scholarly journals A somatic proteoglycan controls Notch-directed germ cell fate

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sandeep Gopal ◽  
Aqilah Amran ◽  
Andre Elton ◽  
Leelee Ng ◽  
Roger Pocock
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Cell Fate ◽  
Notch Receptor ◽  
Cell Behavior ◽  
Cell Fate Decisions ◽  
Calcium Dependent ◽  
Notch Receptors ◽  
Germline Proliferation

AbstractCommunication between the soma and germline optimizes germ cell fate programs. Notch receptors are key determinants of germ cell fate but how somatic signals direct Notch-dependent germ cell behavior is undefined. Here we demonstrate that SDN-1 (syndecan-1), a somatic transmembrane proteoglycan, controls expression of the GLP-1 (germline proliferation-1) Notch receptor in the Caenorhabditis elegans germline. We find that SDN-1 control of a somatic TRP calcium channel governs calcium-dependent binding of an AP-2 transcription factor (APTF-2) to the glp-1 promoter. Hence, SDN-1 signaling promotes GLP-1 expression and mitotic germ cell fate. Together, these data reveal SDN-1 as a putative communication nexus between the germline and its somatic environment to control germ cell fate decisions.

scholarly journals Notch-Directed Germ Cell Proliferation Is Mediated by Proteoglycan-Dependent Transcription

2020 ◽  
Author(s):  
Sandeep Gopal ◽  
Aqilah Amran ◽  
Andre Elton ◽  
Leelee Ng ◽  
Roger Pocock
Keyword(s):  
Cell Proliferation ◽  
Germ Cell ◽  
Cell Fate ◽  
Notch Receptor ◽  
Cell Fate Decisions ◽  
Calcium Dependent ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Germline Proliferation ◽  
Membrane Bound

Notch receptors are essential membrane-bound regulators of cell proliferation and differentiation in metazoa. In the nematode Caenorhabditis elegans, correct expression of GLP-1 (germline proliferation-1), a germline-expressed Notch receptor, is important for germ cell maintenance. However, mechanisms that regulate GLP-1 expression are undefined. Here, we demonstrate that an AP-2 transcription factor (APTF-2) regulates GLP-1 expression through calcium-dependent binding to a conserved motif in the glp-1 promoter. Our data reveals that SDN-1 (syndecan-1), a transmembrane proteoglycan, regulates a TRP calcium channel in the soma to modulate the interaction between APTF-2 and glp-1 promoter - thus providing a potential communication nexus between the germline and its somatic environment to control germ cell fate decisions.

scholarly journals Drosophila Notch receptor activity suppresses Hairless function during adult external sensory organ development.

Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1491-1505
Author(s):  
D F Lyman ◽  
B Yedvobnick
Keyword(s):  
Cell Fate ◽  
Daughter Cell ◽  
Notch Receptor ◽  
Sensory Organ ◽  
Cell Fates ◽  
Gain Of Function ◽  
Over Expression ◽  
Cell Fate Decisions ◽  
Synergistic Enhancement ◽  
Conditional Expression

Abstract The neurogenic Notch locus of Drosophila encodes a receptor necessary for cell fate decisions within equivalence groups, such as proneural clusters. Specification of alternate fates within clusters results from inhibitory communication among cells having comparable neural fate potential. Genetically, Hairless (H) acts as an antagonist of most neurogenic genes and may insulate neural precursor cells from inhibition. H function is required for commitment to the bristle sensory organ precursor (SOP) cell fate and for daughter cell fates. Using Notch gain-of-function alleles and conditional expression of an activated Notch transgene, we show that enhanced signaling produces H-like loss-of-function phenotypes by suppressing bristle SOP cell specification or by causing an H-like transformation of sensillum daughter cell fates. Furthermore, adults carrying Notch gain of function and H alleles exhibit synergistic enhancement of mutant phenotypes. Over-expression of an H+ transgene product suppressed virtually all phenotypes generated by Notch gain-of-function genotypes. Phenotypes resulting from over-expression of the H+ transgene were blocked by the Notch gain-of-function products, indicating a balance between Notch and H activity. The results suggest that H insulates SOP cells from inhibition and indicate that H activity is suppressed by Notch signaling.

scholarly journals The EGL-13 SOX Domain Transcription Factor Affects the Uterine Cell Lineages in Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1623-1628
Author(s):  
Hediye Nese Cinar ◽  
Keri L Richards ◽  
Kavita S Oommen ◽  
Anna P Newman
Keyword(s):  
Transcription Factor ◽  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cell Lineages

Abstract We isolated egl-13 mutants in which the cells of the Caenorhabditis elegans uterus initially appeared to develop normally but then underwent an extra round of cell division. The data suggest that egl-13 is required for maintenance of the cell fate.

