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首页> 外文期刊>Development >Morphogenesis in the absence of integrins: mutation of both Drosophila beta subunits prevents midgut migration.
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Morphogenesis in the absence of integrins: mutation of both Drosophila beta subunits prevents midgut migration.

机译：在没有整合素的情况下的形态发生：果蝇β亚基的两个突变均可阻止中肠迁移。

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摘要

Two integrin beta subunits are encoded in the Drosophila genome. The betaPS subunit is widely expressed and heterodimers containing this subunit are required for many developmental processes. The second betasubunit, betanu, is a divergent integrin expressed primarily in the midgut endoderm. To elucidate its function, we generated null mutations in the gene encoding betanu. We find that betanu is not required for viability or fertility, and overall the mutant flies are normal in appearance. However, we could observe betanu function in the absence of betaPS. Consistent with its expression, removal of betanu only enhanced the phenotype of betaPS in the developing midgut. In embryos lacking the zygotic contribution of betaPS, loss of betanu resulted in enhanced separation between the midgut and the surrounding visceral mesoderm. In the absence of both maternal and zygotic betaPS, a delay in midgut migration was observed, but removing betanu as well blocked migration completely. These results demonstrate that the second beta subunit can partially compensate for loss of betaPS 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 alphaPS3 as a heterodimeric partner for betanu.
机译：果蝇基因组中编码两个整联蛋白β亚基。 betaPS亚基被广泛表达，许多发育过程都需要包含该亚基的异二聚体。第二个β亚基betanu是主要在中肠内胚层表达的整合素。为了阐明其功能，我们在编码甜菜碱的基因中产生了无效突变。我们发现，贝塔努不是生存力或繁殖力所必需的，总体而言，这种突变果蝇外观正常。但是，我们可以在没有betaPS的情况下观察betanu功能。与它的表达一致，去除betanu只会增强发育中肠中betaPS的表型。在缺乏betaPS的合子作用的胚胎中，betanu的缺失导致中肠和周围的内脏中胚层之间的分离增强。在没有母体和合子βPS的情况下，观察到中肠迁移延迟，但是去除βnu也完全阻止了迁移。这些结果表明，第二个β亚基可以部分补偿βPS整合素的损失，并且整合素对于原始中肠细胞的迁移至关重要。这两个β亚基通过不同的机制介导中肠迁移：一种需要塔林，另一种不需要。发育细胞迁移的其他例子，例如原始生殖细胞的迁移，通常在没有整联蛋白的情况下发生。生成了完全消除整联蛋白功能的工具后，我们确认果蝇整联蛋白不能像在哺乳动物中那样控制增殖，并且已确定alphaPS3是甜菜碱的异二聚体伴侣。

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