scholarly journals A JAK-STAT pathway regulates wing vein formation in Drosophila.

1996 ◽  
Vol 93 (12) ◽  
pp. 5842-5847 ◽  
Author(s):  
R. Yan ◽  
H. Luo ◽  
J. E. Darnell ◽  
C. R. Dearolf
Keyword(s):  
Wing Vein ◽  
Vein Formation ◽  
Stat Pathway

Differential Activity of Ras1 during Patterning of the Drosophila Dorsoventral Axis

Genetics ◽  
1996 ◽  
Vol 144 (4) ◽  
pp. 1545-1557 ◽  
Author(s):  
Jon D Schnorr ◽  
Celeste A Berg
Keyword(s):  
Tyrosine Kinases ◽  
P Element ◽  
Embryonic Patterning ◽  
Loss Of Function ◽  
Wing Vein ◽  
Border Cell ◽  
Specific Effects ◽  
Vein Formation ◽  
Allele Specific ◽  
Development Analysis

In Drosophila, the Ras1 gene is required downstream of receptor tyrosine kinases for correct eye development, embryonic patterning, wing vein formation, and border cell migration. Here we characterize a P-element allele of Ras1, Ras15703, that affects viability, eye morphogenesis, and early and late stages of oogenesis. Flies transheterozgyous for Ras15703 and existing EMS-induced Ras1 alleles are viable and exhibit a range of eye and eggshell defects. Differences in the severity of these phenotypes in different tissues suggest that there are allele-specific effects of Ras1 in development. Analysis of rescue constructs demonstrates that these differential phenotypes are due to loss of function in Ras1 alone and not due to effects on neighboring genes. Females mutant at the Ras1 locus lay eggs with reduced or missing dorsal eggshell structures. We observe dominant interactions between Ras1 mutants and other dorsoventral pathway mutants, including and Egfrtop and gurken. Ras1 is also epistatic to K10. Unlike Egfrtop and gurken mutants, however, Ras1 females are moderately fertile, laying eggs with ventralized eggshells that can hatch normal larvae. These results suggest that Ras1 may have a different requirement in the patterning of the eggshell axis than in the patterning of the embryonic axis during oogenesis.

scholarly journals Insights into the molecular mechanisms underlying diversified wing venation among insects

2014 ◽  
Vol 281 (1789) ◽  
pp. 20140264 ◽  
Author(s):  
Osamu Shimmi ◽  
Shinya Matsuda ◽  
Masatsugu Hatakeyama
Keyword(s):  
Molecular Mechanisms ◽  
Positional Information ◽  
Wing Venation ◽  
Wing Vein ◽  
Insect Wing ◽  
Vein Formation ◽  
Key Factor ◽  
Characteristic Features ◽  
Species Specific ◽  
Directional Transport

Insect wings are great resources for studying morphological diversities in nature as well as in fossil records. Among them, variation in wing venation is one of the most characteristic features of insect species. Venation is therefore, undeniably a key factor of species-specific functional traits of the wings; however, the mechanism underlying wing vein formation among insects largely remains unexplored. Our knowledge of the genetic basis of wing development is solely restricted to Drosophila melanogaster . A critical step in wing vein development in Drosophila is the activation of the decapentaplegic (Dpp)/bone morphogenetic protein (BMP) signalling pathway during pupal stages. A key mechanism is the directional transport of Dpp from the longitudinal veins into the posterior crossvein by BMP-binding proteins, resulting in redistribution of Dpp that reflects wing vein patterns. Recent works on the sawfly Athalia rosae , of the order Hymenoptera, also suggested that the Dpp transport system is required to specify fore- and hindwing vein patterns. Given that Dpp redistribution via transport is likely to be a key mechanism for establishing wing vein patterns, this raises the interesting possibility that distinct wing vein patterns are generated, based on where Dpp is transported. Experimental evidence in Drosophila suggests that the direction of Dpp transport is regulated by prepatterned positional information. These observations lead to the postulation that Dpp generates diversified insect wing vein patterns through species-specific positional information of its directional transport. Extension of these observations in some winged insects will provide further insights into the mechanisms underlying diversified wing venation among insects.

