scholarly journals Dominant-negative form of the Pax6 homologeyeless for tissue-specific loss-of-function studies in the developing eye and brain indrosophila

genesis ◽  
2002 ◽  
Vol 34 (1-2) ◽  
pp. 74-75 ◽  
Author(s):  
T. Niimi ◽  
J. Clements ◽  
W.J. Gehring ◽  
P. Callaerts
Keyword(s):  
Dominant Negative ◽  
Loss Of Function ◽  
Tissue Specific ◽  
Specific Loss ◽  
Dominant Negative Form ◽  
Negative Form

scholarly journals An EP overexpression screen for genetic modifiers of Notch pathway function in Drosophila melanogaster

2004 ◽  
Vol 83 (2) ◽  
pp. 71-82 ◽  
Author(s):  
LAUREN E. HALL ◽  
SHAUNA J. ALEXANDER ◽  
MICHAEL CHANG ◽  
NATHANIEL S. WOODLING ◽  
BARRY YEDVOBNICK
Keyword(s):  
Notch Signaling ◽  
Notch Pathway ◽  
Dominant Negative ◽  
Genetic Modifiers ◽  
Loss Of Function ◽  
Partial Loss ◽  
Dominant Negative Form ◽  
Nuclear Component ◽  
Pathway Function ◽  
Negative Form

The Notch pathway comprises a signal transduction cascade required for the proper formation of multiple tissues during metazoan development. Originally described in Drosophila for its role in nervous system formation, the pathway has attracted much wider interest owing to its fundamental roles in a range of developmental and disease-related processes. Despite extensive analysis, Notch signaling is not completely understood and it appears that additional components of the pathway remain to be identified and characterized. Here, we describe a novel genetic strategy to screen for additional Notch pathway genes. The strategy combines partial loss of function for pathway activity with Enhancer-promoter (EP)-induced overexpression of random loci across the dorsoventral wing margin. Mastermind (Mam) is a nuclear component of the Notch signaling cascade. Using a GAL4-UAS-driven dominant-negative form of Mam, we created a genotype that exhibits a completely penetrant dominant wing-nicking phenotype. This phenotype was assayed for enhancement or suppression after outcrossing to several thousand EP lines. The screen identified known components or modifiers of Notch pathway function, as well as several potential new components. Our results suggest that a genetic screen that combines partial loss of function with random gene overexpression might be a useful strategy in the analysis of developmental pathways.

Requirement ofFoxD3-class signaling for neural crest determination inXenopus

Development ◽  
2001 ◽  
Vol 128 (13) ◽  
pp. 2525-2536 ◽  
Author(s):  
Noriaki Sasai ◽  
Kenji Mizuseki ◽  
Yoshiki Sasai
Keyword(s):  
Neural Crest ◽  
Dominant Negative ◽  
Related Factor ◽  
Embryonic Patterning ◽  
Loss Of Function ◽  
Upstream Regulator ◽  
Dominant Negative Form ◽  
Neural Crest Differentiation ◽  
Negative Form

Fox factors (winged-helix transcription factors) play important roles in early embryonic patterning. We show here that FoxD3 (Forkhead 6) regulates neural crest determination in Xenopus embryos. Expression of FoxD3 in the presumptive neural crest region starts at the late gastrula stage in a manner similar to that of Slug, and overlaps with that of Zic-r1. When overexpressed in the embryo and in ectodermal explants, FoxD3 induces expression of neural crest markers. Attenuation of FoxD3-related signaling by a dominant-negative FoxD3 construct (FoxD3delN) inhibits neural crest differentiation in vivo without suppressing the CNS marker Sox2. Interestingly, these loss-of-function phenotypes are reversed by coinjecting Slug. In animal cap explants, neural crest differentiation induced by Slug and Wnt3a is also inhibited by FoxD3delN but not by a dominant-negative form of XBF2. Loss-of-function studies using dominant-negative forms of FoxD3 and Slug indicate that Slug induction by Zic factors requires FoxD3-related signaling, and that FoxD3 and Slug have different requirements in inducing downstream neural crest markers. These data demonstrate that FoxD3 (or its closely related factor) is an essential upstream regulator of neural crest determination.

