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.

The Drosophila actin nucleator DAAM is essential for left-right asymmetry.

Left-Right (LR) asymmetry is essential for organ positioning, shape and function. Myosin 1D (Myo1D) has emerged as an evolutionary conserved chirality determinant in both Drosophila and vertebrates. However, the molecular interplay between Myo1D and the actin cytoskeleton underlying symmetry breaking remains poorly understood.

A standardized nomenclature and atlas of the male terminalia of .

Animal terminalia represent some of the most diverse and rapidly evolving structures in the animal kingdom, and for this reason have been a mainstay in the taxonomic description of species. The terminalia of , with its wide range of experimental tools, have recently become the focus of increased interest in the fields of development, evolution, and behavior. However, studies from different disciplines have often used discrepant terminologies for the same anatomical structures.

The insulin pathway controls expression and dynamic actin-rich protrusions during collective cell migration.

Understanding how different cell types acquire their motile behaviour is central to many normal and pathological processes. border cells represent a powerful model for addressing this issue and to specifically decipher the mechanisms controlling collective cell migration. Here, we identify the Insulin/Insulin-like growth factor signalling (IIS) pathway as a key regulator in controlling actin dynamics in border cells, independently of its function in growth control.

Myosin1D is an evolutionarily conserved regulator of animal left-right asymmetry.

The establishment of left-right (LR) asymmetry is fundamental to animal development, but the identification of a unifying mechanism establishing laterality across different phyla has remained elusive. A cilia-driven, directional fluid flow is important for symmetry breaking in numerous vertebrates, including zebrafish. Alternatively, LR asymmetry can be established independently of cilia, notably through the intrinsic chirality of the acto-myosin cytoskeleton.

A Conserved Role of the Unconventional Myosin 1d in Laterality Determination.

Anatomical and functional asymmetries are widespread in the animal kingdom [1, 2]. In vertebrates, many visceral organs are asymmetrically placed [3]. In snails, shells and inner organs coil asymmetrically, and in Drosophila, genitalia and hindgut undergo a chiral rotation during development.

Polycomb and Hox Genes Control JNK-Induced Remodeling of the Segment Boundary during Drosophila Morphogenesis.

In segmented tissues, anterior and posterior compartments represent independent morphogenetic domains, which are made of distinct lineages separated by boundaries. During dorsal closure of the Drosophila embryo, specific "mixer cells" (MCs) are reprogrammed in a JNK-dependent manner to express the posterior determinant engrailed (en) and cross the segment boundary. Here, we show that JNK signaling induces de novo expression of en in the MCs through repression of Polycomb (Pc) and release of the en locus from the silencing PcG bodies.

Signalling crosstalk at the leading edge controls tissue closure dynamics in the Drosophila embryo.

Tissue morphogenesis relies on proper differentiation of morphogenetic domains, adopting specific cell behaviours. Yet, how signalling pathways interact to determine and coordinate these domains remains poorly understood. Dorsal closure (DC) of the Drosophila embryo represents a powerful model to study epithelial cell sheet sealing.

The Atypical Cadherin Dachsous Controls Left-Right Asymmetry in Drosophila.

Left-right (LR) asymmetry is essential for organ development and function in metazoans, but how initial LR cue is relayed to tissues still remains unclear. Here, we propose a mechanism by which the Drosophila LR determinant Myosin ID (MyoID) transfers LR information to neighboring cells through the planar cell polarity (PCP) atypical cadherin Dachsous (Ds). Molecular interaction between MyoID and Ds in a specific LR organizer controls dextral cell polarity of adjoining hindgut progenitors and is required for organ looping in adults.

Diversity and convergence in the mechanisms establishing L/R asymmetry in metazoa.

Differentiating left and right hand sides during embryogenesis represents a major event in body patterning. Left-Right (L/R) asymmetry in bilateria is essential for handed positioning, morphogenesis and ultimately the function of organs (including the brain), with defective L/R asymmetry leading to severe pathologies in human. How and when symmetry is initially broken during embryogenesis remains debated and is a major focus in the field.

