The study of cell migration has been greatly enhanced by the development of new model systems and analysis protocols to study this process in vivo. Zebrafish embryos have been a principal protagonist because they are easily accessible, genetically tractable, and optically transparent. Neural crest cells, on the other hand, are the ideal system to study cell migration. These cells migrate extensively, using different modalities of movement and sharing many traits with metastatic cancer cells. In this chapter, we present new tools and protocols that allow the study of NC development and migration in vivo.Epithelial-mesenchymal transitions (EMTs) drive the generation of cell diversity during both evolution and development. More and more evidence has pointed to a model where EMT is not a binary switch but a reversible process that can be stabilized at intermediate states. Despite our vast knowledge on the signaling pathways that trigger EMT, we know very little about how EMT happens in a step-wise manner. Live imaging of cells that are undergoing EMT in intact, living, animals will provide us valuable insights into how EMT is executed at both the cellular and molecular levels and help us identify and understand the intermediate states. Here, we describe how to image early stages of EMT in the mesoderm cells of live Drosophila melanogaster embryos and how to image contractile myosin that suspends EMT progression.The evolutionary emergence of the mesenchymal phenotype greatly increased the complexity of tissue architecture and composition in early Metazoan species. At the molecular level, an epithelial-to-mesenchymal transition (EMT) was permitted by the innovation of specific transcription factors whose expression is sufficient to repress the epithelial transcriptional program. The reverse process, mesenchymal-to-epithelial transition (MET), involves direct inhibition of EMT transcription factors by numerous mechanisms including tissue-specific MET-inducing transcription factors (MET-TFs), micro-RNAs, and changes to cell and tissue architecture, thus providing an elegant solution to the need for tight temporal and spatial control over EMT and MET events during development and adult tissue homeostasis.Epithelial Mesenchymal Transition (EMT) initially discovered as a key developmental mechanism is now shown to be indirectly involved in fibrosis and is contributing to the progression of carcinomas. Additionally, to transcription factors driving the morphological transition, novel mechanisms are now described to modulate the different features of the transition. The debate as to whether EMT is essential for the dissemination of carcinoma cells from the primary tumors is likely to be resolved soon, considering that EMT is not a linear transition from an epithelial to a mesenchymal state. Multiple intermediate states can be reached without involving the presence of some of known transcription factors initially described as indispensable for the acquisition of mesenchymal-like phenotypes.As our understanding of Epithelial Mesenchymal Transition (EMT) increases, the original binary concept of E versus M no longer fits with experimental evidence. Re-definition of the EMT paradigm as spectral transitions between a full epithelium and a full mesenchyme suggests the existence of a virtual infinity of intermediate cellular states. The new challenge is to develop technical tools needed to contextualize each of these states and identify biologically significant cellular mechanisms that could be targeted in combatting EMT-related diseases.When referring to the epithelial-to-mesenchymal transition (EMT), readers are familiar with sentences alluding to its pivotal role both in embryonic development and in disease. Following that argument, usually there is a point on the importance of studying the process and the impact it has on the design of therapeutic strategies. However, it is also very common to find arguments on how the EMT is very difficult to tackle, being a somehow obscure and complex process, where the field cannot reach universal conclusions, particularly in pathological contexts. Even worse, it is sometimes defined as a process that cannot be described with universal markers, making it therefore very difficult for cancer studies, where there is a need to use optimal animal models and stratify patients for differential therapeutic strategies.  https://www.selleckchem.com/peptide/octreotide-acetate.html  In the face of all this, the question is whether you have been frightened off working on pathological EMTs, or even if you are not interested anymore and would prefer waiting till the field reaches a steady state of robust knowledge. Do not be afraid and be interested now. It only involves being more plastic, like the EMT itself.The epithelial to mesenchymal transition (EMT) is an enticingly simple mechanism that converts stationary epithelial cells into migratory mesenchymal cells. EMT is meant to provide a unified explanation for phenomena as complex as gastrulation and metastasis. However, cell movements turn out to be diverse, and many are collective. Cells commonly migrate in clusters, strands, sheets, elongating tubes, or in fluid-like masses. Moreover, plenty of cells move without activating the EMT program. Here I propose that EMT can be understood as one of many types of transitions in a broader landscape-or phase space-of cell morphologies and behaviors. Throughout biology, and at multiple scales, complexity arises from the combinatorial deployment of simple, modular components. I propose that diversity of cell shapes and behaviors similarly arises from combinatorial use of modular biomechanical properties.The epithelial-mesenchymal transition (EMT) is a key process required for building the early body plan of metazoa. It involves coordinated and precisely timed changes in multiple cell processes such as de-adhesion, motility, invasion, and cell polarity. While much has been learned about how embryos deploy epithelial-mesenchymal transitions since Betty Hay named the process decades ago, a number of things are still not well understood. Here I will discuss some of the big questions that remain, including how is all of this controlled, how does each of the cell biological events work, and how are they so nicely coordinated with one another?