What is the difference between plasma membrane and basement membrane

When BMs of Ndg mutant animals were examined, dramatic loss of BM integrity was observed only in the fat body and some adult muscles Fig. Structure—function analysis confirmed that Nidogen acts as a link between Collagen IV and Laminin, and defects in fat body BM result from the uncoupling of their networks Dai et al. Why then do the BMs of Ndg mutants break only in certain tissues? One possibility is that BMs of fat body and muscles are subjected to high levels of mechanical stress that make the additional Laminin—Collagen IV link that is provided by Nidogen essential in these tissues to preserve BM integrity.

Indeed, genetic interaction experiments show that loss of Nidogen also enhances the defects seen in the absence of Laminin or Perlecan in other tissues Dai et al. Fat body cells increase their size very quickly during larval stages through polyploidization, which could explain an enhanced requirement for Ndg. However, this is also true of other tissues, such as the salivary glands, in which BMs that lack Nidogen still preserve their integrity.

In summary, while tissue-specific functions of Nidogen and other BM components are well documented, we lack a mechanistic understanding of this phenomenon. The multitude of studies and descriptions of atypical structures reviewed here challenge a strict definition of BMs as planar matrices. Also questionable is the clear distinction between the BM and other types of ECM, such as loose matrices, fibrils and aggregates. Finally, in terms of their composition, there are well-documented examples of laminin, nidogen, collagen IV and perlecan localizing and functioning outside of typical BMs, and of BMs that lack some of these four main BM components.

Although these examples could be dismissed as limiting cases and exceptions to the rule, research in Drosophila , where the numbers of BM studies have exploded in the past decade, indicates that such atypical BM structures are actually quite prevalent.

Even for typical planar BMs, studies repeatedly reveal that each of them is special in its own way, with large gaps in our understanding of their diversity, tissue-specific component requirements and differential properties. Here, I have summarized our precarious knowledge of the mechanisms generating BM diversity and increased thickness or aggregate-like deposition in atypical structures.

Importantly, changes in BM thickness are associated with diseases that affect the blood brain barrier, kidneys, cornea or retina Chew and Lennon, ; Gatseva et al. Furthermore, thick matrix deposits are seen in fibrotic conditions, where the expression of matrix proteins is upregulated, but the mechanisms that make that excess matrix form aberrant structures are unknown.

Uncovering the mechanisms that generate the normal homogeneous thickness of planar BMs and the increased thickness of certain atypical BMs, therefore, may help researchers to understand not only the normal assembly and roles of atypical structures, but also the pathological assembly linked to human diseases. Thanks are due to Marta Rojas, laboratory members and the anonymous referees for comments on the manuscript.

Images in Fig. Research in my laboratory is supported by Natural Science Foundation of China grants , and , and by the Peking-Tsinghua Center for Life Sciences. Read more about our commitment to Open Access. Submit your essay by 1 December for a chance to be published in Journal of Cell Science. Journal of Cell Science is pleased to welcome submissions for consideration for an upcoming special issue, Cell Biology of Motors , which will be guest edited by Anne Straube University of Warwick, UK.

Submission deadline: 15 July Our resident insectivore, Mole, continues his latest series — The Corona Files. Sign In or Create an Account. Advanced Search. User Tools. Sign in. Skip Nav Destination Article Navigation. Close mobile search navigation Article navigation. Volume , Issue 8. Previous Article Next Article. Article contents. Atypical basement membranes and related structures. Atypical basement membranes in Drosophila. Conclusions and perspectives. Article Navigation.

Atypical basement membranes and basement membrane diversity — what is normal anyway? Pastor-Pareja This site. Google Scholar. Author and article information. Competing interests The authors declare no competing or financial interests. Online Issn: National Natural Science Foundation of China Published by The Company of Biologists Ltd. J Cell Sci 8 : jcs Cite Icon Cite. View large Download slide.

Box 1. BM evolution. Table 1. View Large. Search ADS. The Drosophila JNK pathway controls the morphogenesis of imaginal discs during metamorphosis. The retrotransposon and the development of gonadal mesoderm in Drosophila. The PS2 integrin ligand tiggrin is required for proper muscle function in Drosophila. Oriented basement membrane fibrils provide a memory for F-actin planar polarization via the Dystrophin-Dystroglycan complex during tissue elongation.