Starvation induces FoxO-dependent mitotic-to-endocycle switch pausing during Drosophila oogenesis.

When exposed to nutrient challenge, organisms have to adapt their physiology in order to balance reproduction with adult fitness. In mammals, ovarian follicles enter a massive growth phase during which they become highly dependent on gonadotrophic factors and nutrients. Somatic tissues play a crucial role in integrating these signals, controlling ovarian follicle atresia and eventually leading to the selection of a single follicle for ovulation.

The myosin ID pathway and left-right asymmetry in Drosophila.

Drosophila is a classical model to study body patterning, however left-right (L/R) asymmetry had remained unexplored, until recently. The discovery of the conserved myosin ID gene as a major determinant of L/R asymmetry has revealed a novel L/R pathway involving the actin cytoskeleton and the adherens junction. In this process, the HOX gene Abdominal-B plays a major role through the control of myosin ID expression and therefore symmetry breaking.

Drosophila left/right asymmetry establishment is controlled by the Hox gene abdominal-B.

In Drosophila, left/right (LR) asymmetry is apparent in the directional looping of the gut and male genitalia. The dextral orientation of the organs depends on the activity of a single gene, MyosinID (myoID), whose mutation leads to a fully inverted LR axis, thus revealing the activity of a recessive sinistral pathway. Here, we present the identification of the Hox gene Abdominal-B (Abd-B) as an upstream regulator of LR determination.

DE-Cadherin regulates unconventional Myosin ID and Myosin IC in Drosophila left-right asymmetry establishment.

In bilateria, positioning and looping of visceral organs requires proper left-right (L/R) asymmetry establishment. Recent work in Drosophila has identified a novel situs inversus gene encoding the unconventional type ID myosin (MyoID). In myoID mutant flies, the L/R axis is inverted, causing reversed looping of organs, such as the gut, spermiduct and genitalia.

Regulation and activity of JNK signaling in the wing disc peripodial membrane during adult morphogenesis in Drosophila.

Thorax closure in Drosophila is a process during adult morphogenesis in which the anterior ends of the presumptive notum of the two wing imaginal discs fuse to make a seamless thorax. Similar to dorsal closure during embryogenesis, this process is regulated by plegic and JNK signaling pathways. Despite the fact that Peripodial Membrane (PM) cells do not contribute to the formation of any adult structure, they are known to facilitate the process of thorax closure.

Mixer Cell formation during dorsal closure: a new developmental model of JNK-dependent natural cell reprogramming in Drosophila.

What triggers a differentiated cell to naturally change its cell fate? Cell reprogramming is a rare and intriguing phenomenon, from a developmental point of view. It has been mostly involved in boundary sharpening during development, tissue regeneration and cancer. Developmental models of the understanding of pathology-related cell reprogramming are yet to be established.

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.

A mathematical model for dorsal closure.

During embryogenesis, drosophila embryos undergo epithelial folding and unfolding, which leads to a hole in the dorsal epidermis, transiently covered by an extraembryonic tissue called the amnioserosa. Dorsal closure (DC) consists of the migration of lateral epidermis towards the midline, covering the amnioserosa. It has been extensively studied since numerous physical mechanisms and signaling pathways present in DC are conserved in other morphogenetic events and wound healing in many other species (including vertebrates).

Coupling of apoptosis and L/R patterning controls stepwise organ looping.

Handed asymmetry in organ shape and positioning is a common feature among bilateria, yet little is known about the morphogenetic mechanisms underlying left-right (LR) organogenesis. We utilize the directional 360° clockwise rotation of genitalia in Drosophila to study LR-dependent organ looping. Using time-lapse imaging, we show that rotation of genitalia by 360° results from an additive process involving two ring-shaped domains, each undergoing 180° rotation.

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.