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Polarization requires the coordinated interaction of three machineries that modify the basic mechanisms of intracellular protein trafficking and distribution. The integration of these mechanisms into a complex and dynamic network is crucial for normal tissue function and is often defective in disease states.
Conserved proteins of the partitioning defective (PAR), Scribble and Crumbs complexes guide the establishment of cell polarity in various organisms. Small GTPases have also been implicated in cell polarization. How do the polarity complexes and the small GTPases coordinate cellular polarization in different cell types?
Actin and microtubules are dynamic polar polymers that are well suited for providing the structural basis for cell polarity. The actin cytoskeleton generally drives symmetry breaking, whereas microtubules control polarity maintenance. These events are coordinated by bidirectional crosstalk between actin and microtubules.
The positioning of each cytoskeletal or membrane organelle must be coupled to that of other organelles in order to contribute efficiently to cell polarity. The non-random positioning of organelles is preserved and transmitted through cell division.
Tissue structures and shapes can be formed by organizing groups of cells into different polarized arrangements and by coordinating their polarity in space and time. Conserved design principles that underlie tissue polarity are emerging from studies of model organisms and tissues.
Proto-oncogenic pathways, including the insulin-like growth factor-I (IGF-I), Ras and AKT/PKB pathways, have recently been implicated in the ageing process. In simple organisms, proto-oncogene homologues increase DNA damage, whereas in mice they increase cancer incidence. So, can we prevent cancer by chronic downregulation of pro-ageing pathways?
Cell-cycle transitions in higher eukaryotes are regulated by different cyclin-dependent kinases (CDKs) and cyclins. Recent work using gene-targeted mice has led to a revision of this model and revealed overlapping and essential roles of different CDKs and cyclins.