Pericardin, a Drosophila collagen, facilitates accumulation of hemocytes at the heart. The basement membranes of cryofixed or aldehyde-fixed, freeze-substituted tissues are composed of a lamina densa and do not contain a lamina lucida. Pericardin, a Drosophila type IV collagen-like protein is involved in the morphogenesis and maintenance of the heart epithelium during dorsal ectoderm closure.

Extracellular matrix stiffness cues junctional remodeling for 3D tissue elongation. Variations in basement membrane mechanics are linked to epithelial morphogenesis. Inter-adipocyte adhesion and signaling by collagen IV intercellular concentrations in Drosophila. Dissection of Nidogen function in Drosophila reveals tissue-specific mechanisms of basement membrane assembly.

De Las Heras. The Drosophila Hox gene Ultrabithorax controls appendage shape by regulating extracellular matrix dynamics. Modelling the early evolution of extracellular matrix from modern Ctenophores and Sponges.

Collagen IV and basement membrane at the evolutionary dawn of metazoan tissues. The triple helix of collagens — an ancient protein structure that enabled animal multicellularity and tissue evolution. The spatial organization of Descemet's membrane-associated type IV collagen in the avian cornea. Tiggrin, a novel Drosophila extracellular matrix protein that functions as a ligand for Drosophila alpha PS2 beta PS integrins.

The distribution of PS integrins, laminin A and F-actin during key stages in Drosophila wing development. Drosophila PS1 integrin is a laminin receptor and differs in ligand specificity from PS2. Type IV collagen is detectable in most, but not all, basement membranes of caenorhabditis elegans and assembles on tissues that do not express it. A common suite of coagulation proteins function in Drosophila muscle attachment. Hematopoiesis at the onset of metamorphosis: terminal differentiation and dissociation of the Drosophila lymph gland.

The proteoglycan Trol controls the architecture of the extracellular matrix and balances proliferation and differentiation of blood progenitors in the Drosophila lymph gland. Laminin and basement membrane-associated microfilaments in wild-type and mutant Drosophila ovarian follicles. Global tissue revolutions in a morphogenetic movement controlling elongation.

Genetic analysis of laminin a reveals diverse functions during morphogenesis in Drosophila. DSS-induced damage to basement membranes is repaired by matrix replacement and crosslinking. Building from the ground up: basement membranes in Drosophila development. Dynamic regulation of basement membrane protein levels promotes egg chamber elongation in Drosophila. Rabmediated secretion synergizes with tissue movement to build a polarized basement membrane architecture for organ morphogenesis.

Embryo implantation triggers dynamic spatiotemporal expression of the basement membrane toolkit during uterine reprogramming. Collagen secretion screening in Drosophila supports a common secretory machinery and multiple Rab requirements.

Tissue linkage through adjoining basement membranes: the long and the short term of it. Mechanical stress regulates insulin sensitivity through integrin-dependent control of insulin receptor localization. Basement membrane components are key players in specialized extracellular matrices. Laminin A chain: expression during Drosophila development and genomic sequence. The major basement membrane components localize to the chondrocyte pericellular matrix--a cartilage basement membrane equivalent?

Permeation of macromolecules into the renal glomerular basement membrane and capture by the tubules. Le Parco. Stage and tissue-specific expression of a collagen gene during Drosophila melanogaster development.

Basement membrane manipulation in Drosophila wing discs affects Dpp retention but not growth mechanoregulation. JNK and decapentaplegic signaling control adhesiveness and cytoskeleton dynamics during thorax closure in Drosophila. A moving source of matrix components is essential for de novo basement membrane formation. Dynamics of the basement membrane in invasive epithelial clusters in Drosophila.

The role of the peripodial membrane of leg and wing imaginal discs ofDrosophila melanogaster during evagination and differentiation in vitro. Collagen IV alpha 3, alpha 4, and alpha 5 chains in rodent basal laminae: sequence, distribution, association with laminins, and developmental switches.

Evidence for microtubule nucleation at plasma membrane-associated sites in Drosophila. Drosophila substrate adhesion molecule: sequence of laminin B1 chain reveals domains of homology with mouse. Drosophila laminin: sequence of B2 subunit and expression of all three subunits during embryogenesis. Group choreography: mechanisms orchestrating the collective movement of border cells. B-LINK: a hemicentin, plakin, and integrin-dependent adhesion system that links tissues by connecting adjacent basement membranes.

Drosophila matrix metalloproteinases are required for tissue remodeling, but not embryonic development. Drosophila perlecan modulates FGF and hedgehog signals to activate neural stem cell division.

