Transmissible Feline Fibrosarcoma

Snyder, S. P.; Theilen, Gordon H.

doi:10.1038/2211074a0

Cited by 196 publications

(73 citation statements)

References 2 publications

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“…A dfer gain-of-function mutant disrupts dorsal closure Fes/Fer family non-receptor tyrosine kinases were first identified as the retroviral oncogenes, v-fps and v-fes, from avian and feline sarcomas, respectively (Shibuya et al, 1980;Snyder and Theilen, 1969). In v-fes and v-fps, a fragment of the viral GAG protein is fused to the N terminus of the endogenous protein.…”

Section: Research Articlementioning

confidence: 99%

The Fes/Fer non-receptor tyrosine kinase cooperates with Src42A to regulate dorsal closure inDrosophila

et al. 2006

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Fes/Fer non-receptor tyrosine kinases regulate cell adhesion and cytoskeletal reorganisation through the modification of adherens junctions. Unregulated Fes/Fer kinase activity has been shown to lead to tumours in vivo. Here, we show that Drosophila Fer localises to adherens junctions in the dorsal epidermis and regulates a major morphological event, dorsal closure. Mutations in Src42A cause defects in dorsal closure similar to those seen in dfer mutant embryos. Furthermore, Src42A mutations enhance the dfer mutant phenotype, suggesting that Src42A and DFer act in the same cellular process. We show that DFer is required for the formation of the actin cable in leading edge cells and for normal rates of dorsal closure. We have isolated a gain-of-function mutation in dfer (dfer gof ) that expresses an N-terminally fused form of the protein, similar to oncogenic forms of vertebrate Fer. dfer gof blocks dorsal closure and causes axon misrouting. We find that in dfer loss-of-function mutants ␤-catenin is hypophosphorylated, whereas in dfer gof ␤-catenin is hyperphosphorylated. Phosphorylated ␤-catenin is removed from adherens junctions and degraded, thus implicating DFer in the regulation of adherens junctions.KEY WORDS: Drosophila, Fes, Fer, Tyrosine kinase, Src, Adherens junction, Dorsal closure, ␤ ␤-catenin Development 133, 3063-3073 (2006) (Fig. 1B) (Katzen et al., 1991), and shares equal homology with Fes and Fer. Subsequently, a second cDNA encoding a short isoform, p45dfer, was discovered (Paulson et al., 1997) (Fig. 1B). Paulson et al. showed that DFer can transform vertebrate cells (Paulson et al., 1997), suggesting that the molecular pathways through which Fer signals are likely to be conserved.Here, we show that DFer acts in conjunction with Src42A in the process of dorsal closure. dfer mRNA is specifically upregulated in the leading edge cells of the dorsal epidermis. DFer localises to adherens junctions and is required for the formation of the F-actin cable in leading edge cells, and for normal rates of dorsal closure. When mutations in dfer are combined with a mutation in Src42A, dorsal closure fails completely. We have isolated a gain-of-function dfer mutant (dfer gof ) that blocks dorsal closure and causes axon misrouting. The dfer gof mutant expresses an N-terminally fused form of DFer, similar to oncogenic forms of Fer. ␤-catenin phosphorylation levels are reduced in dfer loss-of-function mutants and increased in dfer gof mutants. This supports a role for DFer in the regulation of AJs and cell-cell adhesion, and may begin to explain its role in oncogenesis. MATERIALS AND METHODS Drosophila stocksThe Drosophila lines used in this study are: Wild type (Oregon-P; Bloomington Stock Centre), hep 1 (Glise et al., 1995), UAS-puc (MartinBlanco et al., 1998), UAS-GFP-Actin (Verkhusha et al., 1999) Transgenic flies containing UAS-DFerRB were generated as previously described (Brand and Perrimon, 1993), except that DNA was prepared using a Qiagen Midiprep Kit.To generate DFer mutants by male recombination, w...

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Section: Research Articlementioning

confidence: 99%

The Fes/Fer non-receptor tyrosine kinase cooperates with Src42A to regulate dorsal closure inDrosophila

et al. 2006

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“…During the 1960s and 1970s various retroviruses were found to be associated with solid-tissue fibrosarcomas in mice, 14 cats 15 and monkeys. 16 All were reminiscent of the sarcomas of chickens described by Rous at the turn of the century, caused by 'filterable agents'.…”

Section: Retroviruses In Leukemia and Related Diseasesmentioning

confidence: 99%

Comparative research in leukemia and related diseases. An introduction to a scientific approach

Hehlmann

Essex

1999

Leukemia

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“…17 In the 1960s sarcoma viruses that transmit the disease were also detected in mice, rats, cats and a woolley monkey. 15,16,54,55 The specific feature of these viruses which distinguishes them from leukemia viruses is the presence in the viral genomes of cellular sequences which are responsible for the oncogenic properties (oncogenes). 56 Almost identical sequences are present in the normal cell genomes (proto-oncogenes).…”

Section: Oncogenes and Proto-oncogenesmentioning

confidence: 99%

True

1999

Leukemia

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Transmissible Feline Fibrosarcoma

Cited by 196 publications

References 2 publications

The Fes/Fer non-receptor tyrosine kinase cooperates with Src42A to regulate dorsal closure inDrosophila

The Fes/Fer non-receptor tyrosine kinase cooperates with Src42A to regulate dorsal closure inDrosophila

Comparative research in leukemia and related diseases. An introduction to a scientific approach

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