Cell-autonomous control coupled with tissue context regulates the cessation of migration at the site of organ development
Organ development relies on interactions among different cell types that form three-dimensional structures to carry out specific tasks. This process often involves active migration of progenitor cells toward specific positions within the embryo, where the cells then become immotile and form stable connections among each other and with neighboring cell types. In this work, we study the process of motility loss using zebrafish primordial germ cells as an in vivo model. We show that changes in embryonic tissues as well as cell-autonomous events regulate germ cells' behavior as they arrive at their target region. Importantly, we find that reduction in germ cell motility is correlated with the decay of RNA encoding for Dead end 1 (Dnd1), a conserved vertebrate RNA-binding protein that is essential for PGC migration. Indeed, decreasing or increasing the level of Dnd1 results in a premature or delayed stop to motility, respectively. These findings represent a novel RNA decay-based mechanism for timing the duration of cell migration in vivo. Overall design: To generate spatially-resolved RNA-seq data for 24 hpf (hours post fertilization) old embryos, we cryosectioned samples, extracted RNA from the individual sections, and amplified and barcoded mRNA using the CEL-seq protocol (Hashimshony et al., Cell Reports, 2012) with a few modifications. Libraries were sequenced on Illumina NextSeq500.