The role of Ire1 in Drosophila eye pigmentation revealed by an RNase dead allele

2021 ◽  
Author(s):  
Sahana Mitra ◽  
Hyung Don Ryoo
Keyword(s):  
Drosophila Eye ◽  
Eye Pigmentation

Jun mediates Frizzled-induced R3/R4 cell fate distinction and planar polarity determination in the Drosophila eye

Development ◽  
2000 ◽  
Vol 127 (16) ◽  
pp. 3619-3629 ◽  
Author(s):  
U. Weber ◽  
N. Paricio ◽  
M. Mlodzik
Keyword(s):  
Cell Fate ◽  
Genetic Interaction ◽  
Function Analysis ◽  
Loss Of Function ◽  
Planar Polarity ◽  
Jnk Signaling ◽  
Drosophila Eye ◽  
Polarity Determination ◽  
Signaling Components

Jun acts as a signal-regulated transcription factor in many cellular decisions, ranging from stress response to proliferation control and cell fate induction. Genetic interaction studies have suggested that Jun and JNK signaling are involved in Frizzled (Fz)-mediated planar polarity generation in the Drosophila eye. However, simple loss-of-function analysis of JNK signaling components did not show comparable planar polarity defects. To address the role of Jun and JNK in Fz signaling, we have used a combination of loss- and gain-of-function studies. Like Fz, Jun affects the bias between the R3/R4 photoreceptor pair that is critical for ommatidial polarity establishment. Detailed analysis of jun(−) clones reveals defects in R3 induction and planar polarity determination, whereas gain of Jun function induces the R3 fate and associated polarity phenotypes. We find also that affecting the levels of JNK signaling by either reduction or overexpression leads to planar polarity defects. Similarly, hypomorphic allelic combinations and overexpression of the negative JNK regulator Puckered causes planar polarity eye phenotypes, establishing that JNK acts in planar polarity signaling. The observation that Dl transcription in the early R3/R4 precursor cells is deregulated by Jun or Hep/JNKK activation, reminiscent of the effects seen with Fz overexpression, suggests that Jun is one of the transcription factors that mediates the effects of fz in planar polarity generation.

scholarly journals Analyzing the role of CtBP in Drosophila eye development

2008 ◽  
Vol 319 (2) ◽  
pp. 495-496
Author(s):  
Burnett Micheal ◽  
C.Q. Hoang ◽  
A. Sandoval ◽  
J. Curtiss
Keyword(s):  
Eye Development ◽  
Drosophila Eye

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.

Notch signalling and the initiation of neural development in the Drosophila eye

Development ◽  
2001 ◽  
Vol 128 (20) ◽  
pp. 3889-3898 ◽  
Author(s):  
Antonio Baonza ◽  
Matthew Freeman
Keyword(s):  
Neural Development ◽  
Notch Signalling ◽  
The Other ◽  
Signalling Pathways ◽  
Notch Signalling Pathway ◽  
Drosophila Eye ◽  
Dependent Signal ◽  
Notch Activation ◽  
Number Of Cells

Neural determination in the Drosophila eye occurs progressively. A diffusible signal, Dpp, causes undetermined cells first to adopt a ‘pre-proneural’ state in which they are primed to start differentiating. A second signal is required to trigger the activation of the transcription factor Atonal, which causes the cells to initiate overt photoreceptor neurone differentiation. Both Dpp and the second signal are dependent on Hedgehog (Hh) signalling. Previous work has shown that the Notch signalling pathway also has a proneural role in the eye (as well as a later, opposite function when it restricts the number of cells becoming photoreceptors – a process of lateral inhibition). It is not clear how the early proneural role of Notch integrates with the other signalling pathways involved. We provide evidence that Notch activation by its ligand Delta is the second Hh-dependent signal required for neural determination. Notch activity normally only triggers Atonal expression in cells that have adopted the pre-proneural state induced by Dpp. We also report that Notch drives the transition from pre-proneural to proneural by downregulating two repressors of Atonal: Hairy and Extramacrochaetae.

The role of selectins in Drosophila eye and bristle development

Development ◽  
1997 ◽  
Vol 124 (1) ◽  
pp. 169-180 ◽  
Author(s):  
L.A. Leshko-Lindsay ◽  
V.G. Corces
Keyword(s):  
Protein Interactions ◽  
Transmembrane Domain ◽  
Lectin Binding ◽  
Imaginal Discs ◽  
Binding Domain ◽  
Sensory Organs ◽  
Cell Determination ◽  
Drosophila Eye

Mutations in the furrowed (fw) gene of Drosophila result in defects in the development of the eye and mechanosensory bristles. The eyes are reduced in size, have furrows or crevices in the retina, and show a disturbed patterning of ommatidia. In addition, the ommatidia have an altered morphology and often contain abnormal numbers of cells. The bristles show altered structure and polarity, and are occasionally duplicated or missing. These results suggest that the product of thefw gene is involved in cell determination events within sensory organs. Thefw gene has been cloned and shown to encode a protein homologous to vertebrate selectins. Like selectins, Fw contains a lectin-binding domain, ten complement binding repeats, and a transmembrane domain. The Fw protein is expressed in the larval imaginal discs where it might mediate carbohydrate-protein interactions necessary for proper development of a subset of adult sensory organs.

scholarly journals Dominant Defects in Drosophila Eye Pigmentation Resulting From a Euchromatin-Heterochromatin Fusion Gene

Genetics ◽  
1998 ◽  
Vol 150 (4) ◽  
pp. 1551-1566 ◽  
Author(s):  
Yikang S Rong ◽  
Kent G Golic
Keyword(s):  
Repetitive Dna ◽  
Fusion Gene ◽  
Coding Region ◽  
Dominant Mutation ◽  
Thin Ring ◽  
Drosophila Homolog ◽  
Drosophila Eye ◽  
Methylenetetrahydrofolate Dehydrogenase ◽  
Highly Repetitive Dna ◽  
Eye Pigmentation

Abstract We have isolated a dominant mutation, pugilistDominant (pug D), that causes variegated reductions in pteridine and ommochrome pigmentation of the Drosophila eye. The effect of pugD on pteridine pigmentation is most dramatic: the only remaining pigment consists of a thin ring of pigment around the periphery of the eye with a few scattered spots in the center. The pugD mutation disrupts a gene that encodes a Drosophila homolog of the trifunctional enzyme methylenetetrahydrofolate dehydrogenase (MTHFD; E.C.1.5.1.5, E.C.3.5.4.9, E.C.6.3.4.3). This enzyme produces a cofactor that is utilized in purine biosynthesis. Because pteridines are derived from GTP, the pigment defect may result from an impairment in the production of purines. The mutant allele consists of a portion of the MTHFD coding region fused to ∼1 kb of highly repetitive DNA. Transcription and translation of both parts are required for the phenotype. The repetitive DNA consists of ∼140 nearly perfect repeats of the sequence AGAGAGA, a significant component of centric heterochromatin. The unusual nature of the protein produced by this gene may be responsible for its dominance. The repetitive DNA may also account for the variegated aspect of the phenotype. It may promote occasional association of the pugD locus with centric heterochromatin, accompanied by inactivation of pugD, in a manner similar to the proposed mode of action for brownDominant.

Sign in / Sign up

Export Citation Format

Share Document