Fat facets does a Highwire act at the synapse

BioEssays ◽  
2002 ◽  
Vol 24 (1) ◽  
pp. 13-16 ◽  
Author(s):  
Janice A. Fischer ◽  
Erin Overstreet
Keyword(s):  
Fat Facets

scholarly journals The Ras Target AF-6 is a Substrate of the Fam Deubiquitinating Enzyme

1998 ◽  
Vol 142 (4) ◽  
pp. 1053-1062 ◽  
Author(s):  
Shinichiro Taya ◽  
Takaharu Yamamoto ◽  
Kyoko Kano ◽  
Yoji Kawano ◽  
Akihiro Iwamatsu ◽  
...  
Keyword(s):  
Cell Fate ◽  
Plasma Membranes ◽  
Critical Role ◽  
Amino Acid Sequences ◽  
Cell Contact ◽  
Deubiquitinating Enzyme ◽  
Intact Cells ◽  
Cell Adhesions ◽  
Fat Facets ◽  
Cell Cell

The Ras target AF-6 has been shown to serve as one of the peripheral components of cell–cell adhesions, and is thought to participate in cell–cell adhesion regulation downstream of Ras. We here purified an AF-6-interacting protein with a molecular mass of ∼220 kD (p220) to investigate the function of AF-6 at cell–cell adhesions. The peptide sequences of p220 were identical to the amino acid sequences of mouse Fam. Fam is homologous to a deubiquitinating enzyme in Drosophila, the product of the fat facets gene. Recent genetic analyses indicate that the deubiquitinating activity of the fat facets product plays a critical role in controlling the cell fate. We found that Fam accumulated at the cell–cell contact sites of MDCKII cells, but not at free ends of plasma membranes. Fam was partially colocalized with AF-6 and interacted with AF-6 in vivo and in vitro. We also showed that AF-6 was ubiquitinated in intact cells, and that Fam prevented the ubiquitination of AF-6.

RETRACTED: Stage- and sex-dependent expressions of Usp9x, an X-linked mouse ortholog of Drosophila Fat facets, during gonadal development and oogenesis in mice

2002 ◽  
Vol 2 (1-2) ◽  
pp. 87-91 ◽  
Author(s):  
Takashi Noma ◽  
Yoshiakira Kanai ◽  
Masami Kanai-Azuma ◽  
Maki Ishii ◽  
Masahiko Fujisawa ◽  
...  
Keyword(s):  
Gonadal Development ◽  
Fat Facets

Stage- and sex-dependent expressions of Usp9x, an X-linked mouse ortholog of Drosophila Fat facets, during gonadal development and oogenesis in mice

2002 ◽  
Vol 119 ◽  
pp. S91-S95 ◽  
Author(s):  
Takashi Noma ◽  
Yoshiakira Kanai ◽  
Masami Kanai-Azuma ◽  
Maki Ishii ◽  
Masahiko Fujisawa ◽  
...  
Keyword(s):  
Gonadal Development ◽  
Fat Facets

Control of Cell Fate by a Deubiquitinating Enzyme Encoded by the fat facets Gene

Science ◽  
1995 ◽  
Vol 270 (5243) ◽  
pp. 1828-1831 ◽  
Author(s):  
Y. Huang ◽  
R. T. Baker ◽  
J. A. Fischer-Vize
Keyword(s):  
Cell Fate ◽  
Deubiquitinating Enzyme ◽  
Fat Facets

scholarly journals Spermatogonial deubiquitinase USP9X is essential for proper spermatogenesis in mice

Reproduction ◽  
2017 ◽  
Vol 154 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Kasane Kishi ◽  
Aya Uchida ◽  
Hinako M Takase ◽  
Hitomi Suzuki ◽  
Masamichi Kurohmaru ◽  
...  
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Apoptotic Cell ◽  
Cell Lineage ◽  
Conditional Knockout ◽  
Spermatogenic Cells ◽  
Male Mice ◽  
Conditional Deletion ◽  
Fat Facets

USP9X (ubiquitin-specific peptidase 9, X chromosome) is the mammalian orthologue of Drosophila deubiquitinase fat facets that was previously shown to regulate the maintenance of the germ cell lineage partially through stabilizing Vasa, one of the widely conserved factors crucial for gametogenesis. Here, we demonstrate that USP9X is expressed in the gonocytes and spermatogonia in mouse testes from newborn to adult stages. By using Vasa-Cre mice, germ cell-specific conditional deletion of Usp9x from the embryonic stage showed no abnormality in the developing testes by 1 week and no appreciable defects in the undifferentiated and differentiating spermatogonia at postnatal and adult stages. Interestingly, after 2 weeks, Usp9x-null spermatogenic cells underwent apoptotic cell death at the early spermatocyte stage, and then, caused subsequent aberrant spermiogenesis, which resulted in a complete infertility of Usp9x conditional knockout male mice. These data provide the first evidence of the crucial role of the spermatogonial USP9X during transition from the mitotic to meiotic phases and/or maintenance of early meiotic phase in Usp9x conditional knockout testes.

