TORC2 on the other hand has been less studied but appeared in the past decade as a new regulator of the actin cytoskeleton and of cell migration. In yeast, TORC2 is required for the cell cycle dependent polarization of the actin cytoskeleton, through activation of PKC1, YPK2, and SLM. In Dictyostelium discoideum, TORC2 loss of function leads to severe cell polarity defects and reduced chemotactic speed and directionality. In this system, TORC2 acts in parallel to the PI3K pathway to activate PKB which in turn regulates actin dynamics. In mammalian cells, TORC2 plays a key role in neutrophil chemotaxis by regulating F-actin polarization and myosin II phosphorylation. Contrary to the case in Dictyostelium, in mammalian cells this seems to be independent of Akt but is mediated through PKC, which in turn modulates adenylyl cyclase and cAMP production. TORC2 was also shown to control Prostaglandin E2 dependent chemotaxis of mast cells, and more generally regulates actin dynamics in a number of cell lines. In addition to PKC regulation, TORC2 modulates Rac1 activity, at least in part through activation of the Rac1 GEF P-Rex1. The role of TORC2 in controlling actin dynamics and cell migration is thus now well established in different cell types, and the molecular pathways involved are beginning to be unravelled. However, the functional importance of TORC2 dependent-migration remains unaddressed in metazoans. This most likely stems from the fact that, in mice, knock-out of the TORC2 components sin1 or rictor leads to early embryonic lethality, which has precluded detailed analysis of these mutants. Tissue-specific knock-outs have revealed functions of TORC2 in different organs However, since no major cell migrations take place in these adult tissues, it can be argued that the role of TORC2 in cell migration in vivo has still to be assessed. Here, we used the zebrafish embryo to LY2835219 CDK inhibitor assess the role of TORC2 in controlling cell migrations in vivo. We show that loss of sin1 function leads to defects in prechordal plate migration during gastrulation. Prechordal plate is composed of a group of cells that, during gastrulation, leads the forming embryonic axis. The prechordal plate migrates from the organiser to the animal pole, and later gives rise to the hatching gland. Our analysis reveals that Sin1 controls both cell speed and persistence, and is essential for emission of actin-rich cell protrusions. This effect appears to be Screening Libraries downstream of PI3K, and is mediated through Rac1. In the past decade, it became clear that in addition to the well-studied TORC1 complex, Tor can form a second complex, TORC2, which differs in protein composition and in functions. TORC2 was identified as a regulator of the actin cytoskeleton in yeast, Dictyostelium and mammalian cell lines. However, because of the early embryonic lethality of sin1 and rictor knock downs in mice, the in vivo importance of TORC2 in actin regulation and cell migration had not been addressed. Here we analysed the effect of sin1 loss of function on early zebrafish development and provide evidence that TORC2 controls cell migration in vivo. We found that, in the absence of Sin1, speed of prechordal plate migration is reduced by half. This is due to reductions in both cell speed and cell directionality, which can be attributed to a drastic reduction in the protrusive activity of the cells, and a randomisation of their remaining cytoplasmic extensions. Notably, despite this drastic cellular phenotype, cells lacking Sin1 migrate at a normal pace when transplanted into a wild-type host, and can later differentiate into hatching gland, the prechordal plate derivative.