Neurotrophic interactions occur in Drosophila, but to date, no neurotrophic factor had been found. Neurotrophins are the main vertebrate secreted signalling molecules that link nervous system structure and function: they regulate neuronal survival, targeting, synaptic plasticity, memory and cognition. We have identified a neurotrophic factor in flies, Drosophila Neurotrophin (DNT1), structurally related to all known neurotrophins and highly conserved in insects. By investigating with genetics the consequences of removing DNT1 or adding it in excess, we show that DNT1 maintains neuronal survival, as more neurons die in DNT1 mutants and expression of DNT1 rescues naturally occurring cell death, and it enables targeting by motor neurons. We show that Spätzle and a further fly neurotrophin superfamily member, DNT2, also have neurotrophic functions in flies. Our findings imply that most likely a neurotrophin was present in the common ancestor of all bilateral organisms, giving rise to invertebrate and vertebrate neurotrophins through gene or whole-genome duplications. This work provides a missing link between aspects of neuronal function in flies and vertebrates, and it opens the opportunity to use Drosophila to investigate further aspects of neurotrophin function and to model related diseases.

Development, cancer, neurodegenerative and demyelinating diseases, injury, and stem cell manipulations are characterised by alterations in cell number. Research into development, disease, and the effects of drugs require cell number counts. These are generally indirect estimates, because counting cells in an animal or organ is paradoxically difficult, as well as being tedious and unmanageable. Drosophila is a powerful model organism used to investigate the genetic bases of development and disease. There are Drosophila models for multiple neurodegenerative diseases, characterised by an increase in cell death. However, a fast, reliable, and accurate way to count the number of dying cells in vivo is not available. Here, we present a method based on image filtering and mathematical morphology techniques, to count automatically the number of dying cells in intact fruit-fly embryos. We call the resulting programme DeadEasy Caspase. It has been validated for Drosophila and we present examples of its power to address biological questions. Quantification is automatic, accurate, objective, and very fast. DeadEasy Caspase will be freely available as an ImageJ plug-in, and it can be modified for use in other sample types. It is of interest to the Drosophila and wider biomedical communities. DeadEasy Caspase is a powerful tool for the analysis of cell survival and cell death in development and in disease, such as neurodegenerative diseases and ageing. Combined with the power of Drosophila genetics, DeadEasy expands the tools that enable the use of Drosophila to analyse gene function, model disease and test drugs in the intact nervous system and whole animal.

Trophic interactions in the vertebrate nervous system enable the adjustment of cell number and axon guidance, targeting and connectivity. Computational analysis of the sequenced Drosophila genome failed to identify some of the main trophic factors, the neuregulins and neurotrophins, as well as many other genes. This provoked speculations that the Drosophila nervous system might not require such regulative interactions. Here we review abundant cellular, genetic and functional data that demonstrate the existence of both neurotrophic and gliatrophic interactions in the Drosophila nervous system. Glial survival is maintained by the epidermal growth factor receptor (EGFR) signaling pathway in response to the ligands Spitz, a transforming growth factor-α (TGF-α) signaling molecule, and Vein, a neuregulin homologue. Cellular and genetic evidence predicts the existence of neuronal trophic factors operating at least in the Drosophila embryo during axon guidance and, in the visual system, during the targeting of retinal axons in the brain.

stood. Here, we characterize the role of cebpa during primitive myeloid cell development in Xenopus. We show that cebpa is one of the first known hematopoietic genes expressed in the embryo. Loss-and gain-of-function studies show that it is both necessary and sufficient for the development of functional myeloid cells. In addition, we show that cebpa misexpression leads to the precocious induction of myeloid cell markers in pluripotent prospective ectodermal cells, without the cells transitioning through a general mesodermal state. Finally we use live imaging to show that cebpa expressing cells exhibit many attributes of terminally differentiated myeloid cells, such as highly active migratory behavior, the ability to quickly and efficiently migrate toward wounds and phagocytose bacteria, and the ability to enter the circulation. Thus C/EPB alpha is the first known single factor capable of initiating an entire myelopoeisis pathway in pluripotent cells in the embryo.The shoulder girdle is a key skeletal structure that underwent substantial modifications during the evolutionary transition from fish to quadrupeds. The loss of its dermal bone (cleithral) connec-