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dictyNews Volume 31 Number 04
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.
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Abstracts
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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]
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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]
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[End dictyNews, volume 31, number 4]
