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Drosophila myoblast city encodes a conserved protein that is essential for myoblast fusion, dorsal closure, and cytoskeletal organization.

Erickson MR, Galletta BJ, Abmayr SM - J. Cell Biol. (1997)

Bottom Line: It is also expressed in the pole cells and in ectodermally derived tissues, including the epidermis.Consistent with this latter expression, mbc mutant embryos exhibit defects in dorsal closure and cytoskeletal organization in the migrating epidermis.Both the mesodermal and ectodermal defects are reminiscent of those induced by altered forms of Drac1 and suggest that mbc may function in the same pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology and Center for Gene Regulation, The Pennsylvania State University, University Park, Pennsylvania 16802, USA.

ABSTRACT
The Drosophila myoblast city (mbc) locus was previously identified on the basis of a defect in myoblast fusion (Rushton et al., 1995. Development [Camb.]. 121:1979-1988). We describe herein the isolation and characterization of the mbc gene. The mbc transcript and its encoded protein are expressed in a broad range of tissues, including somatic myoblasts, cardial cells, and visceral mesoderm. It is also expressed in the pole cells and in ectodermally derived tissues, including the epidermis. Consistent with this latter expression, mbc mutant embryos exhibit defects in dorsal closure and cytoskeletal organization in the migrating epidermis. Both the mesodermal and ectodermal defects are reminiscent of those induced by altered forms of Drac1 and suggest that mbc may function in the same pathway. MBC bears striking homology to human DOCK180, which interacts with the SH2-SH3 adapter protein Crk and may play a role in signal transduction from focal adhesions. Taken together, these results suggest the possibility that MBC is an intermediate in a signal transduction pathway from the rho/rac family of GTPases to events in the cytoskeleton and that this pathway may be used during myoblast fusion and dorsal closure.

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Related in: MedlinePlus

Accumulation of filamentous actin and phosphotyrosine in the epidermis of mbc mutant embryos. Confocal micrographs of  embryos stained with Texas red–conjugated phalloidin (A) or an antiphosphotyrosine antibody (B). Anterior is to the left in all panels.  A, a and c, and B, a show stage 14 wild-type embryos. A, b and d, and B, b show stage 14 mbcD11.2 homozygous embryos. Bar, 10 μm.
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Figure 9: Accumulation of filamentous actin and phosphotyrosine in the epidermis of mbc mutant embryos. Confocal micrographs of embryos stained with Texas red–conjugated phalloidin (A) or an antiphosphotyrosine antibody (B). Anterior is to the left in all panels. A, a and c, and B, a show stage 14 wild-type embryos. A, b and d, and B, b show stage 14 mbcD11.2 homozygous embryos. Bar, 10 μm.

Mentions: The cytoskeleton along the leading edge of the epidermis has been implicated in driving the process of dorsal closure (Young et al., 1993). We therefore used fluorescently conjugated phalloidin, which binds filamentous actin, to examine the mbc mutants for defects in cytoskeletal formation and organization. Both wild-type and mbc mutant embryos displayed some variability in the intensity and organization of staining, the range of which is shown in Fig. 9. As shown, the signal in wild-type embryos (Fig. 9 A, a and c) was always stronger than that in mbc mutant embryos (Fig. 9 A, b and d). While frequently more dramatic in cells along the migrating edge, this reduction in signal was also observed throughout the epidermis, consistent with the observed expression of mbc. In addition, it should be noted that ∼20% of the mbc mutant embryos do not exhibit defects in dorsal closure (mentioned above). One might anticipate that these embryos would express relatively normal levels of filamentous actin and exhibit only mild cytoskeletal defects, such as that shown in Fig. 9 A, b. In summary, this analysis suggests that there is a modest but reproducible reduction in cytoskeletal organization in the epidermis of mbc mutant embryos. Unfortunately, examination of the cytoskeletal structure in muscle cells was complicated by the dynamic nature of wild-type muscle cells, making rigorous comparisons with comparable muscle cells in mbc mutant embryos difficult.


