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Abstract:
Organs represent both structural and functional units of the animal body. To fulfill their unique functions, organs develop distinctive morphologies. However, the cellular and molecular mechanisms underlying organ formation remain elusive. Here we report the morphogenesis of Drosophila embryonic gonad. Embryonic gonads consist of primordial germ cells (PGCs) and somatic gonadal precursors (SGPs).The SGPs are specified in the mesoderm, toward which PGCs migrate. Once associated with PGCs, the SGPs initiate gonad coalescence by encapsulating PGCs in a spherical structure. The lack of a proper SGP marker had prevented the detailed analysis of gonad morphogenesis. In this study, however, we developed a membrane GFP marker to examine SGP behavior during gonad morphogenesis. Live imaging demonstrated that normal SGPs in the anterior and posterior edges move inward to compact the gonad. We found that this process is disrupted in an actin regulator enabled (ena) mutant. ena mutant SGPs are flatter than normal SGPs and tilt toward the anterior-posterior axis, leading to incomplete gonad compaction. Previous studies showed that DE-cadherin (DE-cad) affects gonad compaction similarly to ena (Jenkins et al., 2003), and, in this study, we found that ena genetically interacts with DE-cad and β-catenin. Taken together, we propose that ena regulates the actin filament-mediated action of adhesion molecules for proper gonad coalescence.
