Broad-complex, but not ecdysone receptor, is required for progression of the morphogenetic furrow in the Drosophila eye

Development ◽  
2001 ◽  
Vol 128 (1) ◽  
pp. 1-11 ◽  
Author(s):  
C.A. Brennan ◽  
T.R. Li ◽  
M. Bender ◽  
F. Hsiung ◽  
K. Moses
Keyword(s):  
Zinc Finger ◽  
Receptor Gene ◽  
Ecdysone Receptor ◽  
Morphogenetic Furrow ◽  
Response Gene ◽  
Ecdysteroid Receptor ◽  
Receptor Isoforms ◽  
Eye Disc ◽  
Drosophila Eye ◽  
Broad Complex

The progression of the morphogenetic furrow in the developing Drosophila eye is an early metamorphic, ecdysteroid-dependent event. Although Ecdysone receptor-encoded nuclear receptor isoforms are the only known ecdysteroid receptors, we show that the Ecdysone receptor gene is not required for furrow function. DHR78, which encodes another candidate ecdysteroid receptor, is also not required. In contrast, zinc finger-containing isoforms encoded by the early ecdysone response gene Broad-complex regulate furrow progression and photoreceptor specification. br-encoded Broad-complex subfunctions are required for furrow progression and proper R8 specification, and are antagonized by other subfunctions of Broad-complex. There is a switch from Broad complex Z2 to Z1 zinc-finger isoform expression at the furrow which requires Z2 expression and responds to Hedgehog signals. These results suggest that a novel hormone transduction hierarchy involving an uncharacterized receptor operates in the eye disc.

Role of the morphogenetic furrow in establishing polarity in the Drosophila eye

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4085-4094 ◽  
Author(s):  
F. Chanut ◽  
U. Heberlein
Keyword(s):  
Ectopic Expression ◽  
Morphogenetic Furrow ◽  
Eye Disc ◽  
Drosophila Eye ◽  
Retinal Epithelium ◽  
Anteroposterior Polarity ◽  
Crystalline Array

The Drosophila retina is a crystalline array of 800 ommatidia whose organization and assembly suggest polarization of the retinal epithelium along anteroposterior and dorsoventral axes. The retina develops by a stepwise process following the posterior-to-anterior progression of the morphogenetic furrow across the eye disc. Ectopic expression of hedgehog or local removal of patched function generates ectopic furrows that can progress in any direction across the disc leaving in their wake differentiating fields of ectopic ommatidia. We have studied the effect of these ectopic furrows on the polarity of ommatidial assembly and rotation. We find that the anteroposterior asymmetry of ommatidial assembly parallels the progression of ectopic furrows, regardless of their direction. In addition, ommatidia developing behind ectopic furrows rotate coordinately, forming equators in various regions of the disc. Interestingly, the expression of a marker normally restricted to the equator is induced in ectopic ommatidial fields. Ectopic equators are stable as they persist to adulthood, where they can coexist with the normal equator. Our results suggest that ectopic furrows can impart polarity to the disc epithelium, regarding the direction of both assembly and rotation of ommatidia. We propose that these processes are polarized as a consequence of furrow propagation, while more global determinants of dorsoventral and anteroposterior polarity may act less directly by determining the site of furrow initiation.

Hedgehog is an indirect regulator of morphogenetic furrow progression in the Drosophila eye disc

Development ◽  
1997 ◽  
Vol 124 (17) ◽  
pp. 3233-3240 ◽  
Author(s):  
D.I. Strutt ◽  
M. Mlodzik
Keyword(s):  
Pattern Formation ◽  
Imaginal Disc ◽  
Morphogenetic Furrow ◽  
Anterior Edge ◽  
Eye Disc ◽  
Drosophila Eye ◽  
Eye Imaginal Disc ◽  
Inductive Signal ◽  
Rate Of Movement

Pattern formation in the eye imaginal disc of Drosophila occurs in a wave that moves from posterior to anterior. The anterior edge of this wave is marked by a contracted band of cells known as the morphogenetic furrow, behind which photoreceptors differentiate. The movement of the furrow is dependent upon the secretion of the signalling protein Hedgehog (Hh) by more posterior cells, and it has been suggested that Hh acts as an inductive signal to induce cells to enter a furrow fate and begin differentiation. To further define the role of Hh in this process, we have analysed clones of cells lacking the function of the smoothened (smo) gene, which is required for transduction of the Hh signal and allows the investigation of the autonomous requirement for hh signalling. These experiments demonstrate that the function of hh in furrow progression is indirect. Cells that cannot receive/transduce the Hh signal are still capable of entering a furrow fate and differentiating normally. However, hh is required to promote furrow progression and regulate its rate of movement across the disc, since the furrow is significantly delayed in smo clones.