scholarly journals Modulation of flight and feeding behaviours requires presynaptic IP3Rs in dopaminergic neurons

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Anamika Sharma ◽  
Gaiti Hasan
Keyword(s):  
Dopaminergic Neurons ◽  
Calcium Release ◽  
Neural Circuit ◽  
Dominant Negative ◽  
Neuronal Function ◽  
Axonal Projections ◽  
Dominant Negative Form ◽  
Internal States ◽  
Innate Behaviour ◽  
Negative Form

Innate behaviours, although robust and hard wired, rely on modulation of neuronal circuits, for eliciting an appropriate response according to internal states and external cues. Drosophila flight is one such innate behaviour that is modulated by intracellular calcium release through inositol 1,4,5-trisphosphate receptors (IP3Rs). Cellular mechanism(s) by which IP3Rs modulate neuronal function for specific behaviours remain speculative, in vertebrates and invertebrates. To address this, we generated an inducible dominant negative form of the IP3R (IP3RDN). Flies with neuronal expression of IP3RDN exhibit flight deficits. Expression of IP3RDN helped identify key flight-modulating dopaminergic neurons with axonal projections in the mushroom body. Flies with attenuated IP3Rs in these presynaptic dopaminergic neurons exhibit shortened flight bouts and a disinterest in seeking food, accompanied by reduced excitability and dopamine release upon cholinergic stimulation. Our findings suggest that the same neural circuit modulates the drive for food search and for undertaking longer flight bouts.

scholarly journals Suppression of thymic development by the dominant-negative form of Gads

2001 ◽  
Vol 13 (6) ◽  
pp. 777-783 ◽  
Author(s):  
Kazu Kikuchi ◽  
Yoshitada Kawasaki ◽  
Naoto Ishii ◽  
Yoshiteru Sasaki ◽  
Hironobu Asao ◽  
...  
Keyword(s):  
Dominant Negative ◽  
Thymic Development ◽  
Dominant Negative Form ◽  
Negative Form

Wingless blocks bristle formation and morphogenetic furrow progression in the eye through repression of Daughterless

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3393-3402 ◽  
Author(s):  
Kenneth M. Cadigan ◽  
Austin D. Jou ◽  
Roel Nusse
Keyword(s):  
Gene Expression ◽  
Ectopic Expression ◽  
Dominant Negative ◽  
Proneural Gene ◽  
Morphogenetic Furrow ◽  
Heterologous Promoter ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
Dominant Negative Form ◽  
Negative Form

In the developing eye, wingless activity represses proneural gene expression (and thus interommatidial bristle formation) and positions the morphogenetic furrow by blocking its initiation in the dorsal and ventral regions of the presumptive eye. We provide evidence that wingless mediates both effects, at least in part, through repression of the basic helix-loop-helix protein Daughterless. daughterless is required for high proneural gene expression and furrow progression. Ectopic expression of wingless blocks Daughterless expression in the proneural clusters. This repression, and that of furrow progression, can be mimicked by an activated form of armadillo and blocked by a dominant negative form of pangolin/TCF. Placing daughterless under the control of a heterologous promoter blocks the ability of ectopic wingless to inhibit bristle formation and furrow progression. hedgehog and decapentapleigic could not rescue the wingless furrow progression block, indicating that wingless acts downstream of these genes. In contrast, Atonal and Scute, which are thought to heterodimerize with Daughterless to promote furrow progression and bristle formation, respectively, can block ectopic wingless action. These results are summarized in a model where daughterless is a major, but probably not the only, target of wingless action in the eye.

Sign in / Sign up

Export Citation Format

Share Document