Local induction of patterning and programmed cell death in the developing Drosophila retina

Development ◽  
1998 ◽  
Vol 125 (12) ◽  
pp. 2327-2335 ◽  
Author(s):  
D.T. Miller ◽  
R.L. Cagan
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Egf Receptor ◽  
Pigment Cells ◽  
Cell Fates ◽  
Adult Retina ◽  
Ras Pathway ◽  
Cell Ablation ◽  
Cone Cells ◽  
Local Cell

Local cell signaling can pattern the nervous system by directing cell fates, including programmed cell death. In the developing Drosophila retina, programmed cell death is used to remove excess cells between ommatidia. Cell ablation revealed the source and position of signals required for regulating the pattern of programmed cell death among these interommatidial cells. Two types of signals regulate this patterning event. Notch-mediated signals between interommatidial precursors result in removal of unneeded cells. Cone cells and primary pigment cells oppose this signal by supplying a ‘life’-promoting activity; evidence is provided that this signal occurs through localized activation of the EGF Receptor/Ras pathway. Together, these signals refine the highly regular pattern observed in the adult retina.

Cell death in normal and rough eye mutants of Drosophila

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 825-839 ◽  
Author(s):  
T. Wolff ◽  
D.F. Ready
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Compound Eye ◽  
Cell Lineage ◽  
Cell Fates ◽  
Cone Cells ◽  
A Cell ◽  
Retinal Epithelium ◽  
Fly Eye ◽  
Dying Cells

The regular, reiterated cellular pattern of the Drosophila compound eye makes it a sensitive amplifier of defects in cell death. Quantitative and histological methods reveal a phase of cell death between 35 and 50 h of development which removes between 2 and 3 surplus cells per ommatidium. The timing of this epoch is consistent with cell death as the last fate to be specified in the progressive sequence of cell fates that build the ommatidium. An ultrastructural survey of cell death suggests dying cells in the fly eye have similarities as well as differences with standard descriptions of programmed cell death. A failure of cell death to remove surplus cells disorganizes the retinal lattice. A screen of rough eye mutants identifies two genes, roughest and echinus, required for the normal elimination of cells from the retinal epithelium. The use of an enhancer trap as a cell lineage marker shows that the cone cells, like other retinal cells, are not clonally related to each other or to their neighbors.

scholarly journals A Screen for Mutations That Suppress the Phenotype of Drosophila armadillo, the β-Catenin Homolog

Genetics ◽  
2000 ◽  
Vol 155 (4) ◽  
pp. 1725-1740
Author(s):  
Rachel T Cox ◽  
Donald G McEwen ◽  
Denise L Myster ◽  
Robert J Duronio ◽  
Joseph Loureiro ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
Programmed Cell Death ◽  
Cell Survival ◽  
Wnt Pathway ◽  
Genetic Modifier ◽  
Wnt Signaling Pathway ◽  
Adherens Junction ◽  
Cell Fates ◽  
Wnt Signal

Abstract During development signaling pathways coordinate cell fates and regulate the choice between cell survival or programmed cell death. The well-conserved Wingless/Wnt pathway is required for many developmental decisions in all animals. One transducer of the Wingless/Wnt signal is Armadillo/β-catenin. Drosophila Armadillo not only transduces Wingless signal, but also acts in cell-cell adhesion via its role in the epithelial adherens junction. While many components of both the Wingless/Wnt signaling pathway and adherens junctions are known, both processes are complex, suggesting that unknown components influence signaling and junctions. We carried out a genetic modifier screen to identify some of these components by screening for mutations that can suppress the armadillo mutant phenotype. We identified 12 regions of the genome that have this property. From these regions and from additional candidate genes tested we identified four genes that suppress arm: dTCF, puckered, head involution defective (hid), and Dpresenilin. We further investigated the interaction with hid, a known regulator of programmed cell death. Our data suggest that Wg signaling modulates Hid activity and that Hid regulates programmed cell death in a dose-sensitive fashion.

The Drosophila orphan nuclear receptor seven-up requires the Ras pathway for its function in photoreceptor determination

Development ◽  
1995 ◽  
Vol 121 (1) ◽  
pp. 225-235 ◽  
Author(s):  
G. Begemann ◽  
A.M. Michon ◽  
L. vd Voorn ◽  
R. Wepf ◽  
M. Mlodzik
Keyword(s):  
Cell Fate ◽  
Nuclear Receptor ◽  
Egf Receptor ◽  
Cell Transformation ◽  
Orphan Nuclear Receptor ◽  
Loss Of Function ◽  
Cone Cell ◽  
Ras Pathway ◽  
Protein Levels ◽  
Cone Cells

The Drosophila seven-up (svp) gene specifies outer photoreceptor cell fate in eye development and encodes an orphan nuclear receptor with two isoforms. Transient expression under the sevenless enhancer of either svp isoform leads to a dosage-dependent transformation of cone cells into R7 photoreceptors, and at a lower frequency, R7 cells into outer photoreceptors. To investigate the cellular pathways involved, we have taken advantage of the dosage sensitivity and screened for genes that modify this svp-induced phenotype. We show that an active Ras pathway is essential for the function of both Svp isoforms. Loss-of-function mutations in components of the Ras signal transduction cascade act as dominant suppressors of the cone cell transformation, whilst loss-of-function mutations in negative regulators of Ras-activity act as dominant enhancers. Furthermore, Svp-mediated transformation of cone cells to outer photoreceptors, reminiscent of its wild-type function in specifying R3/4 and R1/6 identity, requires an activated Ras pathway in the same cells, or alternatively dramatic increase in ectopic Svp protein levels. Our results indicate that svp is only fully functional in conjunction with activated Ras. Since we find that mutations in the Egf-receptor are also among the strongest suppressors of svp-mediated cone cell transformation, we propose that the Ras activity in cone cells is due to low level Egfr signaling. Several models that could account for the observed svp regulation by the Ras pathway are discussed.