scholarly journals Genetic Analysis of the DrosophilaDNAprimGene: The Function of the 60-kD Primase Subunit of DNA Polymerase Opposes thefat facetsSignaling Pathway in the Developing Eye

Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1787-1795 ◽  
Author(s):  
Xin Chen ◽  
Qinghong Li ◽  
Janice A Fischer
Keyword(s):  
Dna Polymerase ◽  
Dna Sequences ◽  
Compound Eye ◽  
Large Subunit ◽  
Cell Communication ◽  
Dna Primase ◽  
Morphological Defects ◽  
Dependent Cell ◽  
Fat Facets ◽  
Communication Pathway

AbstractThe Drosophila DNAprim gene encodes the large subunit (60 kD) of DNA primase, the part of DNA polymerase α that synthesizes RNA primers during DNA replication. The precise function of the 60-kD subunit is unknown. In a mutagenesis screen for suppressors of the fat facets (faf) mutant eye phenotype, we identified mutations in DNAprim. The faf gene encodes a deubiquitinating enzyme required specifically for patterning the compound eye. The DNA sequences of four DNAprim alleles were determined and these define essential protein domains. We show that while flies lacking DNAprim activity are lethal, flies with reduced DNAprim activity display morphological defects in their eyes, and unlike faf mutants, cell cycle abnormalities in larval eye discs. Mechanisms by which DNA primase levels might influence the faf-dependent cell communication pathway are discussed.

scholarly journals Post-transcriptional modulation of Dscam1 enhances axonal growth in development and after injury

2017 ◽  
Author(s):  
Marta Koch ◽  
Maya Nicolas ◽  
Marlen Zschaetzsch ◽  
Natalie de Geest ◽  
Annelies Claeys ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Axonal Growth ◽  
Cns Injury ◽  
Jnk Pathway ◽  
Protein Levels ◽  
Injury Model ◽  
Central Nervous Systems ◽  
Transcriptional Modulation ◽  
Biochemical Analyses ◽  
Fat Facets

AbstractInjury to the adult central nervous systems (CNS) results in severe long-term disability because damaged CNS connections rarely regenerate. Although several axon regeneration regulators have been proposed, intrinsic regenerative mechanisms remain largely unexplored. Here, we use a Drosophila CNS injury model to identify a novel pro-regeneration signaling pathway. We conducted a genetic screen of approximately three hundred candidate genes and identified three strong inducers of axonal growth and regeneration: the Down Syndrome Cell Adhesion Molecule (Dscam1), the de-ubiquitinating enzyme Fat Facets (Faf)/Usp9x and the Jun N-Terminal Kinase (JNK) pathway transcription factor Kayak (Kay)/Fos. Genetic and biochemical analyses link these genes in a common signaling pathway whereby Faf stabilizes Dscam1 protein levels, by acting on the 3’-UTR of its mRNA, and Dscam1 acts upstream of the growth-promoting JNK signal. The mammalian homolog of Faf, Usp9x/FAM, shares both the regenerative and Dscam1 stabilizing activities, suggesting a conserved mechanism.

Undifferentiated cells in the developing Drosophila eye influence facet assembly and require the Fat facets ubiquitin-specific protease

Development ◽  
1996 ◽  
Vol 122 (10) ◽  
pp. 3207-3216 ◽  
Author(s):  
Y. Huang ◽  
J.A. Fischer-Vize
Keyword(s):  
Compound Eye ◽  
Cell Interactions ◽  
Inhibitory Signal ◽  
Complex Series ◽  
Drosophila Eye ◽  
Undifferentiated Cells ◽  
Specific Protease ◽  
Ubiquitin Specific Protease ◽  
Fat Facets

The Drosophila compound eye develops by a complex series of cell interactions where multiple positive and inhibitory cues guide cells in each facet into their positions and fates. The results of many genetic and molecular experiments have led to the view that facet assembly is directed by cells within developing ommatidial preclusters. Here fat facets mutants and the cloned fat facets gene were used to show that, in order to limit the number of photoreceptors in a facet to eight, undifferentiated cells surrounding assembling facets send an inhibitory signal to extraneous cells within the facet preclusters. Generation of the inhibitory signal requires the ubiquitin-specific protease encoded by the fat facets gene and is thus regulated by ubiquitin-dependent proteolysis.

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