scholarly journals A Genetic Screen for Modifiers of Drosophila Src42A Identifies Mutations in Egfr, rolled and a Novel Signaling Gene

Genetics ◽  
1999 ◽  
Vol 151 (2) ◽  
pp. 697-711
Author(s):  
Qian Zhang ◽  
Qingxia Zheng ◽  
Xiangyi Lu
Keyword(s):  
Tyrosine Kinases ◽  
Egf Receptor ◽  
Photoreceptor Cells ◽  
Mapk Signaling ◽  
Close Relative ◽  
Loss Of Function ◽  
Genetic Screens ◽  
Wing Vein ◽  
Rtk Signaling ◽  
Vein Formation

Abstract Drosophila Src42A, a close relative of the vertebrate c-Src, has been implicated in the Ras-Mapk signaling cascade. An allele of Src42A, Su(Raf)1, dominantly suppresses the lethality of partial loss-of-function Raf mutations. To isolate genes involved in the same pathway where Src42A functions, we carried out genetic screens for dominant suppressor mutations that prevented Su(Raf)1 from suppressing Raf. Thirty-six mutations representing at least five genetic loci were recovered from the second chromosome. These are Drosophila EGF Receptor (Egfr), rolled, Src42A, and two other new loci, one of which was named semang (sag). During embryogenesis, sag affects the development of the head, tail, and tracheal branches, suggesting that it participates in the pathways of Torso and DFGF-R1 receptor tyrosine kinases. sag also disrupts the embryonic peripheral nervous system. During the development of imaginal discs, sag affects two processes known to require Egfr signaling: the recruitment of photoreceptor cells and wing vein formation. Thus sag functions in several receptor tyrosine kinase (RTK)-mediated processes. In addition, sag dominantly enhances the phenotypes associated with loss-of-function Raf and rl, but suppresses those of activated Ras1V12 mutation. This work provides the first genetic evidence that both Src42A and sag are modulators of RTK signaling.

Analysis of the genetic hierarchy guiding wing vein development in Drosophila

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 785-801 ◽  
Author(s):  
M.A. Sturtevant ◽  
E. Bier
Keyword(s):  
Small Group ◽  
Genetic Interactions ◽  
R Genes ◽  
Longitudinal Vein ◽  
Wing Vein ◽  
Pupal Development ◽  
Sequential Model ◽  
Vein Formation ◽  
Wing Veins ◽  
Genetic Hierarchy

The Drosophila rhomboid (rho) and Egf-r genes are members of a small group of genes required for the differentiation of various specific embryonic and adult structures. During larval and early pupal development expression of rho in longitudinal vein primordia mediates the localized formation of wing veins. In this paper we investigate the genetic hierarchy guiding vein development, by testing for genetic interactions between rho alleles and a wide variety of wing vein mutations and by examining the pattern of rho expression in mutant developing wing primordia. We identify a small group of wing vein mutants that interact strongly with rho. Examination of rho expression in these and other key vein mutants reveals when vein development first becomes abnormal. Based on these data and on previous genetic analyses of vein formation we present a sequential model for establishment and differentiation of wing veins.

scholarly journals Developmental genetics of the wing vein pattern of Drosophila

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 612-619 ◽  
Author(s):  
J. Díaz-Benjumea ◽  
M. A. F. González Gaitán ◽  
A. García-Bellido
Keyword(s):  
Cell Proliferation ◽  
Cell Communication ◽  
Wing Disc ◽  
Developmental Genetics ◽  
Developmental Study ◽  
Wing Vein ◽  
Vein Pattern ◽  
Vein Formation ◽  
Cell Proliferation And Differentiation ◽  
Wing Morphogenesis

The developmental study of the wing disc in Drosophila has revealed the progressive appearance of heterogeneities in the anlage formation i.e., of symmetric compartments, of lineage restrictions for vein and intervein regions within compartments, and in mitotic waves. The genetic analysis of alleles in 28 loci that affect vein formation allows us to classify them, according to their phenotypic effects in mutant combinations, in several groups of synergism. These effects include changes in vein differentiation, vein pattern, and growth of the wing anlage. Clonal analyses of mutations of these groups shows that pattern differentiation is associated with changes in cell proliferation dynamics. The study of combinations of mutations from different groups allows us to infer the existence of distinct genetic operations in wing development. A model is presented relating these genetic operations to cell proliferation and cell communication in wing morphogenesis and vein patterning.Key words: pattern formation, morphogenesis, cell proliferation and differentiation.

