scholarly journals Identification of genes involved in the differentiation of R7y and R7p photoreceptor cells in Drosophila

2019 ◽  
Author(s):  
James B Earl ◽  
Lauren A Vanderlinden ◽  
Laura M Saba ◽  
Steven G Britt
Keyword(s):  
Cell Fate ◽  
Compound Eye ◽  
Ectopic Expression ◽  
Photoreceptor Cells ◽  
Biological Processes ◽  
Cell Fate Specification ◽  
Wild Type ◽  
Transposon Insertion ◽  
Yellow Type ◽  
Driver Line

AbstractThe R7 and R8 photoreceptor cells of the Drosophila compound eye mediate color vision. Throughout the majority of the eye, these cells occur in two principal types of ommatidia. Approximately 35% of ommatidia are of the pale type and express Rh3 in R7 cells and Rh5 in R8 cells. The remaining 65% are of the yellow type and express Rh4 in R7 cells and Rh6 in R8 cells. The specification of an R8 cell in a pale or yellow ommatidium depends on the fate of the adjacent R7 cell. However, pale and yellow R7 cells are specified by a stochastic process that requires the genes spineless, tango and klumpfuss. To identify additional genes involved in this process we performed a genetic screen using a collection of 480 P{EP} transposon insertion strains. We identified genes that when inactivated and/or ectopically expressed in R7 cells resulted in a significantly altered percentage of Rh3 expressing R7 cells (Rh3%) from wild-type. 53 strains resulted in altered Rh3% in the heterozygous inactivation arm of the screen. 36 strains resulted in altered Rh3% in the ectopic expression arm of the screen, where the P{EP} insertion strains were crossed to a sevEP-GAL4 driver line. 4 strains showed differential effects between the two screens. Analyses of these results suggest that R7 cell fate specification is sensitive to perturbations in transcription, growth inhibition, glycoprotein ligand binding, WNT signaling, ubiquitin protease activity and Ser/Thr kinase activity, among other diverse signaling and cell biological processes.

scholarly journals Identification of Genes Involved in the Differentiation of R7y and R7p Photoreceptor Cells in Drosophila

2020 ◽  
Vol 10 (11) ◽  
pp. 3949-3958
Author(s):  
James B. Earl ◽  
Lauren A. Vanderlinden ◽  
Thomas L. Jacobsen ◽  
John C. Aldrich ◽  
Laura M. Saba ◽  
...  
Keyword(s):  
Cell Fate ◽  
Protein Modification ◽  
Compound Eye ◽  
Photoreceptor Cells ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Link Type ◽  
Transposon Insertion ◽  
Gtpase Activation ◽  
Yellow Type

The R7 and R8 photoreceptor cells of the Drosophila compound eye mediate color vision. Throughout the majority of the eye, these cells occur in two principal types of ommatidia. Approximately 35% of ommatidia are of the pale type and express Rh3 in R7 cells and Rh5 in R8 cells. The remaining 65% are of the yellow type and express Rh4 in R7 cells and Rh6 in R8 cells. The specification of an R8 cell in a pale or yellow ommatidium depends on the fate of the adjacent R7 cell. However, pale and yellow R7 cells are specified by a stochastic process that requires the genes spineless, tango and klumpfuss. To identify additional genes involved in this process we performed genetic screens using a collection of 480 P{EP} transposon insertion strains. We identified genes in gain of function and loss of function screens that significantly altered the percentage of Rh3 expressing R7 cells (Rh3%) from wild-type. 36 strains resulted in altered Rh3% in the gain of function screen where the P{EP} insertion strains were crossed to a sevEP-GAL4 driver line. 53 strains resulted in altered Rh3% in the heterozygous loss of function screen. 4 strains showed effects that differed between the two screens, suggesting that the effect found in the gain of function screen was either larger than, or potentially masked by, the P{EP} insertion alone. Analyses of homozygotes validated many of the candidates identified. These results suggest that R7 cell fate specification is sensitive to perturbations in mRNA transcription, splicing and localization, growth inhibition, post-translational protein modification, cleavage and secretion, hedgehog signaling, ubiquitin protease activity, GTPase activation, actin and cytoskeletal regulation, and Ser/Thr kinase activity, among other diverse signaling and cell biological processes.

