Establishing and transducing cell polarity: common themes and variations

All cells in vivo have a primary axis of polarity that controls many aspects of their behaviour, such as the direction of protein secretion and signalling, the orientation of cell division and directed cell movement and morphogenesis. Cell polarise in response to extracellular cues or intracellular landmarks that initiate a signal transduction process that establishes complementary cortical domains of conserved polarity factors. These cortical domains then transmit this polarity to the rest of the cell by regulating the organisation of the cytoskeleton and membrane trafficking systems. Here I review work over the past couple of years that has elucidated many key features of how polarity is established and transduced in different systems, but has also revealed unexpected variations in polarity mechanisms depending on context.I am supported by Wellcome Principal Research Fellowship 080007/B/06/Z

Watching gene expression in color.

A combination of two fluorescent proteins with different half-lives allows gene expression to be followed with improved time resolution

Oogenesis: Matrix Revolutions

SummaryThe mechanism of egg-chamber elongation during Drosophila oogenesis has always been mysterious. A new study shows that the egg chambers spin around their long axis laying down polarised extracellular matrix, which acts as a molecular corset to restrict radial expansion

The origin of asymmetry : early polarisation of the Drosophila germline cyst and oocyte.

The anterior-posterior axis of Drosophila is established before fertilisation when the oocyte becomes polarised to direct the localisation of bicoid and oskarmRNAs to opposite poles of the egg. Here we review recent results that reveal that the oocyte acquires polarity much earlier than previously thought, at the time when it acquires its fate. The oocyte arises from a 16 cell germline cyst, and its selection and the initial cue for its polarisation are controlled by the asymmetric segregation of a germline specific organelle called the fusome. Several different downstream pathways then interpret this asymmetry to restrict distinct aspects of oocyte identity to this cell. Mutations in any of the 6 conserved PAR proteins disrupt the early polarisation of the oocyte and lead to a failure to maintain its identity. Surprisingly, mutations affecting the control of the mitotic or meiotic cell cycle also lead to a failure to maintain the oocyte fate, indicating crosstalk between the nuclear and cytoplasmic events of oocyte differentiation. The early polarity of the oocyte initiates a series of reciprocal signalling events between the oocyte and the somatic follicle cells that lead to a reversal of oocyte polarity later in oogenesis, which defines the anterior-posterior axis of the embryo

A rapid method to map mutations in Drosophila.

BACKGROUND: Genetic screens in Drosophila have provided a wealth of information about a variety of cellular and developmental processes. It is now possible to screen for mutant phenotypes in virtually any cell at any stage of development by performing clonal screens using the flp/FRT system. The rate-limiting step in the analysis of these mutants is often the identification of the mutated gene, however, because traditional mapping strategies rely mainly on genetic and cytological markers that are not easily linked to the molecular map. RESULTS: Here we describe the development of a single-nucleotide polymorphism (SNP) map for chromosome arm 3R. The map contains 73 polymorphisms between the standard FRT chromosome, and a mapping chromosome that carries several visible markers (rucuca), at an average density of one SNP per 370 kilobases (kb). Using this collection, we show that mutants can be mapped to a 400 kb interval in a single meiotic mapping cross, with only a few hundred SNP detection reactions. Discovery of further SNPs in the region of interest allows the mutation to be mapped with the same recombinants to a region of about 50 kb. CONCLUSION: The combined use of standard visible markers and molecular polymorphisms in a single mapping strategy greatly reduces both the time and cost of mapping mutations, because it requires at least four times fewer SNP detection reactions than a standard approach. The use of this map, or others developed along the same lines, will greatly facilitate the identification of the molecular lesions in mutants from clonal screens.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Embryonic Pattern Scaling Achieved by Oppositely Directed Morphogen Gradients

Morphogens are proteins, often produced in a localised region, whose concentrations spatially demarcate regions of differing gene expression in developing embryos. The boundaries of expression must be set accurately and in proportion to the size of the one-dimensional developing field; this cannot be accomplished by a single gradient. Here, we show how a pair of morphogens produced at opposite ends of a developing field can solve the pattern-scaling problem. In the most promising scenario, the morphogens effectively interact according to the annihilation reaction $A+B\to\emptyset$ and the switch occurs according to the absolute concentration of $A$ or $B$. In this case embryonic markers across the entire developing field scale approximately with system size; this cannot be achieved with a pair of non-interacting gradients that combinatorially regulate downstream genes. This scaling occurs in a window of developing-field sizes centred at a few times the morphogen decay length.Comment: 24 pages; 11 figures; uses iopar