Analysis of Dominant Enhancers and Suppressors of Activated Notch in Drosophila

Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 1127-1141 ◽  
Author(s):  
Esther M Verheyen ◽  
Karen J Purcell ◽  
Mark E Fortini ◽  
Spyros Artavanis-Tsakonas
Keyword(s):  
Cell Fate ◽  
Notch Signaling Pathway ◽  
Notch Receptor ◽  
Gene Products ◽  
Mutagenesis Screen ◽  
Cell Fate Decisions ◽  
Site Mutagenesis ◽  
Notch Receptor Signaling ◽  
Cellular Transformations ◽  
New Alleles

Abstract The Notch receptor controls cell fate decisions throughout Drosophila development. Truncated, ligand-independent forms of this protein delay or block differentiation. We have previously shown that expression of the intracellular domain of the receptor under the control of the sevenless enhancer/promoter induces a rough eye phenotype in the adult fly. Analysis of the resultant cellular transformations suggested that this form of Notch acts as a constitutively activated receptor. To identify gene products that interact with Notch, a second-site mutagenesis screen was performed to isolate enhancers and suppressors of the eye phenotype caused by expression of these activated Notch molecules. We screened 137,000 mutagenized flies and recovered 290 dominant modifiers. Many new alleles of previously identified genes were isolated, as were mutations defining novel loci that may function in the Notch signaling pathway. We discuss the data with respect to known features of Notch receptor signaling and Drosophila eye development.

glp-1 can substitute for lin-12 in specifying cell fate decisions in Caenorhabditis elegans

Development ◽  
1993 ◽  
Vol 119 (4) ◽  
pp. 1019-1027 ◽  
Author(s):  
K. Fitzgerald ◽  
H.A. Wilkinson ◽  
I. Greenwald
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Effector Proteins ◽  
Regulatory Sequences ◽  
Animal Kingdom ◽  
Cell Fate Decisions ◽  
Notch Gene ◽  
Epidermal Growth ◽  
Differential Gene ◽  
Mutant Phenotypes

Members of the lin-12/Notch gene family encode receptors for intercellular signals and are found throughout the animal kingdom. In many animals, the presence of at least two lin-12/Notch genes raises the issue of the significance of this duplication and divergence. In Caenorhabditis elegans, two lin-12/Notch genes, lin-12 and glp-1, encode proteins that are 50% identical, with different numbers of epidermal growth factor-like motifs in their extracellular domains. Many of the cell fate decisions mediated by lin-12 and glp-1 are distinct. Here, we express glp-1 protein under the control of lin-12 regulatory sequences in animals lacking endogenous lin-12 activity and find that glp-1 can substitute for lin-12 in mediating cell fate decisions. These results imply that the lin-12 and glp-1 proteins are biochemically interchangeable, sharing common ligand and effector proteins, and that the discrete lin-12 and glp-1 mutant phenotypes result from differential gene expression. In addition, these results suggest that the duplicate lin-12/Notch genes found in vertebrates may also be biochemically interchangeable.

scholarly journals Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 1011-1022 ◽  
Author(s):  
T.L. Gumienny ◽  
E. Lambie ◽  
E. Hartwieg ◽  
H.R. Horvitz ◽  
M.O. Hengartner
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Somatic Cell ◽  
Cell Fate ◽  
Germ Cells ◽  
Mapk Pathway ◽  
Apoptotic Cell ◽  
C Elegans ◽  
Pathway Activation

Development of the nematode Caenorhabditis elegans is highly reproducible and the fate of every somatic cell has been reported. We describe here a previously uncharacterized cell fate in C. elegans: we show that germ cells, which in hermaphrodites can differentiate into sperm and oocytes, also undergo apoptotic cell death. In adult hermaphrodites, over 300 germ cells die, using the same apoptotic execution machinery (ced-3, ced-4 and ced-9) as the previously described 131 somatic cell deaths. However, this machinery is activated by a distinct pathway, as loss of egl-1 function, which inhibits somatic cell death, does not affect germ cell apoptosis. Germ cell death requires ras/MAPK pathway activation and is used to maintain germline homeostasis. We suggest that apoptosis eliminates excess germ cells that acted as nurse cells to provide cytoplasmic components to maturing oocytes.