Patterning of the R7 and R8 photoreceptor cells of Drosophila: evidence for induced and default cell-fate specification

Development ◽  
1999 ◽  
Vol 126 (4) ◽  
pp. 607-616 ◽  
Author(s):  
W.H. Chou ◽  
A. Huber ◽  
J. Bentrop ◽  
S. Schulz ◽  
K. Schwab ◽  
...  
Keyword(s):  
Cell Fate ◽  
Compound Eye ◽  
Photoreceptor Cells ◽  
Opsin Gene ◽  
Cell Fate Specification ◽  
Cell Fates ◽  
Independent Manner ◽  
Default State ◽  
Overlapping Sets ◽  
Developmental Switch

Opsin gene expression in the R7 and R8 photoreceptor cells of the Drosophila compound eye is highly coordinated. We have found that the R8 cell specific Rh5 and Rh6 opsins are expressed in non-overlapping sets of R8 cells, in a precise pairwise fashion with Rh3 and Rh4 in the R7 cells of individual ommatidia. Removal of the R7 cells in sevenless, boss or sina mutants, disrupts Rh5 expression and dramatically increases the number of Rh6-expressing R8 cells. This suggests that the expression of Rh5 may be induced by an Rh3-expressing R7 cell, whereas Rh6 expression is most likely a default state of the R8 cell. We found that the paired expression of opsin genes in the R7 and R8 cells occurs in a sevenless and boss independent manner. Furthermore, we found that the generation of both Rh3- and Rh4-expressing R7 cells can occur in the absence of an R8 cell. These results suggest that the specification of opsin expression in the R7 cells may occur autonomously, whereas the R7 photoreceptor cell may be responsible for regulating a binary developmental switch between induced and default cell-fates in the R8 cell.

scholarly journals STY1 and STY2 promote the formation of apical tissues during Arabidopsis gynoecium development

Development ◽  
2002 ◽  
Vol 129 (20) ◽  
pp. 4707-4717 ◽  
Author(s):  
Sandra Kuusk ◽  
Joel J. Sohlberg ◽  
Jeff A. Long ◽  
Ingela Fridborg ◽  
Eva Sundberg
Keyword(s):  
Double Mutant ◽  
Ectopic Expression ◽  
Ring Finger ◽  
Regional Differentiation ◽  
35S Promoter ◽  
Insertion Mutation ◽  
Wild Type ◽  
Transposon Insertion ◽  
Visible Effect ◽  
Gynoecium Development

Gynoecium ontogenesis in Arabidopsis is accomplished by the co-ordinated activity of genes that control patterning and the regional differentiation of tissues, and ultimately results in the formation of a basal ovary, a short style and an apical stigma. A transposon insertion in the STYLISH1 (STY1) gene results in gynoecia with aberrant style morphology, while an insertion mutation in the closely related STYLISH2 (STY2) gene has no visible effect on gynoecium development. However, sty1-1 sty2-1 double mutant plants exhibit an enhanced sty1-1 mutant phenotype and are characterized by a further reduction in the amount of stylar and stigmatic tissues and decreased proliferation of stylar xylem. These data imply that STY1 and STY2 are partially redundant and that both genes promote style and stigma formation and influence vascular development during Arabidopsis gynoecium development. Consistently, STY1 and STY2 are expressed in the apical parts of the developing gynoecium and ectopic expression of either STY1 or STY2 driven by the CaMV 35S promoter is sufficient to transform valve cells into style cells. STY1::GUS and STY2::GUS activity is detected in many other organs as well as the gynoecium, suggesting that STY1 and STY2 may have additional functions. This is supported by the sty1-1 sty2-1 double mutants producing rosette and cauline leaves with a higher degree of serration than wild-type leaves. STY1 and STY2 are members of a small gene family, and encode proteins with a RING finger-like motif. Double mutant analyses indicate that STY1 genetically interacts with SPATULA and possibly also with CRABS CLAW.