scholarly journals Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway

1998 ◽  
Vol 5 (4) ◽  
pp. 262-270 ◽  
Author(s):  
Kazunobu Sawamoto ◽  
Akiko Taguchi ◽  
Yuki Hirota ◽  
Chiharu Yamada ◽  
Ming-hao Jin ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Ras Pathway ◽  
Drosophila Eye

Retinoic acid alters EGF receptor expression during palatogenesis

Development ◽  
1988 ◽  
Vol 102 (4) ◽  
pp. 853-867 ◽  
Author(s):  
B.D. Abbott ◽  
E.D. Adamson ◽  
R.M. Pratt
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Epithelial Cells ◽  
Programmed Cell Death ◽  
Egf Receptor ◽  
Receptor Expression ◽  
Egf Receptors ◽  
Receptor Localization ◽  
All Trans Retinoic Acid ◽  
Fetal Mice

Various growth factors are necessary for normal embryonic development and EGF receptors are present in developing palatal shelves of embryonic/fetal mice at least from day 12 of gestation. The medial epithelium of the palatal shelf undergoes a series of developmental events which do not occur in the oral and nasal epithelia. In utero and in organ culture, the control palatal medial epithelium shows a developmental decline in EGF receptors, demonstrated both by a decrease in the binding of antibody to EGF receptors and a decrease in the binding of 125I-EGF; decreases which are not observed in cells of the adjacent oral or nasal epithelium. During this period, medial cells cease DNA synthesis and undergo programmed cell death. Medial epithelial cells exposed to all-trans-retinoic acid continue to express EGF receptors, bind EGF, proliferate, fail to undergo programmed cell death and exhibit a morphology typical of nasal cells. The data suggest that this disturbance by retinoic acid of EGF receptor localization and subsequent alterations in differentiation of the epithelial cells plays a role in the retinoic-acid-mediated induction of cleft palate.

scholarly journals Necroptosis, pyroptosis and apoptosis: an intricate game of cell death

2021 ◽  
Author(s):  
Damien Bertheloot ◽  
Eicke Latz ◽  
Bernardo S. Franklin
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Embryonic Development ◽  
Immune Responses ◽  
Cell Fates ◽  
Cellular Death ◽  
Key Players ◽  
Different Types ◽  
Living Organisms ◽  
Fine Tune

AbstractCell death is a fundamental physiological process in all living organisms. Its roles extend from embryonic development, organ maintenance, and aging to the coordination of immune responses and autoimmunity. In recent years, our understanding of the mechanisms orchestrating cellular death and its consequences on immunity and homeostasis has increased substantially. Different modalities of what has become known as ‘programmed cell death’ have been described, and some key players in these processes have been identified. We have learned more about the intricacies that fine tune the activity of common players and ultimately shape the different types of cell death. These studies have highlighted the complex mechanisms tipping the balance between different cell fates. Here, we summarize the latest discoveries in the three most well understood modalities of cell death, namely, apoptosis, necroptosis, and pyroptosis, highlighting common and unique pathways and their effect on the surrounding cells and the organism as a whole.

scholarly journals Erratum: Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway

1998 ◽  
Vol 5 (6) ◽  
pp. 548-548 ◽  
Author(s):  
Kazunobu Sawamoto ◽  
Akiko Taguchi ◽  
Yuki Hirota ◽  
Chiharu Yamada ◽  
Ming-hao Jin ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Ras Pathway ◽  
Drosophila Eye

scholarly journals A pathway of signals regulating effector and initiator caspases in the developing Drosophila eye

Development ◽  
2002 ◽  
Vol 129 (13) ◽  
pp. 3269-3278 ◽  
Author(s):  
Sun-Yun Yu ◽  
Soon Ji Yoo ◽  
Lihui Yang ◽  
Cynthia Zapata ◽  
Anu Srinivasan ◽  
...  
Keyword(s):  
Cell Death ◽  
Neural Development ◽  
Egf Receptor ◽  
Extracellular Signals ◽  
Downstream Effector ◽  
Regulated Cell Death ◽  
Effector Caspase ◽  
Cone Cells ◽  
Initiator Caspases

Regulated cell death and survival play important roles in neural development. Extracellular signals are presumed to regulate seven apparent caspases to determine the final structure of the nervous system. In the eye, the EGF receptor, Notch, and intact primary pigment and cone cells have been implicated in survival or death signals. An antibody raised against a peptide from human caspase 3 was used to investigate how extracellular signals controlled spatial patterning of cell death. The antibody crossreacted specifically with dying Drosophila cells and labelled the activated effector caspase Drice. It was found that the initiator caspase Dronc and the proapoptotic gene head involution defective were important for activation in vivo. Dronc may play roles in dying cells in addition to activating downstream effector caspases. Epistasis experiments ordered EGF receptor, Notch, and primary pigment and cone cells into a single pathway that affected caspase activity in pupal retina through hid and Inhibitor of Apoptosis Proteins. None of these extracellular signals appeared to act by initiating caspase activation independently of hid. Taken together, these findings indicate that in eye development spatial regulation of cell death and survival is integrated through a single intracellular pathway.

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