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.

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 and Characterization of Genes That Interact With lin-12 in Caenorhabditis elegans

Genetics ◽  
1997 ◽  
Vol 147 (4) ◽  
pp. 1675-1695 ◽  
Author(s):  
Frans E Tax ◽  
James H Thomas ◽  
Edwin L Ferguson ◽  
H Robert Horvitzt
Keyword(s):  
Cell Fate ◽  
Low Frequency ◽  
Signal Transduction Pathway ◽  
Temperature Shift ◽  
Egg Laying ◽  
Null Alleles ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Suppressor Mutations

Abstract We identified and characterized 14 extragenic mutations that suppressed the dominant egg-laying defect of certain lin-12 gain-of-function mutations. These suppressors defined seven genes: sup-l7, lag-2, sel-4, sel-5, sel-6, sel-7 and sel-8. Mutations in six of the genes are recessive suppressors, whereas the two mutations that define the seventh gene, lag-2, are semi-dominant suppressors. These suppressor mutations were able to suppress other lin-12 gain-of-function mutations. The suppressor mutations arose at a very low frequency per gene, 10-50 times below the typical loss-of-function mutation frequency. The suppressor mutations in sup1 7 and lag-2 were shown to be rare non-null alleles, and we present evidence that null mutations in these two genes cause lethality. Temperature-shift studies for two suppressor genes, sup1 7and lag-2, suggest that both genes act at approximately the same time as lin-12in specifying a cell fate. Suppressor alleles of six of these genes enhanced a temperature-sensitive loss-of-function allele of glp-1, a gene related to lin-12 in structure and function. Our analysis of these suppressors suggests that the majority of these genes are part of a shared lin-12/glp-1 signal transduction pathway, or act to regulate the expression or stability of lin-12 and glp-1.

scholarly journals MKP-3 Has Essential Roles as a Negative Regulator of the Ras/Mitogen-Activated Protein Kinase Pathway during Drosophila Development

2004 ◽  
Vol 24 (2) ◽  
pp. 573-583 ◽  
Author(s):  
Myungjin Kim ◽  
Guang-Ho Cha ◽  
Sunhong Kim ◽  
Jun Hee Lee ◽  
Jeehye Park ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Fate ◽  
Photoreceptor Cells ◽  
Mapk Signaling ◽  
Negative Regulator ◽  
Mitogen Activated Protein Kinase ◽  
Loss Of Function ◽  
Wing Vein ◽  
Mitogen Activated Protein

ABSTRACT Mitogen-activated protein kinase (MAPK) phosphatase 3 (MKP-3) is a well-known negative regulator in the Ras/extracellular signal-regulated kinase (ERK)-MAPK signaling pathway responsible for cell fate determination and proliferation during development. However, the physiological roles of MKP-3 and the mechanism by which MKP-3 regulates Ras/Drosophila ERK (DERK) signaling in vivo have not been determined. Here, we demonstrated that Drosophila MKP-3 (DMKP-3) is critically involved in cell differentiation, proliferation, and gene expression by suppressing the Ras/DERK pathway, specifically binding to DERK via the N-terminal ERK-binding domain of DMKP-3. Overexpression of DMKP-3 reduced the number of photoreceptor cells and inhibited wing vein differentiation. Conversely, DMKP-3 hypomorphic mutants exhibited extra photoreceptor cells and wing veins, and its null mutants showed striking phenotypes, such as embryonic lethality and severe defects in oogenesis. All of these phenotypes were highly similar to those of the gain-of-function mutants of DERK/rl. The functional interaction between DMKP-3 and the Ras/DERK pathway was further confirmed by genetic interactions between DMKP-3 loss-of-function mutants or overexpressing transgenic flies and various mutants of the Ras/DERK pathway. Collectively, these data provide the direct evidences that DMKP-3 is indispensable to the regulation of DERK signaling activity during Drosophila development.

scholarly journals The Classic Lobe Eye Phenotype of Drosophila Is Caused by Transposon Insertion-Induced Misexpression of a Zinc-Finger Transcription Factor

Genetics ◽  
2020 ◽  
Vol 216 (1) ◽  
pp. 117-134
Author(s):  
Wonseok Son ◽  
Kwang-Wook Choi
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Loss Of Function ◽  
Male Recombination ◽  
Link Type ◽  
Transposon Insertion ◽  
Eye Disc ◽  
Dominant Eye ◽  
Allele Specific ◽  
Dominant Mutants

Drosophila Lobe (L) alleles were first discovered ∼100 years ago as spontaneous dominant mutants with characteristic developmental eye defects. However, the molecular basis for L dominant eye phenotypes has not been clearly understood. A previous work reported identification of CG10109/PRAS40 as the L gene, but subsequent analyses suggested that PRAS40 may not be related to L. Here, we revisited the L gene to clarify this discrepancy and understand the basis for the dominance of L mutations. Genetic analysis localized the L gene to Oaz, which encodes a homolog of the vertebrate zinc finger protein 423 (Zfp423) family transcriptional regulators. We demonstrate that RNAi knockdown of Oaz almost completely restores all L dominant alleles tested. Lrev6-3, a revertant allele of the L2 dominant eye phenotype, has an inframe deletion in the Oaz coding sequence. Molecular analysis of L dominant mutants identified allele-specific insertions of natural transposons (roo[ ]L1, hopper[ ]L5, and roo[ ]Lr) or alterations of a preexisting transposon (L2-specific mutations in roo[ ]Mohr) in the Oaz region. In addition, we generated additional L2-reversion alleles by CRISPR targeting at Oaz. These new loss-of-function Oaz mutations suppress the dominant L eye phenotype. Oaz protein is not expressed in wild-type eye disc but is expressed ectopically in L2/+ mutant eye disc. We induced male recombination between Oaz-GAL4 insertions and the L2 mutation through homologous recombination. By using the L2-recombined GAL4 reporters, we show that Oaz-GAL4 is expressed ectopically in L2 eye imaginal disc. Taken together, our data suggest that neomorphic L eye phenotypes are likely due to misregulation of Oaz by spontaneous transposon insertions.

scholarly journals The Drosophila bifocal gene encodes a novel protein which colocalizes with actin and is necessary for photoreceptor morphogenesis.

