# Cell-autonomous control coupled with tissue context regulates the cessation of migration at the site of organ development

## TL;DR

This study explores how cells stop moving during organ development in zebrafish embryos, focusing on the role of an RNA-binding protein called Dnd1.

## Contribution

The study identifies an RNA decay-based mechanism that regulates the timing of cell migration cessation in vivo.

## Key findings

- Germ cell motility reduction correlates with the decay of RNA encoding Dead end 1 (Dnd1).
- Altering Dnd1 levels causes premature or delayed cessation of cell migration.
- Cell-autonomous and tissue-level changes regulate germ cell behavior at their target site.

## Abstract

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 themselves and with neighboring cells. In this work, we study the process of motility loss using zebrafish primordial germ cells (PGC) as an in vivo model. We show that changes in embryonic tissues as well as cell-autonomous events regulate the behavior of germ cells 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 an RNA decay-based mechanism for timing the duration of cell migration in vivo.

Summary: Migratory cells that participate in organ development lose motility upon arrival at their target. This study presents mechanisms governing this process during the early stages of gonad formation in zebrafish embryos.