). The GSK3β consensus site in NeuroD is flanked by an ERK consensus sequence. ERK2 phosphorylates NeuroD at Ser162, Ser259, Ser266, and Ser274 (7). Phosphorylation at these sites can either stimulate or inhibit NeuroD activity depending on the cell or tissue in which NeuroD is expressed. CaMKII (see the record for frantic) phosphorylates NeuroD at Ser336. Mixed-lineage kinase 2 (MLK2) can also phosphorylate NeuroD, resulting in NeuroD stimulation. In Xenopus, Huntingtin protein and Huntington-associated protein 1 (HAP1) interact with NeuroD, subsequently facilitating MLK2-associated NeuroD activation (8). In Xenopus, Id proteins inhibit NeuroD activity (9). NeuroD association with small heterodimer partner (SHP) represses NeuroD-associated reporter activity and p300-enhanced NeuroD transcriptional activity by interfering with p300 (10). Cyclin D is recruited to NeuroD through binding to p300. Cyclin D association with NeuroD represses NeuroD activity (11).
The cruz mutation results in an asparagine (N) to isoleucine (I) substitution at position 148 (N148I). Residue 148 is within the HLH domain.
NeuroD is highly expressed in developing neurons of the peripheral and central nervous systems. During embryonic development, NeuroD is expressed in developing amacrine cells and photoreceptor cells of the retina; NeuroD is also expressed in a subset of mature photoreceptors. NeuroD is expressed in pancreatic endocrine cells as well as endocrine cell lineages in the intestine and brain (12). In the mouse pancreas, Neurod1 is expressed in beta cells throughout development (13). In the adult mouse pancreas, Neurod1 is expressed in mature beta cells and a small fraction (1 to 2%) of alpha cells, but not in delta or PP cells (13). NeuroD is expressed in neuroendocrine cells of the stomach, gut, and lung (13;14). NeuroD is expressed in limbic, hypothalamic, thalamic, cerebral cortical, olfactory/vomeronasal, and hippocampal pyramidal neurons [reviewed in (15)]. NeuroD is also highly expressed in the developing and adult rat pineal gland (16).
NeuroD is essential for the proper development of the nervous and endocrine systems as well as for epithelial-to-mesenchymal transition (17). NeuroD is a neurogenesis differentiation factor that is transiently expressed in the neurons of the central and nervous systems during terminal differentiation into mature neurons (Figure 5) (18). NeuroD activates neuronal differentiation genes by binding directly to regulatory elements in the promoters of the target genes (17). Binding of NeuroD heterodimers to target promoters results in loss of the Polycomb group-associated repressive mark H3K27me3 and loss of repressor protein (e.g., TBX3 and MBD3) binding (17). Concomitantly, there is gain of the active mark H3K27ac and increased chromatin accessibility followed by induced gene expression. In neural precursor cells, NeuroD promotes premature cell cycle exit and differentiation (18). NeuroD is essential for the survival and differentiation of olfactory bulb neurons (19;20). Mice expressing an inducible stem cell-specific deletion of Neurod1 exhibited diminished neuron differentiation in the hippocampus and olfactory bulb (19).
NeuroD is also required for amacrine cell and photoreceptor cell differentiation and survival in the retina (21;22). Neurod1-/- mice exhibited a reduction in amacrine cell differentiation with a concomitant increase in bipolar interneurons (23). Overexpression of NeuroD in retinal explant cultures led to an increased frequency of rod photoreceptor cells (24). Loss of NeuroD expression in cultured retinal cells led to death of a subset of rod photoreceptors, increased number of bipolar cells, delayed amacrine cell differentiation, and increased gliogenesis (23). Neurod1-/- mice exhibited reduced retinal function when assessed by both rod- and cone-driven electroretinograms (21).
NeuroD binds to the E-box binding site in the insulin promoter, which stimulates transcription (Figure 6) (12). In addition, NeuroD is required for proper differentiation of pancreatic islet cells (25). Neurod1-/- mice (129sv/J and C57BL6 mixed genetic background) die by postnatal day five due to severe hyperglycemia (13). Endocrine cells in the Neurod1-/- mice fail to form islets and beta cells undergo cell death starting around embryonic day 17.5; remaining beta cells do not produce enough insulin. Backcrossing Neurod1 heterozygous mice to mice of the 129sv/J strain resulted in more than 60% of the Neurod1-/- mice to survive beyond the neonate stage (26;27); the Neurod1-/- mice on the 129/SvJ genetic background are slightly hyperglycemic and by three weeks of age insulin levels are at normal values (26). NeuroD promotes transcription of the sulfonylurea receptor (SUR1), which forms a potassium channel with Kir6.2 (28). In response to glucose, the potassium channel closes, leading to increased levels of intracellular calcium. Increased calcium is essential for the activation of transcription factors in mature beta cells that promote the transcription of factors that elevate insulin secretion upon glucose stimulation.