1997 ◽  
Vol 17 (9) ◽  
pp. 5521-5529 ◽  
Author(s):  
S M Bahri ◽  
X Yang ◽  
W Chia
Keyword(s):  
Compound Eye ◽  
Photoreceptor Cells ◽  
P Element ◽  
Apical Surface ◽  
Loss Of Function ◽  
Filamentous Actin ◽  
Light Gathering ◽  
Morphological Defects ◽  
Microvillar Structure ◽  
Eye Imaginal Disc

Photoreceptor cells of the Drosophila compound eye begin to develop specialized membrane foldings at the apical surface in midpupation. The microvillar structure ultimately forms the rhabdomere, an actin-rich light-gathering organelle with a characteristic shape and morphology. In a P-element transposition screen, we isolated mutations in a gene, bifocal (bif), which is required for the development of normal rhabdomeres. The morphological defects seen in bif mutant animals, in which the distinct contact domains established by the newly formed rhabdomeres are abnormal, first become apparent during midpupal development. The later defects seen in the mutant adult R cells are more dramatic, with the rhabdomeres enlarged, elongated, and frequently split. bif encodes a novel putative protein of 1063 amino acids which is expressed in the embryo and the larval eye imaginal disc in a pattern identical to that of F actin. During pupal development, Bif localizes to the base of the filamentous actin associated with the forming rhabdomeres along one side of the differentiating R cells. On the basis of its subcellular localization and loss-of-function phenotype, we discuss possible roles of Bif in photoreceptor morphogenesis.

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.

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 A Genetic Screen for Novel Components of the Notch Signaling Pathway During Drosophila Bristle Development

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 211-220 ◽  
Author(s):  
Masahiro J Go ◽  
Spyros Artavanis-Tsakonas
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Genetic Modifier ◽  
Notch Pathway ◽  
Central Element ◽  
Notch Signaling Pathway ◽  
Notch Receptor ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Signaling Mechanism

Abstract The Notch receptor is the central element in a cell signaling mechanism controlling a broad spectrum of cell fate choices. Genetic modifier screens in Drosophila and subsequent molecular studies have identified several Notch pathway components, but the biochemical nature of signaling is still elusive. Here, we report the results of a genetic modifier screen of the bristle phenotype of a gain-of-function Notch allele, Abruptex16. Abruptex mutations interfere with lateral inhibition/specification events that control the segregation of epidermal and sensory organ precursor lineages, thus inhibiting bristle formation. Mutations that reduce Notch signaling suppress this phenotype. This screen of approximately 50,000 flies led to the identification of a small number of dominant suppressors in seven complementation groups. These include known components in the pathway, Notch, mastermind, Delta, and Hairless, as well as two novel mutations. The first, A122, appears to interact with Notch only during bristle development. The other, M285, displays extensive genetic interactions with the Notch pathway elements and appears, in general, capable of suppressing Notch gain-of-function phenotypes while enhancing Notch loss-of-function phenotypes, suggesting that it plays an important role in Notch signaling.

Actin and α-tubulin immuno-EM labelings reveal differences in intra versus interphotoreceptor matrix

1990 ◽  
Vol 48 (3) ◽  
pp. 466-467
Author(s):  
Matti Järvilehto ◽  
Riitta Harjula
Keyword(s):  
Compound Eye ◽  
Frozen Section ◽  
Smooth Muscle Actin ◽  
Photoreceptor Cells ◽  
Immune Serum ◽  
Cell Organelles ◽  
Calliphora Erythrocephala ◽  
Optical Axes ◽  
Interphotoreceptor Matrix ◽  
Similar Kind

The photoreceptor cells in the compound eyes of higher diptera are clustered in groups (ommatidia) of eight receptor cells. The cells from six adjacent ommatidia are organized into optical units, neuro-ommatia sharing the same visual field. In those ommatidia the optical axes of the photopigment containing structures (rhabdomeres) are parallel. The rhabdomeres of the photoreceptor cells are separated from each other by an interstitial i.e innerommatidial space (IOS). In the photoreceptor cell body, besides of the normal cell organelles, a cellular matrix is a structurally apparent component. Similar kind of reticular formation is also found in the IOS containing some unidentified filamentary substance, of which composition and functional significance for optical properties of vision is the aim of this report.The prefixed (2% PA + 0.2% GA in 0.1-n phosphate buffer, pH 7.4, for 1h), frozen section blocks of the compound eye of the blowfly (Calliphora erythrocephala) were prepared by immuno-cryo-techniques. The ultrathin cryosections were incubated with antibodies of monoclonal α-tubulin and polyclonal smooth muscle actin. Control labelings of excess of antigen, non-immune serum and non-present antibody were perforated.

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