Shaping cells and organs in Drosophila by opposing roles of fat body-secreted Collagen IV and perlecan. Invasive cell behavior during Drosophila imaginal disc eversion is mediated by the JNK signaling cascade. Accumulation of laminin monomers in drosophila glia leads to glial endoplasmic reticulum stress and disrupted larval locomotion. Immunolocalization of type IV collagen and laminin in nonbasement membrane structures of murine corneal stroma. A light and electron microscopic study. Physical and functional cell-matrix uncoupling in a developing tissue under tension.

Absence of PS integrins or laminin A affects extracellular adhesion, but not intracellular assembly, of hemiadherens and neuromuscular junctions in Drosophila embryos. A scar-like lesion is apparent in basement membrane after wound repair in vivo. In muscular dystrophy, this protein is defective or missing, and reduces the attachment of muscle cells to their basal lamina.

This reduced attachment results in muscle degeneration and muscle weakness. This picture shows a duct from the kidney, stained with alcian blue, where the basement membrane can be seen more clearly, underlying the cuboidal epithelium.

See if you can identify the lumen of the duct, the simple cuboidal epithelium, and the basement membrane. This diagram shows part of the cuboidal epithelium in the photographs opposite together with its basal lamina. Basal Lamina What is the basal lamina? The basal lamina can be organised in three ways: 1. Components of the basal lamina. Viewed with the electron microscope, three distinct layers of the basal lamina can be described: lamina lucida - electron lucent very little staining in the EM.

Epithelia cells also contain additional structures that facilitate their activities. Epithelial cells involved in absorption often contain microvilli, finger-like projections of the plasma membrane, that increase the surface area of the plasma membrane, allowing for more efficient uptake of material. Some epithelial cells also contain cilia that are long, thin extensions of the plasma membrane.

Cilia are motile and move in wave-like fashion to generate flow in a lumen. This allows epithelial cells to move directionally large particles: ovum in fallopian tubes, mucus in trachea. Epithelial cells are held together through a set of cell to cell interactions along their lateral surface: tight junctions, adhering junctions and desmosomes.

Epithelial cells attach to a specialized kind of extracellular matrix called the basal lamina or basement membrane that separates epithelial cells from the underlying tissue.

Epithelia cells are polarized with an apical surface that faces the lumen of a tube or the external environment and a basal surface that attaches to the basement membrane. The apical and basal surfaces perform different functions and have unique biochemical compositions. Epithelial cells are continuously renewed. Mechanical forces and harsh environmental conditions damage and kill cells.

Every epithelium has a supply of stem cells to replenish lost or damaged cells. Three sets of interactions tether epithelial cells. Adhering junctions and desmosomes were discussed in the Cell to Tissues lecture.

The third complex is tight junctions. The position of these complexes along the lateral surface is ordered from apical to basal: tight junctions, adhering junctions and desmosomes. Tight junctions perform a critical function besides cell adhesion. They restrict the diffusion of molecules between neighboring cells paracellular. Tight junctions regulate the passage of ions and small metabolites, and the tightness of the diffusion barrier varies with the location of the epithelium: brain tight , intestine looser.

In fact, the electrical resistance of some epithelia can differ by over fold. Tight junctions are network of strands that encircle the cell and interact with similar strands on neighboring cells to form a seal around the cells. Tight junctions are linked intracellularly to actin filaments that stabilize the junctions.

There are over 40 proteins that make up a tight junction but claudins are thought to determine the diffusion properties of tight junctions. Claudins contain four transmembrane domains and interact with claudins in neighboring cells.

Their intracellular domains interact with a complex of proteins that associate with actin filaments. The interactions between claudins is thought to create pores that are restrictive to objects as small as 4 angtroms The pores can also be charge-selective, restricting either cations or anions.

There are 24 different claudin genes that show tissue-specific expression, and the type of claudin in an epithelium has been shown to determine the electrical resistance of the epithelium. The paracellular transport of larger molecules sugars, metabolites, peptides is much slower than ions is now thought to proceed by a different mechanism than diffusion through pores.

One model is that the strands of tight junctions are rapidly and sequentially unsealed and resealed to allow stepwise diffusion of some molecules. Besides junctional complexes, epithelial cells also contain gap junctions to facilitate cell to cell communication and coordinate cellular activities.

The basement membrane is form of extracellular matrix that underlies all epithelia.