The role of Wingless signaling in establishing the anteroposterior and dorsoventral axes of the eye disc

Development ◽  
2001 ◽  
Vol 128 (9) ◽  
pp. 1519-1529 ◽  
Author(s):  
J.D. Lee ◽  
J.E. Treisman
Keyword(s):  
Signaling Molecules ◽  
Morphogenetic Furrow ◽  
Wild Type ◽  
Dorsoventral Axis ◽  
Eye Disc ◽  
Wingless Signaling ◽  
Drosophila Eye ◽  
Ectopic Activation ◽  
Lateral Margins

The posteriorly expressed signaling molecules Hedgehog and Decapentaplegic drive photoreceptor differentiation in the Drosophila eye disc, while at the anterior lateral margins Wingless expression blocks ectopic differentiation. We show here that mutations in axin prevent photoreceptor differentiation and lead to tissue overgrowth and that both these effects are due to ectopic activation of the Wingless pathway. In addition, ectopic Wingless signaling causes posterior cells to take on an anterior identity, reorienting the direction of morphogenetic furrow progression in neighboring wild-type cells. We also show that signaling by Decapentaplegic and Hedgehog normally blocks the posterior expression of anterior markers such as Eyeless. Wingless signaling is not required to maintain anterior Eyeless expression and in combination with Decapentaplegic signaling can promote its downregulation, suggesting that additional molecules contribute to anterior identity. Along the dorsoventral axis of the eye disc, Wingless signaling is sufficient to promote dorsal expression of the Iroquois gene mirror, even in the absence of the upstream factor pannier. However, Wingless signaling does not lead to ventral mirror expression, implying the existence of ventral repressors.

wingless inhibits morphogenetic furrow movement in the Drosophila eye disc

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3519-3527 ◽  
Author(s):  
J.E. Treisman ◽  
G.M. Rubin
Keyword(s):  
Posterior Margin ◽  
Ectopic Expression ◽  
Spatial Localization ◽  
Morphogenetic Furrow ◽  
Differentiated Cells ◽  
Repetitive Process ◽  
Eye Disc ◽  
Drosophila Eye ◽  
Lateral Margins ◽  
Eye Imaginal Disc

Differentiation of the Drosophila eye imaginal disc is an asynchronous, repetitive process which proceeds across the disc from posterior to anterior. Its propagation correlates with the expression of decapentaplegic at the front of differentiation, in the morphogenetic furrow. Both differentiation and decapentaplegic expression are maintained by Hedgehog protein secreted by the differentiated cells posterior to the furrow. However, their initiation at the posterior margin occurs prior to hedgehog expression by an unknown mechanism. We show here that the wingless gene contributes to the correct spatial localization of initiation. Initiation of the morphogenetic furrow is restricted to the posterior margin by the presence of wingless at the lateral margins; removal of wingless allows lateral initiation. Ectopic expression of wingless at the posterior margin can also inhibit normal initiation. In addition, the presence of wingless in the center of the disc can prevent furrow progression. These effects of wingless are achieved without altering the expression of decapentaplegic.

Drosophila EcR-B ecdysone receptor isoforms are required for larval molting and for neuron remodeling during metamorphosis

Development ◽  
1998 ◽  
Vol 125 (11) ◽  
pp. 2053-2062 ◽  
Author(s):  
M. Schubiger ◽  
A.A. Wade ◽  
G.E. Carney ◽  
J.W. Truman ◽  
M. Bender
Keyword(s):  
Nervous System ◽  
Wide Spectrum ◽  
Control Cell ◽  
P Element ◽  
Ecdysone Receptor ◽  
Larval Stages ◽  
Receptor Isoforms ◽  
Imprecise Excision ◽  
Cell Type Specific ◽  
Insect Central Nervous System

