一个与左-右对称性有关的基因缺陷

　　

生物通综合:
从苍蝇到人类，身体的左右两边都是不同的。身体的对称性在胚胎发育早期到底是怎样被破坏的是一个谜。但是现在，两个独立工作的研究小组报告了苍蝇的一个基因缺陷，该缺陷也许可帮助揭开这个机制。两个小组都研究了一个内脏反向成环的突变体，发现该突变在一个非传统的肌浆球蛋白中。这个肌浆球蛋白引导右手方向的成环，抑制默认的左手方向的成环。现在，这一发现将基于肌动蛋白的分子马达和肌动蛋白细胞骨架与脊椎动物的左-右手模式的形成联系了起来。

原文:
Nature 440, 798-802 (6 April 2006) | doi:10.1038/nature04625An unconventional myosin in Drosophila reverses the default handedness in visceral organs
Shunya Hozumi1, Reo Maeda1, Kiichiro Taniguchi1, Maiko Kanai1, Syuichi Shirakabe1, Takeshi Sasamura1, Pauline Spéder3, Stéphane Noselli3, Toshiro Aigaki4, Ryutaro Murakami5 and Kenji Matsuno1,2

Top of pageThe internal organs of animals often have left–right asymmetry1, 2. Although the formation of the anterior–posterior and dorsal–ventral axes in Drosophila is well understood, left–right asymmetry has not been extensively studied. Here we find that the handedness of the embryonic gut and the adult gut and testes is reversed (not randomized) in viable and fertile homozygous Myo31DF mutants. Myo31DF encodes an unconventional myosin, Drosophila MyoIA (also referred to as MyoID in mammals; refs 3, 4), and is the first actin-based motor protein to be implicated in left–right patterning. We find that Myo31DF is required in the hindgut epithelium for normal embryonic handedness. Disruption of actin filaments in the hindgut epithelium randomizes the handedness of the embryonic gut, suggesting that Myo31DF function requires the actin cytoskeleton. Consistent with this, we find that Myo31DF colocalizes with the cytoskeleton. Overexpression of Myo61F, another myosin I (ref. 4), reverses the handedness of the embryonic gut, and its knockdown also causes a left–right patterning defect. These two unconventional myosin I proteins may have antagonistic functions in left–right patterning. We suggest that the actin cytoskeleton and myosin I proteins may be crucial for generating left–right asymmetry in invertebrates.