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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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Defects in dorsal closure in  mbc mutants revealed by staining with  Fasciclin III. All panels are dorsal views  with anterior to the left. A–D are wild-type embryos while E and F are mbcF12.7/ Df(3R)mbc-30 transheterozygotes. A  and B show a stage 15 embryo in the  process of dorsal closure. Arrow in B denotes elongated cells at the leading edge.  C and D show a stage 16 embryo that has  completed dorsal closure. E and F show  a stage 16 embryo that has a pronounced  defect in dorsal closure. Arrow denotes  cells that are misshapen and have an improper accumulation of Fasciclin III  along the leading edge. Bars: (A, C, and  E) 50 μm; (B, D, and F) 25 μm.
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Figure 8: Defects in dorsal closure in mbc mutants revealed by staining with Fasciclin III. All panels are dorsal views with anterior to the left. A–D are wild-type embryos while E and F are mbcF12.7/ Df(3R)mbc-30 transheterozygotes. A and B show a stage 15 embryo in the process of dorsal closure. Arrow in B denotes elongated cells at the leading edge. C and D show a stage 16 embryo that has completed dorsal closure. E and F show a stage 16 embryo that has a pronounced defect in dorsal closure. Arrow denotes cells that are misshapen and have an improper accumulation of Fasciclin III along the leading edge. Bars: (A, C, and E) 50 μm; (B, D, and F) 25 μm.

Mentions: Although no epidermal defects had been reported in mbc mutant embryos (Rushton et al., 1995), the early expression of mbc in the ectoderm, which persists in the epidermis into stage 14, led us to reexamine mbc mutant embryos for epidermal defects. Visualization of the epidermis with an antibody to Fasciclin III, a glycoprotein on the cell surface (Patel et al., 1987), revealed defects in dorsal closure in ∼80% of the mutant embryos (Fig. 8, E and F). The extent of completion of dorsal closure varied from a relatively small opening surrounded by puckered misshapen cells (data not shown) to a very large opening (Fig. 8 E). In the normal course of dorsal closure in a wild-type embryo, the epidermal cells elongate as shown in Fig. 8 B, and the epithelium stretches over the entire circumference of the embryo (Young et al., 1993). In the early stages of dorsal closure in mbc mutant embryos, the cells along the leading edge of the epidermis appeared to be normal (data not shown). As dorsal closure neared completion, however, many cells along the leading edge ceased to be elongated, adopted a rounded shape, and expressed Fasciclin III abnormally along their migrating edge (Fig. 8, B, D, and F).


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)

Defects in dorsal closure in  mbc mutants revealed by staining with  Fasciclin III. All panels are dorsal views  with anterior to the left. A–D are wild-type embryos while E and F are mbcF12.7/ Df(3R)mbc-30 transheterozygotes. A  and B show a stage 15 embryo in the  process of dorsal closure. Arrow in B denotes elongated cells at the leading edge.  C and D show a stage 16 embryo that has  completed dorsal closure. E and F show  a stage 16 embryo that has a pronounced  defect in dorsal closure. Arrow denotes  cells that are misshapen and have an improper accumulation of Fasciclin III  along the leading edge. Bars: (A, C, and  E) 50 μm; (B, D, and F) 25 μm.
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Figure 8: Defects in dorsal closure in mbc mutants revealed by staining with Fasciclin III. All panels are dorsal views with anterior to the left. A–D are wild-type embryos while E and F are mbcF12.7/ Df(3R)mbc-30 transheterozygotes. A and B show a stage 15 embryo in the process of dorsal closure. Arrow in B denotes elongated cells at the leading edge. C and D show a stage 16 embryo that has completed dorsal closure. E and F show a stage 16 embryo that has a pronounced defect in dorsal closure. Arrow denotes cells that are misshapen and have an improper accumulation of Fasciclin III along the leading edge. Bars: (A, C, and E) 50 μm; (B, D, and F) 25 μm.
Mentions: Although no epidermal defects had been reported in mbc mutant embryos (Rushton et al., 1995), the early expression of mbc in the ectoderm, which persists in the epidermis into stage 14, led us to reexamine mbc mutant embryos for epidermal defects. Visualization of the epidermis with an antibody to Fasciclin III, a glycoprotein on the cell surface (Patel et al., 1987), revealed defects in dorsal closure in ∼80% of the mutant embryos (Fig. 8, E and F). The extent of completion of dorsal closure varied from a relatively small opening surrounded by puckered misshapen cells (data not shown) to a very large opening (Fig. 8 E). In the normal course of dorsal closure in a wild-type embryo, the epidermal cells elongate as shown in Fig. 8 B, and the epithelium stretches over the entire circumference of the embryo (Young et al., 1993). In the early stages of dorsal closure in mbc mutant embryos, the cells along the leading edge of the epidermis appeared to be normal (data not shown). As dorsal closure neared completion, however, many cells along the leading edge ceased to be elongated, adopted a rounded shape, and expressed Fasciclin III abnormally along their migrating edge (Fig. 8, B, D, and F).

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