Cdc42 is required in a genetically distinct subset of cardiac cells during Drosophila dorsal vessel closure.
Cdc42 is required in a genetically distinct subset of cardiac cells during Drosophila dorsal vessel closure.
复制标题
在果蝇背血管闭合过程中，遗传上不同的心肌细胞亚群需要 Cdc42。
DOI：
10.1016/j.ydbio.2014.05.024
复制
发表时间：
2014
影响因子：
2.7
通讯作者：
Kramer,SunitaG
中科院分区：
文献类型：
--
作者：
Swope,David;Kramer,Joseph;King,TiffanyR;Cheng,Yi-Shan;Kramer,SunitaG
The embryonic heart tube is formed by the migration and subsequent midline convergence of two bilateral heart fields. InDrosophilathe heart fields are organized into two rows of cardioblasts (CBs). While morphogenesis of the dorsal ectoderm, which lies directly above theDrosophiladorsal vessel (DV), has been extensively characterized, the migration and concomitant fundamental factors facilitating DV formation remain poorly understood. Here we provide evidence that DV closure occurs at multiple independent points along the A–P axis of the embryo in a “buttoning” pattern, divergent from the zippering mechanism observed in the overlying epidermis during dorsal closure. Moreover, we demonstrate that a genetically distinct subset of CBs is programmed to make initial contact with the opposing row. To elucidate the cellular mechanisms underlying this process, we examined the role of Rho GTPases during cardiac migration using inhibitory and overexpression approaches. We found that Cdc42 shows striking cell-type specificity during DV formation. Disruption of Cdc42 function specifically prevents CBs that express the homeobox genetinmanfrom completing their dorsal migration, resulting in a failure to make connections with their partnering CBs. Conversely, neighboring CBs that express the orphan nuclear receptor,seven-up, are not sensitive to Cdc42 inhibition. Furthermore, this phenotype was specific to Cdc42 and was not observed upon perturbation of Rac or Rho function. Together with the observation that DV closure occurs through the initial contralateral pairing oftinman-expressingCBs, our studies suggest that the distinct buttoning mechanism we propose for DV closure is elaborated through signaling pathways regulating Cdc42 activity in this cell type.