Role of Notch and achaete-scute complex in the expression of Enhancer of split bHLH proteins

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3745-3752 ◽  
Author(s):  
V. Jennings ◽  
J. de Celis ◽  
C. Delidakis ◽  
A. Preiss ◽  
S. Bray
Keyword(s):  
Cell Fate ◽  
Notch Pathway ◽  
Interaction Mechanism ◽  
Cell Interaction ◽  
Precursor Cell ◽  
Notch Receptor ◽  
Sensory Organ ◽  
Cell Fate Decisions ◽  
Sensory Organ Precursor ◽  
Enhancer Of Split

The proteins encoded by Notch and the Enhancer of split complex are components of a cell-cell interaction mechanism which is important in many cell fate decisions throughout development. One such decision is the formation of the sensory organ precursor cell during the development of the peripheral nervous system in Drosophila. Cells acquire the potential to be neural through the expression of the proneural genes, and the Notch pathway is required to limit neural fate to a single cell from a proneural cluster. However, despite extensive analysis, the precise pathways linking the proneural with Notch and Enhancer of split gene functions remain obscure. For example, it has been suggested that achaete-scute complex proteins directly activate Enhancer of split genes leaving the action of Notch in the pathway unclear. Using monoclonal antibodies that recognise products of the Enhancer of split complex, we show that these proteins accumulate in the cells surrounding the developing sensory organ precursor cell and that their expression is dependent on the activity of Notch and does not directly correlate with expression of Achaete. We further clarify the pathway by showing that ubiquitous expression of an activated Notch receptor leads to widespread accumulation of Enhancer of split proteins even in the absence of achaete-scute complex proteins. Thus Enhancer of split protein expression in response to Notch activity does not require achaete-scute complex proteins.

scholarly journals Exploratory cell dynamics: a sense of touch for cells?

2018 ◽  
Vol 399 (8) ◽  
pp. 809-819 ◽  
Author(s):  
Perihan Nalbant ◽  
Leif Dehmelt
Keyword(s):  
Mechanical Properties ◽  
Cell Fate ◽  
Cell Behavior ◽  
Directional Migration ◽  
Cell Dynamics ◽  
Cell Fate Decisions ◽  
External Cues ◽  
Dynamic Cell ◽  
Sense Of Touch ◽  
Efficient Mechanisms

Abstract Cells need to process multifaceted external cues to steer their dynamic behavior. To efficiently perform this task, cells implement several exploratory mechanisms to actively sample their environment. In particular, cells can use exploratory actin-based cell protrusions and contractions to engage and squeeze the environment and to actively probe its chemical and mechanical properties. Multiple excitable signal networks were identified that can generate local activity pulses to control these exploratory processes. Such excitable signal networks offer particularly efficient mechanisms to process chemical or mechanical signals to steer dynamic cell behavior, such as directional migration, tissue morphogenesis and cell fate decisions.

scholarly journals Ero1L, a thiol oxidase, is required for Notch signaling through cysteine bridge formation of the Lin12-Notch repeats in Drosophila melanogaster

2008 ◽  
Vol 182 (6) ◽  
pp. 1113-1125 ◽  
Author(s):  
An-Chi Tien ◽  
Akhila Rajan ◽  
Karen L. Schulze ◽  
Hyung Don Ryoo ◽  
Melih Acar ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Notch Signaling ◽  
Cell Fate ◽  
Disulfide Bonds ◽  
Cell Communication ◽  
Notch Receptor ◽  
Cell Fate Decisions ◽  
Unfolded Protein ◽  
Thiol Oxidase ◽  
The Unfolded Protein Response

Notch-mediated cell–cell communication regulates numerous developmental processes and cell fate decisions. Through a mosaic genetic screen in Drosophila melanogaster, we identified a role in Notch signaling for a conserved thiol oxidase, endoplasmic reticulum (ER) oxidoreductin 1–like (Ero1L). Although Ero1L is reported to play a widespread role in protein folding in yeast, in flies Ero1L mutant clones show specific defects in lateral inhibition and inductive signaling, two characteristic processes regulated by Notch signaling. Ero1L mutant cells accumulate high levels of Notch protein in the ER and induce the unfolded protein response, suggesting that Notch is misfolded and fails to be exported from the ER. Biochemical assays demonstrate that Ero1L is required for formation of disulfide bonds of three Lin12-Notch repeats (LNRs) present in the extracellular domain of Notch. These LNRs are unique to the Notch family of proteins. Therefore, we have uncovered an unexpected requirement for Ero1L in the maturation of the Notch receptor.

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