scholarly journals Regulation of cone cell formation by Canoe and Ras in the developing Drosophila eye

Development ◽  
1997 ◽  
Vol 124 (14) ◽  
pp. 2671-2680 ◽  
Author(s):  
T. Matsuo ◽  
K. Takahashi ◽  
S. Kondo ◽  
K. Kaibuchi ◽  
D. Yamamoto
Keyword(s):  
Compound Eye ◽  
Gene Dosage ◽  
Active Form ◽  
Cell Formation ◽  
Dominant Negative ◽  
Negative Regulator ◽  
Pigment Cells ◽  
Equivalence Group ◽  
Cone Cell ◽  
Cone Cells

Cone cells are lens-secreting cells in ommatidia, the unit eyes that compose the compound eye of Drosophila. Each ommatidium contains four cone cells derived from precursor cells of the R7 equivalence group which express the gene sevenless (sev). When a constitutively active form of Ras1 (Ras1V12) is expressed in the R7 equivalence group cells using the sev promoter (sev-Ras1V12), additional cone cells are formed in the ommatidium. Expression of Ras1N17, a dominant negative form of Ras1, results in the formation of 1–3 fewer cone cells than normal in the ommatidium. The effects of Ras1 variants on cone cell formation are modulated by changing the gene dosage at the canoe (cno) locus, which encodes a cytoplasmic protein with Ras-binding activity. An increase or decrease in gene dosage potentiates the sev-Ras1v12 action, leading to marked induction of cone cells. A decrease in cno+ activity also enhances the sev-Ras1N17 action, resulting in a further decrease in the number of cone cells contained in the ommatidium. In the absence of expression of sev-Ras1V12 or sev-Ras1N17, an overdose of wild-type cno (cno+) promotes cone cell formation while a significant reduction in cno+ activity results in the formation of 1–3 fewer cone cells than normal in the ommatidium. We propose that there are two signaling pathways in cone cell development, one for its promotion and the other for its repression, and Cno functions as a negative regulator for both pathways. We also postulate that Cno predominantly acts on a prevailing pathway in a given developmental context, thereby resulting in either an increase or a decrease in the number of cone cells per ommatidium. The extra cone cells resulting from the interplay of Ras1v12 and Cno are generated from a pool of undifferentiated cells that are normally fated to develop into pigment cells or undergo apoptosis.

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.

How small can small be: The compound eye of the parasitoid waspTrichogramma evanescens(Westwood, 1833) (Hymenoptera, Hexapoda), an insect of 0.3- to 0.4-mm total body size

2010 ◽  
Vol 28 (4) ◽  
pp. 295-308 ◽  
Author(s):  
STEFAN FISCHER ◽  
CARSTEN H.G. MÜLLER ◽  
V. BENNO MEYER-ROCHOW
Keyword(s):  
Compound Eye ◽  
Uv Light ◽  
Parasitoid Wasp ◽  
Pigment Cells ◽  
Compound Eyes ◽  
Trichogramma Evanescens ◽  
Cone Cells ◽  
Males And Females ◽  
Total Body ◽  
Effective Use

AbstractWith a body length of only 0.3–0.4 mm, the parasitoid waspTrichogramma evanescens(Westwood) is one of the smallest insects known. Yet, despite its diminutive size, it possesses compound eyes that are of oval shapes, measuring across their long axes in dorsoventral direction 63.39 and 71.11μm in males and females, respectively. The corresponding facet diameters are 5.90μm for males and 6.39μm for females. Owing to the small radii of curvature of the eyes in males (34.59μm) and females (42.82μm), individual ommatidia are short with respective lengths of 24.29 and 34.97μm. The eyes are of the apposition kind, and each ommatidium possesses four cone cells of the eucone type and a centrally fused rhabdom, which throughout its length is formed by no more than eight retinula cells. A ninth cell occupies the place of the eighth retinula cell in the distal third of the rhabdom. The cone is shielded by two primary and six secondary pigment cells, all with no apparent extensions to the basement membrane, unlike the case in larger hymenopterans. The regular and dense packing of the rhabdoms reflects an effective use of space. Calculations on the optics of the eyes ofTrichogrammasuggest that the eyes need not be diffraction limited, provided they use mostly shorter wavelengths, that is, UV light. Publications on the visual behavior of these wasps confirmTrichogramma’s sensitivity to UV radiation. On the basis of our findings, some general functional conclusions for very small compound eyes are formulated.