During the metamorphic reorganization of the insect central nervous system, the steroid hormone 20-hydroxyecdysone induces a wide spectrum of cellular responses including neuronal proliferation, maturation, cell death and the remodeling of larval neurons into their adult forms. In Drosophila, expression of specific ecdysone receptor (EcR) isoforms has been correlated with particular responses, suggesting that different EcR isoforms may govern distinct steroid-induced responses in these cells. We have used imprecise excision of a P element to create EcR deletion mutants that remove the EcR-B promoter and therefore should lack EcR-B1 and EcR-B2 expression but retain EcR-A expression. Most of these EcR-B mutant animals show defects in larval molting, arresting at the boundaries between the three larval stages, while a smaller percentage of EcR-B mutants survive into the early stages of metamorphosis. Remodeling of larval neurons at metamorphosis begins with the pruning back of larval-specific dendrites and occurs as these cells are expressing high levels of EcR-B1 and little EcR-A. This pruning response is blocked in the EcR-B mutants despite the fact that adult-specific neurons, which normally express only EcR-A, can progress in their development. These observations support the hypothesis that different EcR isoforms control cell-type-specific responses during remodeling of the nervous system at metamorphosis.

scholarly journals dE2F2-Independent Rescue of Proliferation in Cells Lacking an Activator dE2F1

2007 ◽  
Vol 27 (24) ◽  
pp. 8561-8570 ◽  
Author(s):  
Aaron M. Ambrus ◽  
Brandon N. Nicolay ◽  
Vanya I. Rasheva ◽  
Richard J. Suckling ◽  
Maxim V. Frolov
Keyword(s):  
Cell Cycle ◽  
Morphogenetic Furrow ◽  
Independent Manner ◽  
Dead Box ◽  
Cycle Arrest ◽  
Eye Disc ◽  
Severe Reduction ◽  
Functional Inactivation ◽  
Mutant Cells ◽  
Dependent Mechanism

ABSTRACT In Drosophila melanogaster, the loss of activator de2f1 leads to a severe reduction in cell proliferation and repression of E2F targets. To date, the only known way to rescue the proliferation block in de2f1 mutants was through the inactivation of dE2F2. This suggests that dE2F2 provides a major contribution to the de2f1 mutant phenotype. Here, we report that in mosaic animals, in addition to de2f2, the loss of a DEAD box protein Belle (Bel) also rescues proliferation of de2f1 mutant cells. Surprisingly, the rescue occurs in a dE2F2-independent manner since the loss of Bel does not relieve dE2F2-mediated repression. In the eye disc, bel mutant cells fail to undergo a G1 arrest in the morphogenetic furrow, delay photoreceptor recruitment and differentiation, and show a reduction of the transcription factor Ci155. The down-regulation of Ci155 is important since it is sufficient to partially rescue proliferation of de2f1 mutant cells. Thus, mutation of bel relieves the dE2F2-mediated cell cycle arrest in de2f1 mutant cells through a novel Ci155-dependent mechanism without functional inactivation of the dE2F2 repressor.

Characterization of Star and its interactions with sevenless and EGF receptor during photoreceptor cell development in Drosophila

Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 1731-1745 ◽  
Author(s):  
A.L. Kolodkin ◽  
A.T. Pickup ◽  
D.M. Lin ◽  
C.S. Goodman ◽  
U. Banerjee
Keyword(s):  
Genetic Background ◽  
Egf Receptor ◽  
Transmembrane Domain ◽  
Loss Of Function ◽  
Morphogenetic Furrow ◽  
Eye Disc ◽  
Son Of Sevenless ◽  
Photoreceptor Development ◽  
Star Gene

Loss-of-function mutations in Star impart a dominant rough eye phenotype and, when homozygous, are embryonic lethal with ventrolateral cuticular defects. We have cloned the Star gene and show that it encodes a novel protein with a putative transmembrane domain. Star transcript is expressed in a dynamic pattern in the embryo including in cells of the ventral midline. In the larval eye disc, Star is expressed first at the morphogenetic furrow, then in the developing R2, R5, and R8 cells as well as in the posterior clusters of the disc in additional R cells. Star interacts with Drosophila EGF receptor in the eye and mosaic analysis of Star in the larval eye disc reveals that homozygous Star patches contain no developing R cells. Taken together with the expression pattern at the morphogenetic furrow, these results demonstrate an early role for Star in photoreceptor development. Additionally, loss-of-function mutations in Star act as suppressors of R7 development in a sensitized genetic background involving the Son of sevenless (Sos) locus, and overexpression of Star enhances R7 development in this genetic background. Based on the genetic interactions with Sos, we suggest that Star also has a later role in photoreceptor development including the recruitment of the R7 cell through the sevenless pathway.

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