Drosophila myoblast city encodes a conserved protein that is essential for myoblast fusion, dorsal closure, and cytoskeletal organization.

Erickson MR, Galletta BJ, Abmayr SM - J. Cell Biol. (1997)

Accumulation of filamentous actin and phosphotyrosine in the epidermis of mbc mutant embryos. Confocal micrographs of  embryos stained with Texas red–conjugated phalloidin (A) or an antiphosphotyrosine antibody (B). Anterior is to the left in all panels.  A, a and c, and B, a show stage 14 wild-type embryos. A, b and d, and B, b show stage 14 mbcD11.2 homozygous embryos. Bar, 10 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2141626&req=5

Figure 9: Accumulation of filamentous actin and phosphotyrosine in the epidermis of mbc mutant embryos. Confocal micrographs of embryos stained with Texas red–conjugated phalloidin (A) or an antiphosphotyrosine antibody (B). Anterior is to the left in all panels. A, a and c, and B, a show stage 14 wild-type embryos. A, b and d, and B, b show stage 14 mbcD11.2 homozygous embryos. Bar, 10 μm.
Mentions: The cytoskeleton along the leading edge of the epidermis has been implicated in driving the process of dorsal closure (Young et al., 1993). We therefore used fluorescently conjugated phalloidin, which binds filamentous actin, to examine the mbc mutants for defects in cytoskeletal formation and organization. Both wild-type and mbc mutant embryos displayed some variability in the intensity and organization of staining, the range of which is shown in Fig. 9. As shown, the signal in wild-type embryos (Fig. 9 A, a and c) was always stronger than that in mbc mutant embryos (Fig. 9 A, b and d). While frequently more dramatic in cells along the migrating edge, this reduction in signal was also observed throughout the epidermis, consistent with the observed expression of mbc. In addition, it should be noted that ∼20% of the mbc mutant embryos do not exhibit defects in dorsal closure (mentioned above). One might anticipate that these embryos would express relatively normal levels of filamentous actin and exhibit only mild cytoskeletal defects, such as that shown in Fig. 9 A, b. In summary, this analysis suggests that there is a modest but reproducible reduction in cytoskeletal organization in the epidermis of mbc mutant embryos. Unfortunately, examination of the cytoskeletal structure in muscle cells was complicated by the dynamic nature of wild-type muscle cells, making rigorous comparisons with comparable muscle cells in mbc mutant embryos difficult.

Bottom Line: It is also expressed in the pole cells and in ectodermally derived tissues, including the epidermis.Consistent with this latter expression, mbc mutant embryos exhibit defects in dorsal closure and cytoskeletal organization in the migrating epidermis.Both the mesodermal and ectodermal defects are reminiscent of those induced by altered forms of Drac1 and suggest that mbc may function in the same pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology and Center for Gene Regulation, The Pennsylvania State University, University Park, Pennsylvania 16802, USA.

ABSTRACT
The Drosophila myoblast city (mbc) locus was previously identified on the basis of a defect in myoblast fusion (Rushton et al., 1995. Development [Camb.]. 121:1979-1988). We describe herein the isolation and characterization of the mbc gene. The mbc transcript and its encoded protein are expressed in a broad range of tissues, including somatic myoblasts, cardial cells, and visceral mesoderm. It is also expressed in the pole cells and in ectodermally derived tissues, including the epidermis. Consistent with this latter expression, mbc mutant embryos exhibit defects in dorsal closure and cytoskeletal organization in the migrating epidermis. Both the mesodermal and ectodermal defects are reminiscent of those induced by altered forms of Drac1 and suggest that mbc may function in the same pathway. MBC bears striking homology to human DOCK180, which interacts with the SH2-SH3 adapter protein Crk and may play a role in signal transduction from focal adhesions. Taken together, these results suggest the possibility that MBC is an intermediate in a signal transduction pathway from the rho/rac family of GTPases to events in the cytoskeleton and that this pathway may be used during myoblast fusion and dorsal closure.

Show MeSH
Related in: MedlinePlus