The compound eye of Archichauliodes (Megaloptera)

1971 ◽  
Vol 179 (1054) ◽  
pp. 65-72 ◽  
Keyword(s):  
Electron Microscopy ◽  
Compound Eye ◽  
Systematic Position ◽  
Pigment Cells ◽  
Retinula Cell ◽  
Cell Cytoplasm ◽  
Cone Cell

The ommatidial structure of Archichauliodes , as shown by electron microscopy, agrees with its systematic position as a primitive endopterygote insect. The eight retinula cells form a long column with distally placed nuclei and proximally located rhabdomeres. In the dark-adapted eye four of the retinula cell bodies reach the cone tip but in the light-adapted eye there is a crystalline tract up to 100 µ m long formed by extensions of the cone. Microtubules are abundant in the cells which move on adaptation, i.e. the cone cell cytoplasm and the primary pigment cells which surround the crystalline tract. This paper forms the first of a group on the neuropteran type of compound eye, found also in some Coleoptera and Lepidoptera.

Akt Activation Is Necessary for Growth Factor–Induced Trafficking of Functional KCa Channels in Developing Parasympathetic Neurons

2005 ◽  
Vol 93 (3) ◽  
pp. 1174-1182 ◽  
Author(s):  
Kwon-Seok Chae ◽  
Miguel Martin-Caraballo ◽  
Marc Anderson ◽  
Stuart E. Dryer
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Developmental Regulation ◽  
Active Form ◽  
Transforming Growth Factor Β1 ◽  
Dominant Negative ◽  
Negative Regulator ◽  
Akt Inhibitor ◽  
Akt Phosphorylation ◽  
Akt Activation

The protein kinase Akt is a crucial regulator of neuronal survival and apoptosis. Here we show that Akt activation is necessary for mobilization of large-conductance KCa channels in ciliary ganglion (CG) neurons evoked by β-neuregulin-1 (NRG1) and transforming growth factor-β1 (TGFβ1). Application of NRG1 to embryonic day 9 (E9) CG neurons increased Akt phosphorylation, as observed previously for TGFβ1. NRG1- and TGFβ1-evoked stimulation of KCa is blocked by inhibitors of PI3K by overexpression of a dominant-negative form of Akt, by overexpression of CTMP, an endogenous negative regulator of Akt, and by application of the Akt inhibitor 1L-6-hydroxymethyl-chiro-inositol 2-( R)-2- O-methyl-3- O-octadecylcarbonate (HIMO). Conversely, overexpression of a constitutively-active form of Akt was sufficient by itself to increase mobilization of functional KCa channels. NRG1 and TGFβ1 evoked an Akt-dependent increase in cell-surface SLO α-subunits. These procedures have no effect on voltage-activated Ca2+ currents. Thus Akt plays an essential role in the developmental regulation of excitability in CG neurons.

scholarly journals p38 Mitogen-Activated Protein Kinase Can Be Involved in Transforming Growth Factor β Superfamily Signal Transduction in Drosophila Wing Morphogenesis

1999 ◽  
Vol 19 (3) ◽  
pp. 2322-2329 ◽  
Author(s):  
Takashi Adachi-Yamada ◽  
Makoto Nakamura ◽  
Kenji Irie ◽  
Yoshinori Tomoyasu ◽  
Yorikata Sano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Transforming Growth Factor ◽  
Gene Dosage ◽  
Active Form ◽  
Fruit Fly ◽  
Transforming Growth Factor Β ◽  
Dominant Negative ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein

ABSTRACT p38 mitogen-activated protein kinase (p38) has been extensively studied as a stress-responsive kinase, but its role in development remains unknown. The fruit fly, Drosophila melanogaster, has two p38 genes, D-p38a and D-p38b. To elucidate the developmental function of the Drosophilap38’s, we used various genetic and pharmacological manipulations to interfere with their functions: expression of a dominant-negative form of D-p38b, expression of antisense D-p38b RNA, reduction of theD-p38 gene dosage, and treatment with the p38 inhibitor SB203580. Expression of a dominant-negative D-p38b in the wing imaginal disc caused a decapentaplegic (dpp)-like phenotype and enhanced the phenotype of a dpp mutant. Dpp is a secretory ligand belonging to the transforming growth factor β superfamily which triggers various morphogenetic processes through interaction with the receptor Thick veins (Tkv). Inhibition of D-p38b function also caused the suppression of the wing phenotype induced by constitutively active Tkv (TkvCA). Mosaic analysis revealed that D-p38b regulates the Tkv-dependent transcription of theoptomotor-blind (omb) gene in non-Dpp-producing cells, indicating that the site of D-p38b action is downstream of Tkv. Furthermore, forced expression of TkvCA induced an increase in the phosphorylated active form(s) of D-p38(s). These results demonstrate that p38, in addition to its role as a transducer of emergency stress signaling, may function to modulate Dpp signaling.

scholarly journals Differential Regulation of Retinoblastoma Tumor Suppressor Protein by G1 Cyclin-Dependent Kinase Complexes In Vivo

