The big brain gene of Drosophila functions to control the number of neuronal precursors in the peripheral nervous system

Development ◽  
1992 ◽  
Vol 116 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Y. Rao ◽  
R. Bodmer ◽  
L.Y. Jan ◽  
Y.N. Jan
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Cell Fate ◽  
Neural Development ◽  
Mutant Phenotype ◽  
Neurogenic Genes ◽  
Neuronal Precursors ◽  
Sensory Nervous System ◽  
The One ◽  
Multiple Stages

big brain (bib) is one of the six known zygotic neurogenic genes involved in the decision of an ectodermal cell to take on the neurogenic or the epidermogenic cell fate. Previous studies suggest that bib functions in a pathway separate from the one involving Notch and other known neurogenic genes. For a better understanding of the bib function, it is essential first to characterize the mutant phenotype in detail. Our mutant analyses show that loss of bib function approximately doubles the number of neuronal precursors and their progeny cells in the embryonic peripheral nervous system. Mosaic studies reveal a hypertrophy of sensory bristles in bib mutant patches in adult flies. Our observations are compatible with a function of bib in specifying neuronal precursors of both the embryonic and adult sensory nervous system. This is in contrast to the function of Notch, which continues to be required at multiple stages of neural development subsequent to this initial determination event.

scholarly journals A Gain-of-Function Screen for Genes That Affect the Development of the Drosophila Adult External Sensory Organ

Genetics ◽  
2000 ◽  
Vol 155 (2) ◽  
pp. 733-752 ◽  
Author(s):  
Salim Abdelilah-Seyfried ◽  
Yee-Ming Chan ◽  
Chaoyang Zeng ◽  
Nicholas J Justice ◽  
Susan Younger-Shepherd ◽  
...  
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Cell Fate ◽  
P Element ◽  
External Support ◽  
Sensory Organ ◽  
Sensory Organs ◽  
Gain Of Function ◽  
Asymmetric Cell Divisions ◽  
Single Precursor

Abstract The Drosophila adult external sensory organ, comprising a neuron and its support cells, is derived from a single precursor cell via several asymmetric cell divisions. To identify molecules involved in sensory organ development, we conducted a tissue-specific gain-of-function screen. We screened 2293 independent P-element lines established by P. Rørth and identified 105 lines, carrying insertions at 78 distinct loci, that produced misexpression phenotypes with changes in number, fate, or morphology of cells of the adult external sensory organ. On the basis of the gain-of-function phenotypes of both internal and external support cells, we subdivided the candidate lines into three classes. The first class (52 lines, 40 loci) exhibits partial or complete loss of adult external sensory organs. The second class (38 lines, 28 loci) is associated with increased numbers of entire adult external sensory organs or subsets of sensory organ cells. The third class (15 lines, 10 loci) results in potential cell fate transformations. Genetic and molecular characterization of these candidate lines reveals that some loci identified in this screen correspond to genes known to function in the formation of the peripheral nervous system, such as big brain, extra macrochaetae, and numb. Also emerging from the screen are a large group of previously uncharacterized genes and several known genes that have not yet been implicated in the development of the peripheral nervous system.

Glide directs glial fate commitment and cell fate switch between neurones and glia

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 131-139 ◽  
Author(s):  
S. Vincent ◽  
J.L. Vonesch ◽  
A. Giangrande
Keyword(s):  
Nervous System ◽  
Drosophila Melanogaster ◽  
Peripheral Nervous System ◽  
Glial Cell ◽  
Cell Fate ◽  
Glial Cells ◽  
Neuronal Development ◽  
Precursor Cells ◽  
A Cell ◽  
Glial Fate

Glial cells constitute the second component of the nervous system and are important during neuronal development. In this paper we describe a gene, glial cell deficient, (glide), that is necessary for glial cell fate commitment in Drosophila melanogaster. Mutations at the glide locus prevent glial cell determination in the embryonic central and peripheral nervous system. Moreover, we show that the absence of glial cells is the consequence of a cell fate switch from glia to neurones. This suggests the existence of a multipotent precursor cells in the nervous system. glide mutants also display defects in axonal navigation, which confirms and extends previous results indicating a role for glial cells in these processes.

