Initiation of lumen formation from junctions via differential actomyosin contractility regulated by dynamic recruitment of Rasip1.

De novo lumen formation necessitates the precise segregation of junctional proteins from apical surfaces, yet the underlying mechanisms remain unclear. Using a zebrafish model, we develop a series of molecular reporters, photo-convertible and optogenetic tools to study the establishment of apical domains. Our study identifies Rasip1 as one of the earliest apical proteins recruited, which suppresses actomyosin contractility at junctional patches by inhibiting NMII, thereby allowing for the sustained outward flow of junctional complexes.

Interferon-γ drives macrophage reprogramming, cerebrovascular remodelling, and cognitive dysfunction in a zebrafish and a mouse model of ion imbalance and pressure overload.

Aims: Dysregulated immune response contributes to inefficiency of treatment strategies to control hypertension and reduce the risk of end-organ damage. Uncovering the immune pathways driving the transition from the onset of hypertensive stimulus to the manifestation of multi-organ dysfunction are much-needed insights for immune targeted therapy.

Methods And Results: To aid visualization of cellular events orchestrating multi-organ pathogenesis, we modelled hypertensive cardiovascular remodelling in zebrafish.

Vinculin strengthens the endothelial barrier during vascular development.

Remodelling of cell-cell junctions is crucial for proper tissue development and barrier function. The cadherin-based adherens junctions anchor via β-catenin and α-catenin to the actomyosin cytoskeleton, together forming a junctional mechanotransduction complex. Tension-induced conformational changes in the mechanosensitive α-catenin protein induce junctional vinculin recruitment.

Vinculin controls endothelial cell junction dynamics during vascular lumen formation.

Blood vessel morphogenesis is driven by coordinated endothelial cell behaviors. Active remodeling of cell-cell junctions promotes cellular plasticity while preserving vascular integrity. Here, we analyze the dynamics of endothelial adherens junctions during lumen formation in angiogenic sprouts in vivo.

Probing the Effects of the FGFR-Inhibitor Derazantinib on Vascular Development in Zebrafish Embryos.

Angiogenesis is a fundamental developmental process and a hallmark of cancer progression. Receptor tyrosine kinases (RTK) are targets for cancer therapy which may include their action as anti-angiogenic agents. Derazantinib (DZB) is an inhibitor of the fibroblast growth factor receptors (FGFRs) 1-3 as well as other kinase targets including vascular endothelial growth factor receptor 2 (VEGFR2), colony stimulating factor-1 receptor (CSF1R) and platelet-derived growth factor beta receptor (PDGFRbeta).

Sprouting and anastomosis in the Drosophila trachea and the vertebrate vasculature: Similarities and differences in cell behaviour.

Branching morphogenesis is a fascinating process whereby a simple network of biological tubes increases its complexity by adding new branches to existing ones, generating an enlarged structure of interconnected tubes. Branching morphogenesis has been studied extensively in animals and much has been learned about the regulation of branching at the cellular and molecular level. Here, we discuss studies of the Drosophila trachea and of the vertebrate vasculature, which have revealed how new branches are formed and connect (anastomose), leading to the establishment of complex tubular networks.

Author Correction: Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo.

The original version of this Article contained an error in the spelling of the author Alexandra Schambony, which was incorrectly given as Alexandra Schambon. This has now been corrected in both the PDF and HTML versions of the Article.

Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo.

Connexins are the primary components of gap junctions, providing direct links between cells under many physiological processes. Here, we demonstrate that in addition to this canonical role, Connexins act as transcriptional regulators. We show that Connexin 43 (Cx43) controls neural crest cell migration in vivo by directly regulating N-cadherin transcription.

The Leishmania donovani histidine acid ecto-phosphatase LdMAcP: insight into its structure and function.

Acid ecto-phosphatase activity has been implicated in Leishmania donovani promastigote virulence. In the present study, we report data contributing to the molecular/structural and functional characterization of the L. donovani LdMAcP (L.

Connexins in migration during development and cancer.

Connexins, the gap junction proteins, through their multitude of actions are implicated in a variety of cell processes during animal development and cancer. They allow direct or paracrine/autocrine cell communication through their channel and hemi-channel functions. They enable adhesion and interact with a plethora of signalling molecules.

Lamellipodin and the Scar/WAVE complex cooperate to promote cell migration in vivo.

Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism.