Zeitlinger J, Kockel L, Peverali F A, Jackson D B, Mlodzik M, Bohmann D
EMBL, Meyerhofstr. 1, 69117 Heidelberg, Germany.
EMBO J. 1997 Dec 15;16(24):7393-401. doi: 10.1093/emboj/16.24.7393.
Drosophila kayak mutant embryos exhibit defects in dorsal closure, a morphogenetic cell sheet movement during embryogenesis. Here we show that kayak encodes D-Fos, the Drosophila homologue of the mammalian proto-oncogene product, c-Fos. D-Fos is shown to act in a similar manner to Drosophila Jun: in the cells of the leading edge it is required for the expression of the TGFbeta-like Decapentaplegic (Dpp) protein, which is believed to control the cell shape changes that take place during dorsal closure. Defects observed in mutant embryos, and adults with reduced Fos expression, are reminiscent of phenotypes caused by 'loss of function' mutations in the Drosophila JNKK homologue, hemipterous. These results indicate that D-Fos is required downstream of the Drosophila JNK signal transduction pathway, consistent with a role in heterodimerization with D-Jun, to activate downstream targets such as dpp.
果蝇kayak突变体胚胎在背闭合过程中表现出缺陷，背闭合是胚胎发育期间一种形态发生细胞层运动。我们在此表明，kayak编码D-Fos，即哺乳动物原癌基因产物c-Fos的果蝇同源物。已证明D-Fos的作用方式与果蝇Jun相似：在前缘细胞中，它是TGFβ样的Decapentaplegic（Dpp）蛋白表达所必需的，据信该蛋白控制背闭合期间发生的细胞形状变化。在突变体胚胎以及Fos表达降低的成虫中观察到的缺陷，让人联想到果蝇JNKK同源物hemipterous中“功能丧失”突变所导致的表型。这些结果表明，D-Fos在果蝇JNK信号转导途径的下游发挥作用，这与它和D-Jun异源二聚化以激活诸如dpp等下游靶标的作用一致。
