The shape of biological tubes is optimized for supporting efficient circulation of liquid and gas and to maintain organismal homeostasis. Maintaining a constant tube diameter and fitting tube length to body size are two requirements for proper tube function. The tracheal system of the Drosophila embryo is established through branching of ectodermal epithelia in the absence of environmental air, and the branching pattern and geometry of this system are genetically specified. Recent studies identified apical extracellular matrix (aECM) as a crucial regulator of tube expansion and elongation. Evidence suggests that aECM coordinates apical membrane growth and cell contractility to control tube growth at the tissue level. In the present review, we will discuss the physical mechanisms underlying this interaction.

•Adult segment of Perinereis is formed by stepwise posterior addition of 5 cell rows•Cell cycle entry and change in chromatin modification accompany segment formation•Wingless signaling is activated in posteriorly decaying gradient in each segment•Elevation of Wingless signaling increased segment width and decreased segment numberSegmentation is a body-patterning strategy in which new segments are specified from a segment-addition zone containing uncommitted cells. However, the cell-recruitment process is poorly understood. Here we investigated in detail the segmentation in a polychaete annelid, Perinereis nuntia (Lophotrochozoa), in which new segments emerge at the boundary between the posterior end of the segmented region and the terminal pygidium. Cells at this border synchronously remodel their chromatin, enter the cell cycle, and undergo oriented cell division, before being added to new segments. wingless is expressed at the posterior edge of the pre-existing segment, abutted by hedgehog in the first row of the new segment. Overstimulation of Wingless signaling caused excess cells to enter the cell cycle, prolonging segmentation and widening the new segment. Thus, segment addition may occur by a homeogenetic mechanism, in which Wingless expressed in the differentiated segment coordinates the stepwise recruitment of undifferentiated cells from the segment/pygidium boundary.

Dorsal closure in Drosophila embryogenesis involves expansion of the dorsal epidermis, followed by closure of the opposite epidermal edges. This process is driven by contractile force generated by an extraembryonic epithelium covering the yolk syncytium known as the amnioserosa. The secreted signaling molecule Dpp is expressed in the leading edge of the dorsal epidermis and is essential for dorsal closure. We found that the outermost row of amnioserosa cells (termed pAS) maintains a tight basolateral cell–cell adhesion interface with the leading edge of dorsal epidermis throughout the dorsal closure process. pAS was subject to altered cell motility in response to Dpp emanating from the dorsal epidermis, and this response was essential for dorsal closure. αPS3 and βPS integrin subunits accumulated in the interface between pAS and dorsal epidermis, and were both required for dorsal closure. Looking at αPS3, type I Dpp receptor, and JNK mutants, we found that pAS cell motility was altered and pAS and dorsal epidermis adhesion failed under the mechanical stress of dorsal closure, suggesting that a Dpp-mediated mechanism connects the squamous pAS to the columnar dorsal epidermis to form a single coherent epithelial layer.

IKK-related kinases are key regulators of innate immunity and oncogenesis. While their effects on transcription are well characterized, their cytoplasmic functions remain poorly understood. Drosophila IKK-related kinase, IKKɛ, regulates cytoskeletal organization and cell elongation. Here, we demonstrate that IKKɛ is activated locally at the tip of growing mechanosensory bristles and regulates the rapid shuttling of recycling endosomes, independent of its roles in F-actin organization and caspase signaling. IKKɛ regulates the localization of recycling endosome regulators Rab11 and Dynein and phosphorylates their adaptor molecule, Nuclear fallout (Nuf). Nuf's negative regulation by IKKɛ suggests that local activation of IKKɛ inhibits Dynein on incoming recycling endosomes, converting them for outward transport. Mammalian IKK-related kinases also regulate the recycling endosomes' distribution by phosphorylating the Nuf homolog Rab11-FIP3. Our results establish an evolutionarily conserved function of IKK-related kinases in regulating recycling endosome dynamics and point to a key role of endosome dynamics in cell morphogenesis.Graphical AbstractDownload high-res image (412KB)Download full-size imageHighlights► Recycling endosomes shuttle along the proximal-distal axis of growing bristles ► IKKɛ locally antagonizes Rab11 effector Nuf at the bristle tip by phosphorylation ► Nuf-endosome pathway is independent of actin cytoskeleton or DIAP1-caspase pathway ► Mammalian IKK-related kinases antagonize Rab11-FIP3 through phosphorylation

Domain boundary formation in development involves sorting of different types of cells into separate spatial domains. The segment boundary between tarsus 5 (Ta5) and the pretarsus (Pre) of the Drosophila leg initially appears at the center of the leg disc and progressively sharpens and expands to its final position, accompanied by down-regulation of the cell recognition molecule Capricious and Tartan and cell displacement from Ta5 to Pre across the boundary. Capricious and Tartan are controlled by transcription factor Bar and Al, and their loss of function leads to reduction of cell affinity to wild type neighbors and cell displacement activities. In addition, although the mutant cells formed Ta5/Pre boundary, its progression and sharpening were compromised. Cells overexpressing Capricious or Tartan became invasive within Ta5 and Pre, sometimes escaping the compartmental restriction of cell movement. Dynamic spatiotemporal regulation of cell affinity mediated by Capricious and Tartan is a key property of refinement of the Ta5/Pre boundary.

The interaction of heterologous tissues involves cell adhesion mediated by the extracellular matrix and its receptor integrins. The Drosophila wing disc is an ectodermal invagination that contacts specific tracheal branches at the basolateral cell surface. We show that an α subunit of laminin, encoded by wing blister (wb), is essential for the establishment of the interaction between the wing and trachea. During embryogenesis, wing disc cells present Wb at their basolateral surface and extend posteriorly, expanding their association to more posteriorly located tracheal branches. These migratory processes are impaired in the absence of the trachea, Wb, or integrins. Time-lapse and transmission electron microscopy analyses suggest that Wb facilitates integrin-dependent contact over a large surface and controls the cellular behavior of the wing cells, including their exploratory filopodial activity. Our data identify Wb laminin as an extracellular matrix ligand that is essential for integrin-dependent cellular migration in Drosophila.