Alternative cell fate choice induced by low-level expression of a regulator of protein phosphatase 2A in the Drosophila peripheral nervous system

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1591-1599 ◽  
Author(s):  
K. Shiomi ◽  
M. Takeichi ◽  
Y. Nishida ◽  
Y. Nishi ◽  
T. Uemura
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Cell Fate ◽  
Protein Phosphatase ◽  
Regulatory Subunit ◽  
Loss Of Function ◽  
B Subunit ◽  
Accessory Cells ◽  
Phosphatase 2A ◽  
Altered Cell

The Drosophila gene twins encodes the regulatory B subunit of type 2A protein phosphatase. Here we report that its partial loss-of-function mutations caused abnormal morphogenesis in the adult peripheral nervous system. In wild-type flies, the mechanoreceptor, one major class of sensory organs, is composed of four specialized cells (one neuron and three accessory cells) that are derived from a single precursor cell. The hypomorphic twins mutations did not block division of this precursor, but most likely altered cell fate in this lineage to produce only accessory cells that form sensory structures. Stepwise reductions of twins protein enhanced this transformation. In these mutants, another regulatory subunit, A, and the catalytic subunit, C, of the phosphatase were expressed at normal levels. Therefore, the modulation of the phosphatase activity by the B subunit appears to be crucial for specification of neural cell identity.

scholarly journals Isolation of a Murine Homologue of the Drosophila neuralized Gene, a Gene Required for Axonemal Integrity in Spermatozoa and Terminal Maturation of the Mammary Gland

2001 ◽  
Vol 21 (21) ◽  
pp. 7481-7494 ◽  
Author(s):  
Benedikt Vollrath ◽  
Jeffrey Pudney ◽  
Sylvia Asa ◽  
Philip Leder ◽  
Kevin Fitzgerald
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mammary Gland ◽  
Cell Fate ◽  
Suppressor Gene ◽  
Neurogenic Genes ◽  
Malignant Astrocytomas ◽  
Tail Movement ◽  
Murine Homologue ◽  
The Central Nervous System

ABSTRACT The Drosophila neuralized gene shows genetic interactions with Notch, Enhancer of split, and other neurogenic genes and is thought to be involved in cell fate specification in the central nervous system and the mesoderm. In addition, a human homologue of the Drosophila neuralizedgene has been described as a potential tumor suppressor gene in malignant astrocytomas. We have isolated a murine homologue of theDrosophila and human Neuralized genes and, in an effort to understand its physiological function, derived mice with a targeted deletion of this gene. Surprisingly, mice homozygous for the introduced mutation do not show aberrant cell fate specifications in the central nervous system or in the developing mesoderm. This is in contrast to mice with targeted deletions in other vertebrate homologues of neurogenic genes such as Notch, Delta, andCbf-1. Male Neuralized null mice, however, are sterile due to a defect in axoneme organization in the spermatozoa that leads to highly compromised tail movement and sperm immotility. In addition, female Neuralized null animals are defective in the final stages of mammary gland maturation during pregnancy.

scholarly journals p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 1027-1033 ◽  
Author(s):  
K.F. Lee ◽  
A.M. Davies ◽  
R. Jaenisch
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Neural Development ◽  
Dorsal Root ◽  
Sympathetic Neurons ◽  
Mutant Mice ◽  
Neurotrophin Receptor ◽  
Cervical Ganglion ◽  
Response Specificity

To understand the role of low-affinity neurotrophin receptor p75 in neural development, we previously generated mice carrying a null mutation in the p75 locus (Lee, K. F., Li, E., Huber, L. J., Landis, S. C., Sharpe, A. H., Chao, M. V. and Jaenisch, R. (1992) Cell 69, 737–749). To elucidate the mechanisms leading to deficits in the peripheral nervous system in p75 mutant mice, we have employed dissociated cultures to examine the responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. We found that p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 (E15) and postnatal day 3 (P3), respectively, ages that coincide with the peak of naturally occurring cell death. Furthermore, while p75-deficient E15 DRG neurons did not change their response specificity to BDNF, NT-3, and NT-4/5, P3 SCG neurons became more responsive to NT-3 at higher concentrations (nanomolar ranges). These results may help explain the deficits in the peripheral nervous system in p75 mutant mice and provide evidence that p75 can modulate neurotrophin sensitivity in some neurons.

