Ultrastructural Changes in the Surface Layers of the Newt's Egg in Relation to the Mechanism of Its Cleavage

1970 ◽  
Vol 6 (1) ◽  
pp. 207-227 ◽  
Author(s):  
G. G. SELMAN ◽  
M. M. PERRY
Keyword(s):  
Plasma Membrane ◽  
Leading Edge ◽  
Ultrastructural Changes ◽  
Cortical Layers ◽  
Active Growth ◽  
Structural Modifications ◽  
Cell Cleavage ◽  
Surface Irregularities ◽  
Dense Band ◽  
10 Nm Filaments

The surface and cortical layers of an uncleaved newt egg have a characteristic ultrastructure which remains unaltered during cleavage; ultrastructural changes are confined to the region of the furrow. At the onset of cleavage there is a dipping inwards of the rough heavily pigmented animal surface to form a groove. Along the bottom of the groove the surface irregularities are reduced and a dense band (0.1 µm thick and 16 µm wide) is formed immediately below the plasma membrane. Within this band there are parallel filaments, 8-10 nm in diameter, oriented in the direction of the future furrow. No structural modifications were observed below the cortical layers of the leading part of the furrow apart from accumulations of granules and the mid-bodies of the spindle remnant. It is proposed that the dipping-in of the groove is due to contraction within the filamentous band, rather than contraction in a sheet of subcortical gel as proposed previously. The filamentous band persists below the furrow during the later stages of cleavage. The new unpigmented surface first forms as a strip across the animal surface and begins to grow at the bottom of the groove. Over most of its area, it is much smoother than the pigmented surface and has less material on the outside of the plasma membrane. There are microvilli along the bottom of the groove. The join between the new unpigmented and the old pigmented surface is abrupt. As the new unpigmented surface grows in extent, a narrow furrow forms below the lowest part of the groove and progresses towards the vegetal surface. For most of its length the furrow is between 10-nm and 0.5 µm wide, but at its leading edge it is 2 µ wide with microvilli on its surface and 10-nm filaments below the plasma membrane. It is concluded that the progressive formation of the furrow is due to active growth of new unpigmented cell surface. At late cleavage a ridge 10 µm high forms at the join between the new and old surface. After cleavage the ridges approach and meet to form the intercellular junction by which daughter blastomeres are held together along the animal surface. The mechanism of cell cleavage in the newt egg and in other forms is discussed in the light of the present observations.

scholarly journals The MADD-3 LAMMER Kinase Interacts with a p38 MAP Kinase Pathway to Regulate the Display of the EVA-1 Guidance Receptor in Caenorhabditis elegans

PLoS Genetics ◽  
2016 ◽  
Vol 12 (4) ◽  
pp. e1006010 ◽  
Author(s):  
Serena A. D’Souza ◽  
Luckshi Rajendran ◽  
Rachel Bagg ◽  
Louis Barbier ◽  
Derek M. van Pel ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Motor Neurons ◽  
Leading Edge ◽  
P38 Map Kinase ◽  
Endosomal Trafficking ◽  
Guidance Cue ◽  
Map Kinase Pathway ◽  
Kinase Pathway

The proper display of transmembrane receptors on the leading edge of migrating cells and cell extensions is essential for their response to guidance cues. We previously discovered that MADD-4, which is an ADAMTSL secreted by motor neurons in Caenorhabditis elegans, interacts with an UNC-40/EVA-1 co-receptor complex on muscles to attract plasma membrane extensions called muscle arms. In nematodes, the muscle arm termini harbor the post-synaptic elements of the neuromuscular junction. Through a forward genetic screen for mutants with disrupted muscle arm extension, we discovered that a LAMMER kinase, which we call MADD-3, is required for the proper display of the EVA-1 receptor on the muscle’s plasma membrane. Without MADD-3, EVA-1 levels decrease concomitantly with a reduction of the late-endosomal marker RAB-7. Through a genetic suppressor screen, we found that the levels of EVA-1 and RAB-7 can be restored in madd-3 mutants by eliminating the function of a p38 MAP kinase pathway. We also found that EVA-1 and RAB-7 will accumulate in madd-3 mutants upon disrupting CUP-5, which is a mucolipin ortholog required for proper lysosome function. Together, our data suggests that the MADD-3 LAMMER kinase antagonizes the p38-mediated endosomal trafficking of EVA-1 to the lysosome. In this way, MADD-3 ensures that sufficient levels of EVA-1 are present to guide muscle arm extension towards the source of the MADD-4 guidance cue.

