Effect of the wingless (wg1) mutation on wing and haltere development in Drosophila melanogaster

Sharma, R. P.; Chopra, V. L.

doi:10.1016/0012-1606(76)90108-1

Cited by 300 publications

(167 citation statements)

References 5 publications

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“…Nine null alleles of wg are embryonic lethal, two hypomorphic alleles are lethal at the pupal stage (van den Heuvel et al 1993), and the least severe hypomorphic allele results in viable adults that lack one or both wings (Sharma and Chopra 1976). The range of viability observed in the wg allelic series corresponds to the embryonic lethal, perinatal lethal, and adult viable phenotypes observed in mice with varied amounts of The example provided by Wnt3a suggests that the use of gene targeting to generate hypomorphic alleles of other mammalian Wnt genes could be enlightening.…”

Section: G E N E S and Developmentmentioning

confidence: 99%

Analysis of the vestigial tail mutation demonstrates that Wnt-3a gene dosage regulates mouse axial development.

Greco¹,

Takada²,

Newhouse³

et al. 1996

Genes Dev.

235

161

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Mice homozygous for the recessive mutation vestigial tail (v-t), which arose spontaneously on Chromosome 11, exhibit vertebral abnormalities, including loss of caudal vertebrae leading to shortening of the tail. Wnt-3a, a member of the wingless family of secreted glycoproteins, maps to the same chromosome. Embryos homozygous for a null mutation in Wnt-3a (Wnt-3a "e°) have a complete absence of tail bud development and are truncated rostral to the hindlimbs. Several lines of evidence reveal that vt is a hypomorphic allele of Wnt-3a. We show that Wnt-3a and vt eosegregate in a high-resolution backcross and fail to complement, suggesting that Wnt-3a "~° and vt are allelic. Embryos heterozygous for both alleles have a phenotype intermediate between that of Wnt-3a n~° and vt homozygotes, lacking a tail, but developing thoracic and a variable number of lumbar vertebrae. Although no gross alteration in the Wnt-3a gene was detected in vt mice and the Wnt-3a coding region was normal, Wnt-3a expression was markedly reduced in vt/rt embryos consistent with a regulatory mutation in Wnt-3a. Furthermore, the analysis of allelic combinations indicates that Wnt-3a is required throughout the period of tail bud development for caudal somitogenesis. Interestingly, increasing levels of Wnt-3a activity appear to be necessary for the formation of more posterior derivatives of the paraxial mesoderm.

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Section: G E N E S and Developmentmentioning

confidence: 99%

Analysis of the vestigial tail mutation demonstrates that Wnt-3a gene dosage regulates mouse axial development.

Greco¹,

Takada²,

Newhouse³

et al. 1996

Genes Dev.

235

161

View full text Add to dashboard Cite

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“…2 Attention was attracted to these genes in the mammalian system when it was discovered that both function as proto-oncogenes. Nusse and Varmus 3 discovered the Wnt gene (then termed Int1) as an integration site for mouse mammary-tumor viruses.…”

Section: Introductionmentioning

confidence: 99%

Notch and Wnt signaling in T-lymphocyte development and acute lymphoblastic leukemia

2006

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Many acute lymphoblastic leukemias can be considered as malignant counterparts of cells in the various stages of normal lymphoid development in bone marrow and thymus. T-cell development in the thymus is an ordered and tightly controlled process. Two evolutionary conserved signaling pathways, which were first discovered in Drosophila, control the earliest steps of T-cell development. These are the Notch and Wnt-signaling routes, which both are deregulated in several types of leukemias. In this review we discuss both pathways, with respect to their signaling mechanisms, functions during T-cell development and their roles in development of leukemias, especially T-cell acute lymphoblastic leukemia.

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“…It is required for patterning of the embryonic epidermis (1,2), for the proper establishment of the embryonic nervous system (3)(4)(5)(6), and also for the specification, growth, and cell-fate assignment of adult appendages, such as the wing and the leg (7,8). In the developing wing imaginal disk, wg is first involved in the definition of the wing versus notum primordium (9,10). Later, Wg is secreted at the dorsoventral (D͞V) compartment boundary of the wing disk, where it directs the formation of wing margin structures (11) and from where it acts as a morphogen to organize gene expression (12,13).…”

mentioning

confidence: 99%

Requirement for Pangolin/dTCF in Drosophila Wingless signaling

Schweizer

Nellen

Basler

2003

Proc. Natl. Acad. Sci. U.S.A.

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The Wingless (Wg) protein is a secreted glycoprotein involved in intercellular signaling. On activation of the Wg signaling pathway, Armadillo is stabilized, causing target genes to be activated by the transcription factor Pangolin (Pan). This study investigated the roles of Pan in the developing wing of Drosophila by clonal analysis. Three different aspects of wing development were examined: cell proliferation, wing margin specification, and wg self-refinement. Our results indicate that Pan function is critically required for all three of these processes. Consequently, lack of pan causes a severe reduction in the activity of the Wg target genes Distalless and vestigial within their normal domain of expression. Loss of pan function does not, however, lead to a derepression of these genes outside this domain. Thus, although Pan is positively required for the induction of Wg targets in the wing imaginal disk, it does not appear to play a default repressor function in the absence of Wg input. In contrast, lack of zygotic pan function causes a milder phenotype than that caused by the lack of wg function in the embryo. We show that this difference cannot be attributed to maternally provided pan product, indicating that a Pan repressor function usually prevents the expression of embryonic Wg targets. Together, our results suggest that for embryonic patterning the activator as well as repressor forms of Pan play important roles, while for wing development Pan operates primarily in the activator mode.W ingless (Wg) plays important roles in Drosophila development. It is required for patterning of the embryonic epidermis (1, 2), for the proper establishment of the embryonic nervous system (3-6), and also for the specification, growth, and cell-fate assignment of adult appendages, such as the wing and the leg (7,8). In the developing wing imaginal disk, wg is first involved in the definition of the wing versus notum primordium (9, 10). Later, Wg is secreted at the dorsoventral (D͞V) compartment boundary of the wing disk, where it directs the formation of wing margin structures (11) and from where it acts as a morphogen to organize gene expression (12,13). Wg also plays a role in restricting its own expression to cells immediately adjacent to the D͞V boundary, a phenomenon referred to as wg self-refinement (14).Wg exerts most if not all effects on cell-fate specification by regulating the transcription of target genes in responding cells. The key regulatory event in the Wg transduction pathway appears to be the posttranscriptional up-regulation of the ␤-catenin homolog Armadillo (Arm). Arm, in turn, confers transcriptional activator activity to the lymphoid-enhancing factor (LEF)͞T cell factor (TCF) homolog Pangolin (Pan)͞dTCF (15,16). LEF͞TCF proteins belong to the family of high-mobilitygroup transcription factors that bind to specific DNA sequences. Because the loss-of-pan-function phenotypes resemble those caused by loss of Wg signaling, it is likely that Pan acts as a transcriptional activator for Wg target genes. It w...

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Effect of the wingless (wg1) mutation on wing and haltere development in Drosophila melanogaster

Cited by 300 publications

References 5 publications

Analysis of the vestigial tail mutation demonstrates that Wnt-3a gene dosage regulates mouse axial development.

Analysis of the vestigial tail mutation demonstrates that Wnt-3a gene dosage regulates mouse axial development.

Notch and Wnt signaling in T-lymphocyte development and acute lymphoblastic leukemia

Requirement for Pangolin/dTCF in Drosophila Wingless signaling

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