scholarly journals ngn-1/neurogenin Activates Transcription of Multiple Terminal Selector Transcription Factors in the Caenorhabditis elegans Nervous System

2020 ◽  
Vol 10 (6) ◽  
pp. 1949-1962 ◽  
Author(s):  
Elyse L. Christensen ◽  
Alexandra Beasley ◽  
Jessica Radchuk ◽  
Zachery E. Mielko ◽  
Elicia Preston ◽  
...  
Keyword(s):  
Nervous System ◽  
Transcription Factors ◽  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Neural Development ◽  
System Development ◽  
Neuronal Cell ◽  
Nervous System Development ◽  
Link Type ◽  
Neuroblast Migration

Proper nervous system development is required for an organism’s survival and function. Defects in neurogenesis have been linked to neurodevelopmental disorders such as schizophrenia and autism. Understanding the gene regulatory networks that orchestrate neural development, specifically cascades of proneural transcription factors, can better elucidate which genes are most important during early neurogenesis. Neurogenins are a family of deeply conserved factors shown to be both necessary and sufficient for the development of neural subtypes. However, the immediate downstream targets of neurogenin are not well characterized. The objective of this study was to further elucidate the role of ngn-1/neurogenin in nervous system development and to identify its downstream transcriptional targets, using the nematode Caenorhabditis elegans as a model for this work. We found that ngn-1 is required for axon outgrowth, nerve ring architecture, and neuronal cell fate specification. We also showed that ngn-1 may have roles in neuroblast migration and epithelial integrity during embryonic development. Using RNA sequencing and comparative transcriptome analysis, we identified eight transcription factors (hlh-34/NPAS1, unc-42/PROP1, ceh-17/PHOX2A, lim-4/LHX6, fax-1/NR2E3, lin-11/LHX1, tlp-1/ZNF503, and nhr-23/RORB) whose transcription is activated, either directly or indirectly, by ngn-1. Our results show that ngn-1 has a role in transcribing known terminal regulators that establish and maintain cell fate of differentiated neural subtypes and confirms that ngn-1 functions as a proneural transcription factor in C. elegans neurogenesis.

scholarly journals P-element mutations affecting embryonic peripheral nervous system development in Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1663-1678 ◽  
Author(s):  
A Kania ◽  
A Salzberg ◽  
M Bhat ◽  
D D'Evelyn ◽  
Y He ◽  
...  
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Neural Development ◽  
Molecular Mechanisms ◽  
Nervous System Development ◽  
P Element ◽  
Phenotypic Characterization ◽  
Specific Marker ◽  
Element Insertion ◽  
Complementation Groups

Abstract The Drosophila embryonic peripheral nervous system (PNS) is an excellent model system to study the molecular mechanisms governing neural development. To identify genes controlling PNS development, we screened 2000 lethal P-element insertion strains. The PNS of mutant embryos was examined using the neural specific marker MAb 22C10, and 92 mutant strains were retained for further analysis. Genetic and cytological analysis of these strains shows that 42 mutations affect previously isolated genes that are known to be required for PNS development: longitudinals lacking (19), mastermind (15), numb (4), big brain (2), and spitz (2). The remaining 50 mutations were classified into 29 complementation groups and the P-element insertions were cytologically mapped. The mutants were classified in five major classes on the basis of their phenotype: gain of neurons, loss of neurons, organizational defects, pathfinding defects and morphological defects. Herein we report the preliminary phenotypic characterization of each of these complementation groups as well as the embryonic lacZ expression pattern of each P-element strain. Our analysis indicates that in most of the P-element insertion strains, the lacZ reporter gene is not expressed in the developing PNS.

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