Ectopic expression of either the Drosophila gooseberry-distal or proximal gene causes alterations of cell fate in the epidermis and central nervous system

Development ◽  
1994 ◽  
Vol 120 (5) ◽  
pp. 1151-1161 ◽  
Author(s):  
Y. Zhang ◽  
A. Ungar ◽  
C. Fresquez ◽  
R. Holmgren
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Fate ◽  
Ectopic Expression ◽  
Cell Fate Specification ◽  
Single Function ◽  
Independent Functions ◽  
Segment Polarity ◽  
The Central Nervous System ◽  
The Common

Previous studies have shown that the segment polarity locus gooseberry, which contains two closely related transcripts gooseberry-proximal and gooseberry-distal, is required for proper development in both the epidermis and the central nervous system of Drosophila. In this study, the roles of the gooseberry proteins in the process of cell fate specification have been examined by generating two fly lines in which either gooseberry-distal or gooseberry-proximal expression is under the control of an hsp70 promoter. We have found that ectopic expression of either gooseberry protein causes cell fate transformations that are reciprocal to those of a gooseberry deletion mutant. Our results suggest that the gooseberry-distal protein is required for the specification of naked cuticle in the epidermis and specific neuroblasts in the central nervous system. These roles may reflect independent functions in neuroblasts and epidermal cells or a single function in the common ectodermal precursor cells. The gooseberry-proximal protein is also found in the same neuroblasts as gooseberry-distal and in the descendants of these cells.

Ectopic Expression of the Immune Adaptor Protein CD3zeta in Neural Stem/Progenitor Cells Disrupts Cell-Fate Specification

2011 ◽  
Vol 46 (2) ◽  
pp. 431-441 ◽  
Author(s):  
Julie Angibaud ◽  
Stéphane J. Baudouin ◽  
Antoine Louveau ◽  
Véronique Nerrière-Daguin ◽  
Virginie Bonnamain ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Ectopic Expression ◽  
Adaptor Protein ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Neural Stem Progenitor Cells

scholarly journals Translational Control of Cell Fate: Availability of Phosphorylation Sites on Translational Repressor 4E-BP1 Governs Its Proapoptotic Potency

2002 ◽  
Vol 22 (8) ◽  
pp. 2853-2861 ◽  
Author(s):  
Shunan Li ◽  
Nahum Sonenberg ◽  
Anne-Claude Gingras ◽  
Mark Peterson ◽  
Svetlana Avdulov ◽  
...  
Keyword(s):  
Cell Fate ◽  
Translational Control ◽  
Phosphorylation Site ◽  
Ectopic Expression ◽  
Initiation Factor ◽  
Wild Type ◽  
Internal Ribosomal Entry Sites ◽  
Translational Repressor ◽  
Eukaryotic Initiation Factor 4E ◽  
Quantitative Changes

ABSTRACT Translational control has been recently added to well-recognized genomic, transcriptional, and posttranslational mechanisms regulating apoptosis. We previously found that overexpressed eukaryotic initiation factor 4E (eIF4E) rescues cells from apoptosis, while ectopic expression of wild-type eIF4E-binding protein 1 (4E-BP1), the most abundant member of the 4E-BP family of eIF4E repressor proteins, activates apoptosis—but only in transformed cells. To test the possibility that nontransformed cells require less cap-dependent translation to suppress apoptosis than do their transformed counterparts, we intensified the level of translational repression in nontransformed fibroblasts. Here, we show that inhibition of 4E-BP1 phosphorylation by rapamycin triggers apoptosis in cells ectopically expressing wild-type 4E-BP1 and that expression of 4E-BP1 phosphorylation site mutants potently activates apoptosis in a phosphorylation site-specific manner. In general, proapoptotic potency paralleled repression of cap-dependent translation. However, this relationship was not a simple monotone. As repression of cap-dependent translation intensified, apoptosis increased to a maximum value. Further repression resulted in less apoptosis—a state associated with activation of translation through internal ribosomal entry sites. These findings show: that phosphorylation events govern the proapoptotic potency of 4E-BP1, that 4E-BP1 is proapoptotic in normal as well as transformed fibroblasts, and that malignant transformation is associated with a higher requirement for cap-dependent translation to inhibit apoptosis. Our results suggest that 4E-BP1-mediated control of apoptosis occurs through qualitative rather than quantitative changes in protein synthesis, mediated by a dynamic interplay between cap-dependent and cap-independent processes.

