A dynamic and mosaic basement membrane controls cell intercalation in ovaries.

Basement membranes (BM) are extracellular matrices assembled into complex and highly organized networks essential for organ morphogenesis and function. However, little is known about the tissue origin of BM components and their dynamics Here, we unravel the assembly and role of the BM main component, Collagen type IV (ColIV), in ovarian stalk morphogenesis. Stalks are short strings of cells assembled through cell intercalation that link adjacent follicles and maintain ovarian integrity.

Polycomb controls gliogenesis by regulating the transient expression of the Gcm/Glide fate determinant.

The Gcm/Glide transcription factor is transiently expressed and required in the Drosophila nervous system. Threshold Gcm/Glide levels control the glial versus neuronal fate choice, and its perdurance triggers excessive gliogenesis, showing that its tight and dynamic regulation ensures the proper balance between neurons and glia. Here, we present a genetic screen for potential gcm/glide interactors and identify genes encoding chromatin factors of the Trithorax and of the Polycomb groups.

Asymmetric localisation of cytokine mRNA is essential for JAK/STAT activation during cell invasiveness.

The transition from immotile epithelial cells to migrating cells occurs in all organisms during normal embryonic development, as well as during tumour metastasis. During Drosophila oogenesis, border cells (BCs) are recruited and delaminate from the follicular epithelium. This process is triggered by the polar cells (PCs), which secrete the cytokine Unpaired (Upd) and activate the JAK/STAT pathway in neighbouring cells, turning them into invasive BCs.

Cell migration: MIM takes the driver's seat.

A recent study reports a novel and conserved function for the I-BAR protein MIM in guiding cell migration: MIM has an anti-endocytic activity that moderates intracellular signalling of guidance cues by sequestration of cortactin.

A bioinformatics search pipeline, RNA2DSearch, identifies RNA localization elements in Drosophila retrotransposons.

mRNA localization is a widespread mode of delivering proteins to their site of function. The embryonic axes in Drosophila are determined in the oocyte, through Dynein-dependent transport of gurken/TGF-alpha mRNA, containing a small localization signal that assigns its destination. A signal with a similar secondary structure, but lacking significant sequence similarity, is present in the I factor retrotransposon mRNA, also transported by Dynein.

gurken and the I factor retrotransposon RNAs share common localization signals and machinery.

Drosophila gurken mRNA is localized by dynein-mediated transport to a crescent near the oocyte nucleus, thus targeting the TGFalpha signal and forming the primary embryonic axes. Here, we show that gurken and the I factor, a non-LTR retrotransposon, share a small consensus RNA stem loop of defined secondary structure, which forms a conserved signal for dynein-mediated RNA transport to the oocyte nucleus. Furthermore, gurken and the I factor compete in vivo for the same localization machinery.

Time-lapse and cell ablation reveal the role of cell interactions in fly glia migration and proliferation.

Migration and proliferation have been mostly explored in culture systems or fixed preparations. We present a simple genetic model, the chains of glia moving along fly wing nerves, to follow such dynamic processes by time-lapse in the whole animal. We show that glia undergo extensive cytoskeleton and mitotic apparatus rearrangements during division and migration.

mRNA localisation gets more complex.

Recent advances in techniques for visualising mRNA movement in living cells have led to rapid progress in understanding the mechanism of mRNA localisation in the cytoplasm. There is an emerging consensus that in many cases the mRNA signals that determine intracellular destination are more complex and difficult to define than was first anticipated. Furthermore, the transacting factors that interpret the mRNA signals are numerous and their combinations change during the life of an mRNA, perhaps allowing the selection of many sub-destinations in the cell.

Transcriptional regulation of glial cell specification.

Neuronal differentiation relies on proneural factors that also integrate positional information and contribute to the specification of the neuronal type. The molecular pathway triggering glial specification is not understood yet. In Drosophila, all lateral glial precursors and glial-promoting activity have been identified, which provides us with a unique opportunity to dissect the regulatory pathways controlling glial differentiation and specification.

Novel features of dFMR1, the Drosophila orthologue of the fragile X mental retardation protein.

FMRP belongs to a family of widely expressed proteins that contain RNA-binding domains. Although lack of human FMRP results in mental retardation, correlated with subtle synaptic changes, the precise role of FMRP remains elusive. The Drosophila genome contains a single gene homologous to the FXR family.

glide/gcm: at the crossroads between neurons and glia.

Neurons and glia are generated by multipotent precursors. Recent studies indicate that the choice between the two fates depends on the combined activity of extracellular influences and factors that respond to precise spatial and temporal cues. Drosophila provides a simple genetic model to study the cellular and molecular mechanisms controlling fate choice, mode of precursor division and generation of cell diversity.

Precocious expression of the Glide/Gcm glial-promoting factor in Drosophila induces neurogenesis.

Neurons and glial cells depend on similar developmental pathways and often originate from common precursors; however, the differentiation of one or the other cell type depends on the activation of cell-specific pathways. In Drosophila, the differentiation of glial cells depends on a transcription factor, Glide/Gcm. This glial-promoting factor is both necessary and sufficient to induce the central and peripheral glial fates at the expense of the neuronal fate.