Drosophila wing development in the absence of dorsal identity

Development ◽  
2001 ◽  
Vol 128 (5) ◽  
pp. 703-710 ◽  
Author(s):  
D.D. O'Keefe ◽  
J.B. Thomas
Keyword(s):  
Wing Disc ◽  
Wing Development ◽  
Integrin Subunit ◽  
Wing Vein ◽  
Vein Formation ◽  
Downstream Effectors ◽  
Adult Wing ◽  
Wing Structures ◽  
Distinct Lineage ◽  
Dorsal Cells

The developing wing disc of Drosophila is divided into distinct lineage-restricted compartments along both the anterior/posterior (A/P) and dorsal/ventral (D/V) axes. At compartment boundaries, morphogenic signals pattern the disc epithelium and direct appropriate outgrowth and differentiation of adult wing structures. The mechanisms by which affinity boundaries are established and maintained, however, are not completely understood. Compartment-specific adhesive differences and inter-compartment signaling have both been implicated in this process. The selector gene apterous (ap) is expressed in dorsal cells of the wing disc and is essential for D/V compartmentalization, wing margin formation, wing outgrowth and dorsal-specific wing structures. To better understand the mechanisms of Ap function and compartment formation, we have rescued aspects of the ap mutant phenotype with genes known to be downstream of Ap. We show that Fringe (Fng), a secreted protein involved in modulation of Notch signaling, is sufficient to rescue D/V compartmentalization, margin formation and wing outgrowth when appropriately expressed in an ap mutant background. When Fng and alphaPS1, a dorsally expressed integrin subunit, are co-expressed, a nearly normal-looking wing is generated. However, these wings are entirely of ventral identity. Our results demonstrate that a number of wing development features, including D/V compartmentalization and wing vein formation, can occur independently of dorsal identity and that inter-compartmental signaling, refined by Fng, plays the crucial role in maintaining the D/V affinity boundary. In addition, it is clear that key functions of the ap selector gene are mediated by only a small number of downstream effectors.

Identification of Chromosomal Regions Involved in decapentaplegic Function in Drosophila

Genetics ◽  
1998 ◽  
Vol 149 (1) ◽  
pp. 203-215 ◽  
Author(s):  
Russell E Nicholls ◽  
William M Gelbart
Keyword(s):  
Growth Factor ◽  
Pattern Formation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Genetic Interactions ◽  
Genetic Approach ◽  
Wing Vein ◽  
Vein Formation ◽  
Embryonic Lethal ◽  
Β Function

AbstractSignaling molecules of the transforming growth factor β (TGF-β) family contribute to numerous developmental processes in a variety of organisms. However, our understanding of the mechanisms which regulate the activity of and mediate the response to TGF-β family members remains incomplete. The product of the Drosophila decapentaplegic (dpp) locus is a well-characterized member of this family. We have taken a genetic approach to identify factors required for TGF-β function in Drosophila by testing for genetic interactions between mutant alleles of dpp and a collection of chromosomal deficiencies. Our survey identified two deficiencies that act as maternal enhancers of recessive embryonic lethal alleles of dpp. The enhanced individuals die with weakly ventralized phenotypes. These phenotypes are consistent with a mechanism whereby the deficiencies deplete two maternally provided factors required for dpp's role in embryonic dorsal-ventral pattern formation. One of these deficiencies also appears to delete a factor required for dpp function in wing vein formation. These deficiencies remove material from the 54F-55A and 66B-66C polytene chromosomal regions, respectively. As neither of these regions has been previously implicated in dpp function, we propose that each of the deficiencies removes a novel factor or factors required for dpp function.