Cell fate control in the Drosophila retina by the orphan receptor seven-up: its role in the decisions mediated by the ras signaling pathway

Development ◽  
1995 ◽  
Vol 121 (5) ◽  
pp. 1361-1372 ◽  
Author(s):  
S. Kramer ◽  
S.R. West ◽  
Y. Hiromi
Keyword(s):  
Signaling Pathway ◽  
Cell Fate ◽  
Compound Eye ◽  
Gene Dosage ◽  
Ectopic Expression ◽  
Orphan Receptor ◽  
Ras Signaling ◽  
Cell Type ◽  
Cone Cells ◽  
Ras Signaling Pathway

Drosophila seven-up is an orphan receptor of the steroid receptor family that is required to specify photoreceptor neuron subtypes in the developing compound eye. Expression of seven-up is confined to four of the eight photoreceptor precursors, R3/R4/R1/R6. We show that misexpression of seven-up in any of the other cell types within the developing ommatidium interferes with their differentiation. Each cell type responds differently to seven-up misexpression. For example, ectopic expression in the non-neuronal cone cells using the sevenless promoter/enhancer (sev-svp) causes the cone cells to take on a neuronal identity. Ectopic expression of seven-up in R2/R5 using the rough enhancer (ro-svp) causes these neurons to lose aspects of their photoreceptor subtype identity while remaining neuronal. Each cell type appears to have a different developmental time window that is sensitive to misexpressed seven-up. The temporal order of responsiveness of each cell type to misexpressed seven-up is similar but not identical to the order of neuronal differentiation. This suggests that there are processes of specification that are distinct from the specification to become a photoreceptor neuron. We have identified members of the ras signaling pathway as suppressors of the cone cell to R7 neuron transformation caused by sev-svp. Suppression of the sev-svp phenotype can be achieved by decreasing the gene-dosage of any of the members of the ras-pathway. This suggests that the function of seven-up in the cone cells requires ras signaling. However, a decrease in ras signaling results in enhancement of the phenotype caused by the ro-svp transgene. We discuss the relationship between decisions controlled by seven-up and those controlled by ras signaling.

Evidence of functional long-range Wnt/Wg in the developing Drosophila wing epithelium

2018 ◽  
Author(s):  
Varun Chaudhary ◽  
Michael Boutros
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Target Gene ◽  
Secreted Proteins ◽  
Cell Fate Specification ◽  
Wild Type ◽  
Fate Specification ◽  
Drosophila Wing ◽  
Wnt Proteins ◽  
Insight Into

SUMMARYWnts are secreted proteins that regulate cell fate specification during development of all metazoans. Wnt proteins were proposed to spread over several cell diameters to activate signalling directly at a distance. In the Drosophila wing epithelium, an extracellular gradient of Wingless (Wg, the homolog of Wnt1) was observed extending over several cells away from producing cells. However, it was also recently shown that a membrane-tethered Neurotactin-Wg fusion protein (NRT-Wg) can rescue the loss-of endogenous Wg, leading to proper patterning of the wing. Therefore, whether Wg spreading is required for correct tissue patterning during development remains controversial and the functional range of wild-type Wg is unclear. Here, by capturing secreted Wg on distally located cells we show that the Wg gradient acts directly up to eleven cell distances. Cells located outside the reach of extracellular Wg depend on the Frizzled2 receptor to maintain target gene expression. We find that NRT-Wg is not restricted to the producing cells and propose that it can rescue signalling defects by perdurance in the receiving cells. These results provide insight into the mechanisms by which Wnt proteins mediate patterning of a rapidly growing tissue.

