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Development ePress online publication date 6 Oct 2004
doi: 10.1242/dev.01427

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Research article

Morphogenesis in the absence of integrins: mutation of both Drosophila {beta} subunits prevents midgut migration


Danelle Devenport and Nicholas H. Brown*
* Author for correspondence (e-mail: n.brown{at}gurdon.cam.ac.uk)

Two integrin {beta} subunits are encoded in the Drosophila genome. The {beta}PS subunit is widely expressed and heterodimers containing this subunit are required for many developmental processes. The second {beta} subunit, {beta}{nu}, is a divergent integrin expressed primarily in the midgut endoderm. To elucidate its function, we generated null mutations in the gene encoding {beta}{nu}. We find that {beta}{nu} is not required for viability or fertility, and overall the mutant flies are normal in appearance. However, we could observe {beta}{nu} function in the absence of {beta}PS. Consistent with its expression, removal of {beta}{nu} only enhanced the phenotype of {beta}PS in the developing midgut. In embryos lacking the zygotic contribution of {beta}PS, loss of {beta}{nu} resulted in enhanced separation between the midgut and the surrounding visceral mesoderm. In the absence of both maternal and zygotic {beta}PS, a delay in midgut migration was observed, but removing {beta}{nu} as well blocked migration completely. These results demonstrate that the second {beta} subunit can partially compensate for loss of {beta}PS integrins, and that integrins are essential for migration of the primordial midgut cells. The two {beta} subunits mediate midgut migration by distinct mechanisms: one that requires talin and one that does not. Other examples of developmental cell migration, such as that of the primordial germ cells, occurred normally in the absence of integrins. Having generated the tools to eliminate integrin function completely, we confirm that Drosophila integrins do not control proliferation as they do in mammals, and have identified {alpha}PS3 as a heterodimeric partner for {beta}{nu}.
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