scholarly journals Control of Growth and Differentiation byDrosophila RasGAP, a Homolog of p120 Ras–GTPase-Activating Protein

1999 ◽  
Vol 19 (3) ◽  
pp. 1928-1937 ◽  
Author(s):  
Pascale Feldmann ◽  
Eva N. Eicher ◽  
Sally J. Leevers ◽  
Ernst Hafen ◽  
David A. Hughes
Keyword(s):  
Tyrosine Kinases ◽  
Receptor Tyrosine Kinases ◽  
Intracellular Localization ◽  
Ectopic Expression ◽  
Gtpase Activating Protein ◽  
Wing Vein ◽  
Sh2 Domains ◽  
Ras Gtpase ◽  
Vein Formation

ABSTRACT Mammalian Ras GTPase-activating protein (GAP), p120 Ras-GAP, has been implicated as both a downregulator and effector of Ras proteins, but its precise role in Ras-mediated signal transduction pathways is unclear. To begin a genetic analysis of the role of p120 Ras-GAP we identified a homolog from the fruit flyDrosophila melanogaster through its ability to complement the sterility of a Schizosaccharomyces pombe (fission yeast) gap1 mutant strain. Like its mammalian homolog,Drosophila RasGAP stimulated the intrinsic GTPase activity of normal mammalian H-Ras but not that of the oncogenic Val12 mutant. RasGAP was tyrosine phosphorylated in embryos and its Src homology 2 (SH2) domains could bind in vitro to a small number of tyrosine-phosphorylated proteins expressed at various developmental stages. Ectopic expression of RasGAP in the wing imaginal disc reduced the size of the adult wing by up to 45% and suppressed ectopic wing vein formation caused by expression of activated forms of Breathless and Heartless, two Drosophila receptor tyrosine kinases of the fibroblast growth factor receptor family. The in vivo effects of RasGAP overexpression required intact SH2 domains, indicating that intracellular localization of RasGAP through SH2-phosphotyrosine interactions is important for its activity. These results show that RasGAP can function as an inhibitor of signaling pathways mediated by Ras and receptor tyrosine kinases in vivo. Genetic interactions, however, suggested a Ras-independent role for RasGAP in the regulation of growth. The system described here should enable genetic screens to be performed to identify regulators and effectors of p120 Ras-GAP.

Calmodulin Point Mutations Affect Drosophila Development and Behavior

Genetics ◽  
1997 ◽  
Vol 147 (4) ◽  
pp. 1783-1798 ◽  
Author(s):  
Heidi B Nelson ◽  
Robert G Heiman ◽  
Clare Bolduc ◽  
Gae E Kovalick ◽  
Penn Whitley ◽  
...  
Keyword(s):  
Point Mutations ◽  
Coding Region ◽  
Wing Vein ◽  
Protein Coding ◽  
Vein Formation ◽  
Intracellular Calcium Signaling ◽  
The Individual ◽  
Mutant Phenotypes ◽  
And Behavior ◽  
Drosophila Mutant

Abstract Calmodulin (CAM) is recognized as a major intermediary in intracellular calcium signaling, but as yet little is known of its role in developmental and behavioral processes. We have generated and studied mutations to the endogenous Cam gene of Drosophila melanogaster that change single amino acids within the protein coding region. One of these mutations produces a striking pupal lethal phenotype involving failure of head eversion. Various mutant combinations produce specific patterns of ectopic wing vein formation or melanotic scabs on the cuticle. Anaphase chromosome bridging is also seen as a maternal effect during the early embryonic nuclear divisions. In addition, specific behavioral defects such as poor climbing and flightlessness are detected among these mutants. Comparisons with other Drosophila mutant phenotypes suggests potential CAM targets that may mediate these developmental and behavioral effects, and analysis of the CAM crystal structure suggests the structural consequences of the individual mutations.

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