There are several NeuroD target genes, which mediate endocrine-related functions or neuronal differentiation (Table 1).
Mutations in NEUROD1 are linked to maturity-onset diabetes of the young 6 (OMIM: #606394) (43) and noninsulin-dependent diabetes mellitus (OMIM: #125853) (44-46). In addition, mutations in NEUROD1 have been attributed to cases of nonsyndromic autosomal recessive retinitis pigmentosa (47). One study described a patient with a NEUROD1 mutation that exhibited permanent neonatal diabetes and a consistent pattern of neurological abnormalities including cerebellar hypoplasia, learning difficulties, sensorineural deafness, and visual impairment (44).
NeuroD functions in inner ear development by promoting the survival and differentiation of inner ear sensory neurons (48-50). Neurod1-deficient (Neurod1-/-) mice exhibited loss of sound response, hyperactivity, head tilting, circling, spontaneous seizures, impaired motor coordination (i.e., hindlimb clutching when suspended), and ataxia due to a reduction of sensory neurons in the cochlear-vestibular ganglion as well as cerebellar defects (49;51;52). Conditional deletion of Neurod1 in the inner ear resulted in formation of hair cells within the inner ear sensory ganglia (53). The aberrant formation of hair cells in the inner ear was proposed to be due to loss of the suppressive function of NeuroD on hair cell differentiation in sensory ganglia (53). Loss of NeuroD expression in the inner ear led to loss of spiral and many vestibular neurons as well as defects in the projection of vestibular and cochlear afferents, which resulted in the vestibular and cochlear afferents entering the cochlear nucleus as a single mixed nerve (54).
cruz(F):5'- GGGCTTTCAAAGAAGGGCTC -3'
cruz(R):5'- AGGACGAGCTTGAAGCCATG -3'
cruz_seq(F):5'- CTTTCAAAGAAGGGCTCCAGAG -3'
cruz_seq(R):5'- CGAGCTTGAAGCCATGAATGC -3'
1. Mehmood, R., Yasuhara, N., Oe, S., Nagai, M., and Yoneda, Y. (2009) Synergistic Nuclear Import of NeuroD1 and its Partner Transcription Factor, E47, Via Heterodimerization. Exp Cell Res. 315, 1639-1652.
2. Longo, A., Guanga, G. P., and Rose, R. B. (2008) Crystal Structure of E47-NeuroD1/beta2 bHLH Domain-DNA Complex: Heterodimer Selectivity and DNA Recognition. Biochemistry. 47, 218-229.
3. Qiu, Y., Guo, M., Huang, S., and Stein, R. (2004) Acetylation of the BETA2 Transcription Factor by p300-Associated Factor is Important in Insulin Gene Expression. J Biol Chem. 279, 9796-9802.
4. Andrali, S. S., Qian, Q., and Ozcan, S. (2007) Glucose Mediates the Translocation of NeuroD1 by O-Linked Glycosylation. J Biol Chem. 282, 15589-15596.
5. Marcus, E. A., Kintner, C., and Harris, W. (1998) The Role of GSK3beta in Regulating Neuronal Differentiation in Xenopus Laevis. Mol Cell Neurosci. 12, 269-280.
6. Moore, K. B., Schneider, M. L., and Vetter, M. L. (2002) Posttranslational Mechanisms Control the Timing of bHLH Function and Regulate Retinal Cell Fate. Neuron. 34, 183-195.
7. Khoo, S., Griffen, S. C., Xia, Y., Baer, R. J., German, M. S., and Cobb, M. H. (2003) Regulation of Insulin Gene Transcription by ERK1 and ERK2 in Pancreatic Beta Cells. J Biol Chem. 278, 32969-32977.
8. Marcora, E., Gowan, K., and Lee, J. E. (2003) Stimulation of NeuroD Activity by Huntingtin and Huntingtin-Associated Proteins HAP1 and MLK2. Proc Natl Acad Sci U S A. 100, 9578-9583.
9. Liu, K. J., and Harland, R. M. (2003) Cloning and Characterization of Xenopus Id4 Reveals Differing Roles for Id Genes. Dev Biol. 264, 339-351.
10. Kim, J. Y., Chu, K., Kim, H. J., Seong, H. A., Park, K. C., Sanyal, S., Takeda, J., Ha, H., Shong, M., Tsai, M. J., and Choi, H. S. (2004) Orphan Nuclear Receptor Small Heterodimer Partner, a Novel Corepressor for a Basic Helix-Loop-Helix Transcription Factor BETA2/neuroD. Mol Endocrinol. 18, 776-790.
11. Ratineau, C., Petry, M. W., Mutoh, H., and Leiter, A. B. (2002) Cyclin D1 Represses the Basic Helix-Loop-Helix Transcription Factor, BETA2/NeuroD. J Biol Chem. 277, 8847-8853.
12. Naya, F. J., Stellrecht, C. M., and Tsai, M. J. (1995) Tissue-Specific Regulation of the Insulin Gene by a Novel Basic Helix-Loop-Helix Transcription Factor. Genes Dev. 9, 1009-1019.
13. Naya, F. J., Huang, H. P., Qiu, Y., Mutoh, H., DeMayo, F. J., Leiter, A. B., and Tsai, M. J. (1997) Diabetes, Defective Pancreatic Morphogenesis, and Abnormal Enteroendocrine Differentiation in BETA2/neuroD-Deficient Mice. Genes Dev. 11, 2323-2334.
14. Ito, T., Udaka, N., Yazawa, T., Okudela, K., Hayashi, H., Sudo, T., Guillemot, F., Kageyama, R., and Kitamura, H. (2000) Basic Helix-Loop-Helix Transcription Factors Regulate the Neuroendocrine Differentiation of Fetal Mouse Pulmonary Epithelium. Development. 127, 3913-3921.
15. Chae, J. H., Stein, G. H., and Lee, J. E. (2004) NeuroD: The Predicted and the Surprising. Mol Cells. 18, 271-288.
16. Munoz, E. M., Bailey, M. J., Rath, M. F., Shi, Q., Morin, F., Coon, S. L., Moller, M., and Klein, D. C. (2007) NeuroD1: Developmental Expression and Regulated Genes in the Rodent Pineal Gland. J Neurochem. 102, 887-899.
17. Pataskar, A., Jung, J., Smialowski, P., Noack, F., Calegari, F., Straub, T., and Tiwari, V. K. (2016) NeuroD1 Reprograms Chromatin and Transcription Factor Landscapes to Induce the Neuronal Program. EMBO J. 35, 24-45.
18. Lee, J. E., Hollenberg, S. M., Snider, L., Turner, D. L., Lipnick, N., and Weintraub, H. (1995) Conversion of Xenopus Ectoderm into Neurons by NeuroD, a Basic Helix-Loop-Helix Protein. Science. 268, 836-844.
19. Gao, Z., Ure, K., Ables, J. L., Lagace, D. C., Nave, K. A., Goebbels, S., Eisch, A. J., and Hsieh, J. (2009) Neurod1 is Essential for the Survival and Maturation of Adult-Born Neurons. Nat Neurosci. 12, 1090-1092.
20. Boutin, C., Hardt, O., de Chevigny, A., Core, N., Goebbels, S., Seidenfaden, R., Bosio, A., and Cremer, H. (2010) NeuroD1 Induces Terminal Neuronal Differentiation in Olfactory Neurogenesis. Proc Natl Acad Sci U S A. 107, 1201-1206.
21. Pennesi, M. E., Cho, J. H., Yang, Z., Wu, S. H., Zhang, J., Wu, S. M., and Tsai, M. J. (2003) BETA2/NeuroD1 Null Mice: A New Model for Transcription Factor-Dependent Photoreceptor Degeneration. J Neurosci. 23, 453-461.
22. Cherry, T. J., Wang, S., Bormuth, I., Schwab, M., Olson, J., and Cepko, C. L. (2011) NeuroD Factors Regulate Cell Fate and Neurite Stratification in the Developing Retina. J Neurosci. 31, 7365-7379.
23. Morrow, E. M., Furukawa, T., Lee, J. E., and Cepko, C. L. (1999) NeuroD Regulates Multiple Functions in the Developing Neural Retina in Rodent. Development. 126, 23-36.
24. Yan, R. T., and Wang, S. Z. (1998) NeuroD Induces Photoreceptor Cell Overproduction in Vivo and De Novo Generation in Vitro. J Neurobiol. 36, 485-496.
25. Chao, C. S., Loomis, Z. L., Lee, J. E., and Sussel, L. (2007) Genetic Identification of a Novel NeuroD1 Function in the Early Differentiation of Islet Alpha, PP and Epsilon Cells. Dev Biol. 312, 523-532.
