dictyNews Electronic Edition Volume 31, number 4 July 25, 2008 Please submit abstracts of your papers as soon as they have been accepted for publication by sending them to dicty@northwestern.edu or by using the form at http://dictybase.org/db/cgi-bin/dictyBase/abstract_submit. Back issues of dictyNews, the Dicty Reference database and other useful information is available at dictyBase - http://dictybase.org. ========= Abstracts ========= Chemotaxis, chemokine receptors and human disease Tian Jin(1), Xuehua Xu(2) and Dale Hereld(3) (1) Chemotaxis Signal Section, Laboratory of Immunogenetics, NIAID, NIH, Rockville, Maryland 20852. (2) Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057. (3) Division of Metabolism and Health Effects, NIAAA, NIH, Rockville, Maryland 20852 Cytokine, in press Cell migration is involved in diverse physiological processes including embryogenesis, immunity, and diseases such as cancer and chronic inflammatory disease. The movement of many cell types is directed by extracellular gradients of diffusible chemicals. This phenomenon, referred to as "chemotaxis", was first described in 1888 by Leber who observed the movement of leukocytes toward sites of inflammation. We now know that a large family of small proteins, chemokines, serves as the extracellular signals and a family of G-protein-coupled receptors (GPCRs), chemokine receptors, detects gradients of chemokines and guides cell movement in vivo. Currently, we still know little about the molecular machineries that control chemokine gradient sensing and migration of immune cells. Fortunately, the molecular mechanisms that control these fundamental aspects of chemotaxis appear to be evolutionarily conserved, and studies in lower eukaryotic model systems allowed us to form concepts, uncover molecular components, develop new techniques, and test models of chemotaxis. These studies have helped our current understanding of this complicated cell behavior. In this review, we wish to mention landmark discoveries in the chemotaxis research field that shaped our current understanding of this fundamental cell behavior and lay out key questions that remain to be addressed in the future. Submitted by: Dale Hereld [hereldd@mail.nih.gov] -------------------------------------------------------------------------------- Phagocytosis and host-pathogen interactions in Dictyostelium with a look at macrophages. S. Bozzaro, C. Bucci and M. Steinert Int. Rev. Cytol., in press Research into phagocytosis and host-pathogen interactions in the lower eukaryote Dictyostelium discoideum has flourished in recent years. This review presents a glimpse of where this research stands, with emphasis on the cell biology of the phagocytic process and on the wealth of molecular genetic data that have been gathered. The basic mechanistic machinery and most of the underlying genes appear to be evolutionarily conserved, reflecting the fact that phagocytosis arose as an efficient way to ingest food in single protozoan cells devoid of a rigid cell wall. In spite of some differences, the signal transduction pathways regulating phagosome biogenesis are also emerging as similar between Dictyostelium and macrophages. Both cell types are host for many pathogenic invasive bacteria, which exploit phagocytosis to grow intracellularly. We present an overwiew, based on the analysis of mutants, on how Dictyostelium contributes as a genetic model system to decipher the complexity of host-pathogen interactions. Table of content: 1. Introduction 2. The dynamics of phagocytosis 3. Cellular mechanisms of phagocytosis 3.1 Bacterial adhesion to the cell surface: the search for phagocytosis receptors 3.2 Actin cytoskeleton in phagocytosis 3.3 Phagosome fusion with endo-lysosomal vesicles and the killing of bacteria 4. Regulatory pathways controlling phagocytosis 4.1 Heterotrimeric G proteins 4.2 Phosphoinositides and calcium ions 4.3 Small G proteins of Ras and Rac families and tyrosine kinases 4.4 The Rab family and intracellular phagosome maturation 5. Host-pathogen interactions: a versatile new model host 5.1 Resistance/susceptibility genes of the host to infection by Mycobacteria, Legionella and Klebsiella 5.2 Nramp family in Dictyostelium and Nramp1 as the host defence factor 6. Concluding remarks Submitted by: Salvo Bozzaro [salvatore.bozzaro@unito.it] ============================================================== [End dictyNews, volume 31, number 4]