2001 ◽  
Vol 21 (14) ◽  
pp. 4773-4784 ◽  
Author(s):  
Sergei A. Ezhevsky ◽  
Alan Ho ◽  
Michelle Becker-Hapak ◽  
Penny K. Davis ◽  
Steven F. Dowdy
Keyword(s):  
Cyclin E ◽  
Active Form ◽  
Dominant Negative ◽  
Tumor Suppressor Protein ◽  
Cyclin D ◽  
Cyclin Dependent Kinase ◽  
Retinoblastoma Tumor Suppressor Protein ◽  
Retinoblastoma Tumor Suppressor ◽  
Retinoblastoma Tumor

ABSTRACT The retinoblastoma tumor suppressor protein (pRB) negatively regulates early-G1 cell cycle progression, in part, by sequestering E2F transcription factors and repressing E2F-responsive genes. Although pRB is phosphorylated on up to 16 cyclin-dependent kinase (Cdk) sites by multiple G1 cyclin-Cdk complexes, the active form(s) of pRB in vivo remains unknown. pRB is present as an unphosphorylated protein in G0 quiescent cells and becomes hypophosphorylated (∼2 mol of PO4 to 1 mol of pRB) in early G1 and hyperphosphorylated (∼10 mol of PO4 to 1 mol of pRB) in late G1 phase. Here, we report that hypophosphorylated pRB, present in early G1, represents the biologically active form of pRB in vivo that is assembled with E2Fs and E1A but that both unphosphorylated pRB in G0 and hyperphosphorylated pRB in late G1 fail to become assembled with E2Fs and E1A. Furthermore, using transducible dominant-negative TAT fusion proteins that differentially target cyclin D-Cdk4 or cyclin D-Cdk6 (cyclin D-Cdk4/6) and cyclin E-Cdk2 complexes, namely, TAT-p16 and TAT–dominant-negative Cdk2, respectively, we found that, in vivo, cyclin D-Cdk4/6 complexes hypophosphorylate pRB in early G1 and that cyclin E-Cdk2 complexes inactivate pRB by hyperphosphorylation in late G1. Moreover, we found that cycling human tumor cells expressing deregulated cyclin D-Cdk4/6 complexes, due to deletion of the p16 INK4a gene, contained hypophosphorylated pRB that was bound to E2Fs in early G1and that E2F-responsive genes, including those for dihydrofolate reductase and cyclin E, were transcriptionally repressed. Thus, we conclude that, physiologically, pRB is differentially regulated by G1 cyclin-Cdk complexes.

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.

Developing compound eye in lozenge mutants of Drosophila : lozenge expression in the R7 equivalence group

1997 ◽  
Vol 206 (8) ◽  
pp. 481-493 ◽  
Author(s):  
J. R. Crew ◽  
Philip Batterham ◽  
J. A. Pollock
Keyword(s):  
Compound Eye ◽  
Equivalence Group

scholarly journals Activation of Hepatitis B Virus S Promoter by a Cell Type-Restricted IRE1-Dependent Pathway Induced by Endoplasmic Reticulum Stress

2005 ◽  
Vol 25 (17) ◽  
pp. 7522-7533 ◽  
Author(s):  
Zhi-Ming Huang ◽  
Thomas Tan ◽  
Hiderou Yoshida ◽  
Kazutoshi Mori ◽  
Yanjun Ma ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Er Stress ◽  
Transcriptional Activation ◽  
Active Form ◽  
Dominant Negative ◽  
Dependent Manner ◽  
Cell Type ◽  
B Virus

ABSTRACT IRE1-alpha is an integral membrane protein of the endoplasmic reticulum (ER) that is a key sensor in the cellular transcriptional response to stress in the ER. Upon induction of ER stress, IRE1-alpha is activated, resulting in the synthesis of the active form of the transcription factor XBP1 via IRE1-mediated splicing of its mRNA. In this report, we have examined the role of IRE1-alpha and XBP1 in activation of the hepatitis B virus S promoter by ER stress. Cotransfection experiments revealed that overexpression of either IRE1-alpha or XBP1 activated this promoter. Conversely, cotransfected dominant-negative IRE1-alpha or small interfering RNA directed against XBP1 decreased the activation of the S promoter by ER stress, confirming an important role for the IRE1-alpha/XBP1 signaling pathway in activation of the S promoter. However, XBP1 does not bind directly to the S promoter; rather, a novel S promoter-binding complex that does not contain XBP1 is induced in cells undergoing ER stress in an XBP1-dependent manner. This complex, as well as transcriptional activation of the S promoter, is induced by ER stress in hepatocytes but not in fibroblasts, despite the presence of active XBP1 in the latter. Thus, the hepatitis B virus S promoter responds to a novel, cell type-restricted transcriptional pathway downstream of IRE1-alpha and XBP1.

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