scholarly journals A Screen for Genes That Function Downstream of Ras1 During Drosophila Eye Development

Genetics ◽  
1996 ◽  
Vol 143 (1) ◽  
pp. 315-329 ◽  
Author(s):  
Felix D Karim ◽  
Henry C Chang ◽  
Marc Themen ◽  
David A Wassarman ◽  
Todd Laverty ◽  
...  
Keyword(s):  
Cell Fate ◽  
Photoreceptor Cells ◽  
Type I ◽  
Cell Fate Specification ◽  
Phosphatase 2A ◽  
Ras Oncogenes ◽  
Geranylgeranyl Transferase ◽  
Sevenless Receptor Tyrosine Kinase ◽  
Mutant Genes ◽  
Photoreceptor Development

Abstract Cell-fate specification of the R7 photoreceptor cell is controlled by the sevenless receptor tyrosine kinase (SevRTK) and Ras1, the Drosophila homologue of mammalian H-ras, K-ras and N-ras oncogenes. An activated form of Ras1 expressed under control of the sevenless enhancer/promoter (sev-Ras1v12) induces production of supernumerary R7 photoreceptor cells, which causes the eye to become rough in appearance. To isolate mutations in genes functioning downstream of Ras1, we carried out a screen for dominant suppressors and enhancers of this rough eye phenotype. Approximately 850,000 mutagenized flies were screened, and 282 dominant suppressors and 577 dominant enhancers were isolated. Mutations in the Drosophila homologues of Raf, MEK, MAPK, type I Geranylgeranyl Transferase and Protein Phosphatase 2A were isolated, as were mutations in several novel signaling genes. Some of these mutant genes appear to be general signaling factors that function in other Ras1 pathways, while one seems to be more specific for photoreceptor development. At least two suppressors appear to function either between Ras1 and Raf or in parallel to Raf.

A unique mutation in the Enhancer of split gene complex affects the fates of the mystery cells in the developing Drosophila eye

Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 89-101 ◽  
Author(s):  
J.A. Fischer-Vize ◽  
P.D. Vize ◽  
G.M. Rubin
Keyword(s):  
Compound Eye ◽  
Photoreceptor Cells ◽  
Neural Cells ◽  
Loss Of Function ◽  
Wild Type ◽  
Partial Loss ◽  
Eye Disc ◽  
Mutant Cells ◽  
Enhancer Of Split

An unusual recessive allele of the Drosophila groucho gene, which encodes a transducin-like protein, affects the fates of specific cells in the eye disc. groucho is one of several transcription units in the Enhancer of split complex. Most groucho mutations are zygotic lethal due to the proliferation of embryonic neural cells at the expense of epidermal cells. In contrast, flies homozygous for the mutant allele described here, groBFP2, are viable but have abnormal eyes. The Drosophila compound eye is composed of several hundred identical facets, or ommatidia, each of which contains eight photoreceptor cells, R1-R8. In groBFP2 mutant retinas, most of the facets contain eight normally determined photoreceptor cells and one or two additional R-cells of the R3/4 subtype. The extra photoreceptors appear to arise from the mystery cells, which are part of the precluster that initiates the ommatidium, but do not normally become neurons. groBFP2 behaves as a partial loss-of-function mutant. Analysis of ommatidia mosaic for wild-type and groBFP2 mutant cells suggests that the focus of action of the groBFP2 mutation is outside of the photoreceptor cells. These results imply that one function of groucho is in a pathway whereby neuralization of the mystery cells is inhibited by other non-neural cells in the eye disc. In addition, determination of R3/4 photoreceptors usually requires contact with R2 and R5. Specification of the mystery cells as ectopic R3/4 subtype photoreceptors in groBFP2 mutant eye discs implies that induction by R2 or R5 is not absolutely necessary for R3/4 cell determination.

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