Lachesin is a component of a septate junction-based mechanism that controls tube size and epithelial integrity in theDrosophilatracheal system

Abstract

Organ morphogenesis requires the coordinated activity of many mechanisms involved in cell rearrangements, size control, cell proliferation and organ integrity. Here we report that Lachesin (Lac), a cell surface protein, is required for the proper morphogenesis of the Drosophila tracheal system. Homozygous embryos for Lac mutations, which we find fail to complement the previous identified bulbous (

The Drosophila Claudin Kune-kune Is Required for Septate Junction Organization and Tracheal Tube Size Control

“…Kune is required for tracheal tube size control: Since almost all characterized SJ proteins are required for tracheal tube size control (Behr et al 2003;Paul et al 2003;Faivre-Sarrailh et al 2004;Llimargas et al 2004;Hijazi et al 2009;Wu et al 2007), we examined the tracheal system of kune embryos.…”

A UDP-GalNAc:Polypeptide N-Acetylgalactosaminyltransferase Is Required for Epithelial Tube Formation

“…Like mutations in septate junction proteins, pgant35A mutations resulted in a defective diffusion barrier across the tracheal tube. Furthermore, the tracheal tube shape is altered in much the same way as is seen for mutations in the claudin transmembrane proteins, Megatrachea and Sinuous (18,19), as well as the cell adhesion protein, Lachesin (21). Given the phenotypic similarities, it is possible that these membrane-bound proteins may be substrates of PGANT35A, requiring O-glycans for proper function.…”

“…Along the lateral surfaces, septate junctions are functionally analogous to vertebrate tight junctions and are responsible for establishing the transepithelial diffusion barrier of the tracheal tube (2, 16 -19). Additionally, septate junctions influence cell shape and tube size, since some septate junction proteins have been found to limit the extent of apical cell surface formation (16,20), and others severely alter tracheal tube morphology (2,19,21). All of these studies point to an incredibly complex interplay of many components to ensure proper cell polarity, morphology, and epithelial barrier formation.…”

Mechanisms of Lumen Development in Drosophila Tubular Organs

“…Restriction of tracheal tube length also depends on genes encoding components of the SJs, a structure located basal to the adherens junctions, which like the vertebrate tight junctions functions as a paracellular diffusion barrier and is comprised in part by the claudin family proteins (Behr et al, 2003;Nelson et al, 2010;Tepass et al, 2001;Wu et al, 2004). Mutations in several SJ proteins affect both tracheal tube length and diameter but not early aspects of tracheal development (Behr et al, 2003;Beitel and Kransnow, 2000;Llimargas et al, 2004;Paul et al, 2003;Wu et al, 2004). One mechanism by which SJ proteins control tracheal tube size is through apical secretion of Verm and Serp (Luschnig et al, 2006;Wang et al, 2006).…”

“…Thus, independent of Verm/Serp-dependent chitin modification, tracheal lumen length is controlled by a Yurt/Cora pathway dependent on Crb activity, and by a Scrib pathway independent of Crb. SJs likely control tracheal tube size by other mechanisms, such as cell shape since mutations in the SJ proteins, encoded by megatrachea and lachesin, cause tracheal cells to adopt an irregularly stretched morphology (Behr et al, 2003;Llimargas et al, 2004).…”