26. Liu, M., Pleasure, S. J., Collins, A. E., Noebels, J. L., Naya, F. J., Tsai, M. J., and Lowenstein, D. H. (2000) Loss of BETA2/NeuroD Leads to Malformation of the Dentate Gyrus and Epilepsy. Proc Natl Acad Sci U S A. 97, 865-870.
27. Huang, H. P., Chu, K., Nemoz-Gaillard, E., Elberg, D., and Tsai, M. J. (2002) Neogenesis of Beta-Cells in Adult BETA2/NeuroD-Deficient Mice. Mol Endocrinol. 16, 541-551.
28. Kim, J. W., Seghers, V., Cho, J. H., Kang, Y., Kim, S., Ryu, Y., Baek, K., Aguilar-Bryan, L., Lee, Y. D., Bryan, J., and Suh-Kim, H. (2002) Transactivation of the Mouse Sulfonylurea Receptor I Gene by BETA2/NeuroD. Mol Endocrinol. 16, 1097-1107.
29. Poulin, G., Turgeon, B., and Drouin, J. (1997) NeuroD1/beta2 Contributes to Cell-Specific Transcription of the Proopiomelanocortin Gene. Mol Cell Biol. 17, 6673-6682.
30. Sharma, S., Jhala, U. S., Johnson, T., Ferreri, K., Leonard, J., and Montminy, M. (1997) Hormonal Regulation of an Islet-Specific Enhancer in the Pancreatic Homeobox Gene STF-1. Mol Cell Biol. 17, 2598-2604.
31. Mutoh, H., Fung, B. P., Naya, F. J., Tsai, M. J., Nishitani, J., and Leiter, A. B. (1997) The Basic Helix-Loop-Helix Transcription Factor BETA2/NeuroD is Expressed in Mammalian Enteroendocrine Cells and Activates Secretin Gene Expression. Proc Natl Acad Sci U S A. 94, 3560-3564.
32. Itkin-Ansari, P., Marcora, E., Geron, I., Tyrberg, B., Demeterco, C., Hao, E., Padilla, C., Ratineau, C., Leiter, A., Lee, J. E., and Levine, F. (2005) NeuroD1 in the Endocrine Pancreas: Localization and Dual Function as an Activator and Repressor. Dev Dyn. 233, 946-953.
33. Lieberman, S. M., Evans, A. M., Han, B., Takaki, T., Vinnitskaya, Y., Caldwell, J. A., Serreze, D. V., Shabanowitz, J., Hunt, D. F., Nathenson, S. G., Santamaria, P., and DiLorenzo, T. P. (2003) Identification of the Beta Cell Antigen Targeted by a Prevalent Population of Pathogenic CD8+ T Cells in Autoimmune Diabetes. Proc Natl Acad Sci U S A. 100, 8384-8388.
34. Moates, J. M., Nanda, S., Cissell, M. A., Tsai, M. J., and Stein, R. (2003) BETA2 Activates Transcription from the Upstream Glucokinase Gene Promoter in Islet Beta-Cells and Gut Endocrine Cells. Diabetes. 52, 403-408.
35. Martin, C. C., Svitek, C. A., Oeser, J. K., Henderson, E., Stein, R., and O'Brien, R. M. (2003) Upstream Stimulatory Factor (USF) and Neurogenic differentiation/beta-Cell E Box Transactivator 2 (NeuroD/BETA2) Contribute to Islet-Specific Glucose-6-Phosphatase Catalytic-Subunit-Related Protein (IGRP) Gene Expression. Biochem J. 371, 675-686.
36. Noma, T., Yoon, Y. S., and Nakazawa, A. (1999) Overexpression of NeuroD in PC12 Cells Alters Morphology and Enhances Expression of the Adenylate Kinase Isozyme 1 Gene. Brain Res Mol Brain Res. 67, 53-63.
37. Konishi, Y., Ohkawa, N., Makino, Y., Ohkubo, H., Kageyama, R., Furuichi, T., Mikoshiba, K., and Tamura, T. (1999) Transcriptional Regulation of Mouse Type 1 Inositol 1,4,5-Trisphosphate Receptor Gene by NeuroD-Related Factor. J Neurochem. 72, 1717-1724.
38. Hutcheson, D. A., and Vetter, M. L. (2001) The bHLH Factors Xath5 and XNeuroD can Upregulate the Expression of XBrn3d, a POU-Homeodomain Transcription Factor. Dev Biol. 232, 327-338.
39. Pozzoli, O., Bosetti, A., Croci, L., Consalez, G. G., and Vetter, M. L. (2001) Xebf3 is a Regulator of Neuronal Differentiation during Primary Neurogenesis in Xenopus. Dev Biol. 233, 495-512.
40. Kim, W. Y. (2012) NeuroD1 is an Upstream Regulator of NSCL1. Biochem Biophys Res Commun. 419, 27-31.
42. Huang, P., Kishida, S., Cao, D., Murakami-Tonami, Y., Mu, P., Nakaguro, M., Koide, N., Takeuchi, I., Onishi, A., and Kadomatsu, K. (2011) The Neuronal Differentiation Factor NeuroD1 Downregulates the Neuronal Repellent Factor Slit2 Expression and Promotes Cell Motility and Tumor Formation of Neuroblastoma. Cancer Res. 71, 2938-2948.
43. Malecki, M. T., Jhala, U. S., Antonellis, A., Fields, L., Doria, A., Orban, T., Saad, M., Warram, J. H., Montminy, M., and Krolewski, A. S. (1999) Mutations in NEUROD1 are Associated with the Development of Type 2 Diabetes Mellitus. Nat Genet. 23, 323-328.
44. Rubio-Cabezas, O., Minton, J. A., Kantor, I., Williams, D., Ellard, S., and Hattersley, A. T. (2010) Homozygous Mutations in NEUROD1 are Responsible for a Novel Syndrome of Permanent Neonatal Diabetes and Neurological Abnormalities. Diabetes. 59, 2326-2331.
45. Hansen, L., Jensen, J. N., Urioste, S., Petersen, H. V., Pociot, F., Eiberg, H., Kristiansen, O. P., Hansen, T., Serup, P., Nerup, J., and Pedersen, O. (2000) NeuroD/BETA2 Gene Variability and Diabetes: No Associations to Late-Onset Type 2 Diabetes but an A45 Allele may Represent a Susceptibility Marker for Type 1 Diabetes among Danes. Danish Study Group of Diabetes in Childhood, and the Danish IDDM Epidemiology and Genetics Group. Diabetes. 49, 876-878.
46. Cinek, O., Drevinek, P., Sumnik, Z., Bendlova, B., Sedlakova, P., Kolouskova, S., Snajderova, M., and Vavrinec, J. (2003) NEUROD Polymorphism Ala45Thr is Associated with Type 1 Diabetes Mellitus in Czech Children. Diabetes Res Clin Pract. 60, 49-56.
47. Wang, F., Li, H., Xu, M., Li, H., Zhao, L., Yang, L., Zaneveld, J. E., Wang, K., Li, Y., Sui, R., and Chen, R. (2014) A Homozygous Missense Mutation in NEUROD1 is Associated with Nonsyndromic Autosomal Recessive Retinitis Pigmentosa. Invest Ophthalmol Vis Sci. 56, 150-155.
48. Fritzsch, B. (2003) Development of Inner Ear Afferent Connections: Forming Primary Neurons and Connecting them to the Developing Sensory Epithelia. Brain Res Bull. 60, 423-433.
49. Liu, M., Pereira, F. A., Price, S. D., Chu, M. J., Shope, C., Himes, D., Eatock, R. A., Brownell, W. E., Lysakowski, A., and Tsai, M. J. (2000) Essential Role of BETA2/NeuroD1 in Development of the Vestibular and Auditory Systems. Genes Dev. 14, 2839-2854.
50. Kim, W. Y., Fritzsch, B., Serls, A., Bakel, L. A., Huang, E. J., Reichardt, L. F., Barth, D. S., and Lee, J. E. (2001) NeuroD-Null Mice are Deaf due to a Severe Loss of the Inner Ear Sensory Neurons during Development. Development. 128, 417-426.
51. Crawley, J. N., and Paylor, R. (1997) A Proposed Test Battery and Constellations of Specific Behavioral Paradigms to Investigate the Behavioral Phenotypes of Transgenic and Knockout Mice. Horm Behav. 31, 197-211.
52. Miyata, T., Maeda, T., and Lee, J. E. (1999) NeuroD is Required for Differentiation of the Granule Cells in the Cerebellum and Hippocampus. Genes Dev. 13, 1647-1652.
53. Jahan, I., Pan, N., Kersigo, J., and Fritzsch, B. (2010) Neurod1 Suppresses Hair Cell Differentiation in Ear Ganglia and Regulates Hair Cell Subtype Development in the Cochlea. PLoS One. 5, e11661.
|Science Writers||Anne Murray|
|Authors||Marleen de Groot, Jamie Russell, and Bruce Beutler|
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