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1.
Development ; 147(2)2020 01 22.
Article in English | MEDLINE | ID: mdl-31862845

ABSTRACT

The development of tissues and organs requires close interaction of cells. To achieve this, cells express adhesion proteins such as the neural cell adhesion molecule (NCAM) or its Drosophila ortholog Fasciclin 2 (Fas2). Both are members of the Ig-domain superfamily of proteins that mediate homophilic adhesion. These proteins are expressed as isoforms differing in their membrane anchorage and their cytoplasmic domains. To study the function of single isoforms, we have conducted a comprehensive genetic analysis of Fas2 We reveal the expression pattern of all major Fas2 isoforms, two of which are GPI anchored. The remaining five isoforms carry transmembrane domains with variable cytoplasmic tails. We generated Fas2 mutants expressing only single isoforms. In contrast to the null mutation, which causes embryonic lethality, these mutants are viable, indicating redundancy among the different isoforms. Cell type-specific rescue experiments showed that glial-secreted Fas2 can rescue the Fas2 mutant phenotype to viability. This demonstrates that cytoplasmic Fas2 domains have no apparent essential functions and indicate that Fas2 has function(s) other than homophilic adhesion. In conclusion, our data suggest novel mechanistic aspects of a long-studied adhesion protein.


Subject(s)
Cell Adhesion Molecules, Neuronal/metabolism , Drosophila melanogaster/cytology , Drosophila melanogaster/metabolism , Signal Transduction , Animals , Cell Adhesion , Cell Adhesion Molecules, Neuronal/chemistry , Cell Adhesion Molecules, Neuronal/genetics , Cell Movement , Drosophila melanogaster/embryology , Drosophila melanogaster/genetics , Embryo, Nonmammalian/cytology , Embryo, Nonmammalian/metabolism , Gene Editing , Gene Expression Regulation, Developmental , Glycosylphosphatidylinositols/metabolism , Mutation/genetics , Neuroglia/metabolism , Protein Domains , Protein Isoforms/metabolism , Trachea/embryology , Trachea/metabolism
2.
Dev Biol ; 301(1): 27-37, 2007 Jan 01.
Article in English | MEDLINE | ID: mdl-17157832

ABSTRACT

A prominent feature of glial cells is their ability to migrate along axons to finally wrap and insulate them. In the embryonic Drosophila PNS, most glial cells are born in the CNS and have to migrate to reach their final destinations. To understand how migration of the peripheral glia is regulated, we have conducted a genetic screen looking for mutants that disrupt the normal glial pattern. Here we present an analysis of two of these mutants: Notch and numb. Complete loss of Notch function leads to an increase in the number of glial cells. Embryos hemizygous for the weak Notch(B-8X) allele display an irregular migration phenotype and mutant glial cells show an increased formation of filopodia-like structures. A similar phenotype occurs in embryos carrying the Notch(ts1) allele when shifted to the restrictive temperature during the glial cell migration phase, suggesting that Notch must be activated during glial migration. This is corroborated by the fact that cell-specific reduction of Notch activity in glial cells by directed numb expression also results in similar migration phenotypes. Since the glial migration phenotypes of Notch and numb mutants resemble each other, our data support a model where the precise temporal and quantitative regulation of Numb and Notch activity is not only required during fate decisions but also later during glial differentiation and migration.


Subject(s)
Cell Movement/physiology , Drosophila Proteins/physiology , Drosophila/cytology , Juvenile Hormones/physiology , Neuroglia/cytology , Receptors, Notch/physiology , Animals , Drosophila/embryology , Drosophila Proteins/genetics , Immunohistochemistry , Juvenile Hormones/genetics , Mutagenesis , Receptors, Notch/genetics , Signal Transduction
3.
Neuron ; 52(6): 969-80, 2006 Dec 21.
Article in English | MEDLINE | ID: mdl-17178401

ABSTRACT

In both vertebrates and invertebrates, glial cells wrap axonal processes to ensure electrical conductance. Here we report that Crooked neck (Crn), the Drosophila homolog of the yeast Clf1p splicing factor, is directing peripheral glial cell maturation. We show that crooked neck is expressed and required in glial cells to control migration and axonal wrapping. Within the cytoplasm, Crn interacts with the RNA-binding protein HOW and then translocates to the nucleus where the Crn/HOW complex controls glial differentiation by facilitating splicing of specific target genes. By using a GFP-exon trap approach, we identified some of the in vivo target genes that encode proteins localized in autocellular septate junctions. In conclusion, here we show that glial cell differentiation is controlled by a cytoplasmic assembly of splicing components, which upon translocation to the nucleus promote the splicing of genes involved in the assembly of cellular junctions.


Subject(s)
Cell Movement/physiology , Drosophila Proteins/physiology , Neuroglia/physiology , Nuclear Proteins/physiology , RNA-Binding Proteins/physiology , Animals , Animals, Genetically Modified , Cell Differentiation/physiology , Cell Growth Processes , Cell Line , Cell Nucleus/metabolism , Drosophila , Drosophila Proteins/genetics , Embryo, Nonmammalian , Female , Genes, Insect/physiology , Green Fluorescent Proteins/metabolism , Male , Microscopy, Electron, Transmission/methods , Mutation/physiology , Neuroglia/ultrastructure , Nuclear Proteins/genetics , RNA Splicing/physiology , RNA-Binding Proteins/genetics , Transfection/methods , Wings, Animal/growth & development
4.
Mech Dev ; 120(4): 401-13, 2003 Apr.
Article in English | MEDLINE | ID: mdl-12676319

ABSTRACT

In the midline glia of the embryonic ventral nerve cord of Drosophila, differentiation as well as the subsequent regulation of cell number is under the control of EGF-receptor signaling. During pupal stages apoptosis of all midline glial cells is initiated by ecdysone signaling. In a genetic screen we have identified mutations in disembodied, rippchen, spook, shade, shadow, shroud and tramtrack that all share a number of phenotypic traits, including defects in cuticle differentiation and nervous system development. Some of these genes were previously placed in the so-called 'Halloween-group' and were shown to affect ecdysone synthesis during embryogenesis. Here we demonstrate that the Halloween mutations not only affect glial differentiation but also lead to an increase in the number of midline glial cells, suggesting that during embryogenesis ecdysone signaling is required to adjust glial cell number similar to pupal stages. Finally we isolated a P-element-induced mutation of shroud, which controls the expression of ecdysone inducible genes. The P-element insertion occurs in one of the promoters of the Drosophila fos gene for which we present a yet undescribed complex genomic organization. The recently described kayak alleles affect only one of the six different Fos isoforms. This work for the first time links ecydsone signaling to Fos function and shows that during embryonic and pupal stages similar developmental mechanisms control midline glia survival.


Subject(s)
Drosophila Proteins/physiology , Ecdysone/physiology , Gene Expression Regulation, Developmental , Neuroglia/metabolism , Amino Acid Sequence , Animals , Cell Differentiation , Drosophila , Drosophila Proteins/genetics , Ecdysone/genetics , Genotype , Immunohistochemistry , Molecular Sequence Data , Mutation , Neurons/metabolism , Phenotype , Protein Isoforms , Sequence Homology, Amino Acid
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