scholarly journals Ultrastructural Changes in Bovine Lingual Epithelium Infected with Vesicular Stomatitis Virus

1975 ◽  
Vol 12 (5-6) ◽  
pp. 362-377 ◽  
Author(s):  
S. J. Proctor ◽  
K. C. Sherman
Keyword(s):  
Plasma Membrane ◽  
Vesicular Stomatitis Virus ◽  
Ultrastructural Changes ◽  
Intercellular Spaces ◽  
Lingual Epithelium ◽  
Vesicular Stomatitis

Vesicular stomatitis virus was inoculated into the dorsal lingual epithelium of three cows. The reaction that developed in 72 h was characterized by severe acute diffuse glossitis with intercellular edema and necrosis of keratinocytes. Virions budded from the plasma membrane and were in the intercellular spaces. Reduplication of desmosomes was a prominent alteration, and normal desmosomes were within the cytoplasm. Intracytoplasmic desmosomes appeared to be formed by endocytosis after breaks occurred in the plasma membrane of one cell; endocytosis of loops of plasma membrane containing desmosomes; and formation of desmosomes on invagination of the plasma membrane.

scholarly journals Anchorage of secretion-competent dense granules on the plasma membrane of bovine platelets in the absence of secretory stimulation.

1990 ◽  
Vol 111 (1) ◽  
pp. 79-86 ◽  
Author(s):  
T Morimoto ◽  
S Ogihara ◽  
H Takisawa
Keyword(s):  
Plasma Membrane ◽  
Average Distance ◽  
Ultrastructural Changes ◽  
Thin Sections ◽  
Regulated Exocytosis ◽  
Permeabilized Cells ◽  
Dense Granules ◽  
Amorphous Structures ◽  
Stimulation Of

The ultrastructural changes in electropermeabilized bovine platelets that accompany the Ca2(+)-induced secretion of serotonin were investigated in ultra-thin sections of chemically fixed cells. Such preparations permitted us to study both the localization of and the structures associated with serotonin-containing dense granules. Localization of dense granules within cells was examined by measuring the shortest distances between the granular membranes and the plasma membrane. About 40% of total granules were located close to the plasma membrane at an average distance of 10.8 +/- 1.6 nm. 71% of the total number of granules were localized at a similar average distance of 12.5 +/- 2.7 nm in intact platelets. The percentage of granules apposed to the plasma membrane corresponded closely to the percentage of total serotonin that was maximally secreted after stimulation of the permeabilized (38 +/- 4.9%) and the intact platelets (72 +/- 3.6%). Furthermore, the percentage of granules anchored to the membrane, but not of those in other regions of permeabilized cells, decreased markedly when cells were stimulated for 30 s by extracellularly added Ca2+. The decrease in the numbers of granules in the vicinity of the plasma membrane corresponded to approximately 22% of the total number of dense granules that were used for measurements of the distances between the two membranes and corresponded roughly to the overall decrease (15%) in the average number of the granules per cell. Most dense granules were found to be associated with meshwork structures of microfilaments. Upon secretory stimulation, nonfilamentous, amorphous structures found between the plasma membrane and the apposed granules formed a bridge-like structure that connected both membranes without any obvious accompanying changes in the microfilament structures. These results suggest that the dense granules that are susceptible to secretory stimulation are anchored to the plasma membrane before stimulation, and that the formation of the bridge-like structure may participate in the Ca2(+)-regulated exocytosis.

Ultrastructural changes in the cell surface of Coelomomyces punctatus infecting mosquito larvae

1976 ◽  
Vol 54 (13) ◽  
pp. 1419-1437 ◽  
Author(s):  
Martha J. Powell
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Granular Material ◽  
Fat Body ◽  
Vegetative Stage ◽  
Ultrastructural Changes ◽  
Anopheles Quadrimaculatus ◽  
Advanced Stages ◽  
Hyphal Bodies ◽  
Hyphal Body

As the fungus Coelomomyces punctatus develops in the coelomic cavity of the mosquito Anopheles quadrimaculatus, the conformation of the plasma membrane and extracellular coat of the fungus changes markedly. The vegetative stage was surrounded by a granular and fibrillar extracellular coat which reacted positively in the silver methenamine procedure for the localization of polysaccharides. Numerous simple, branched or contorted cytoplasmic protuberances covered the irregularly shaped hyphal bodies. The surface of the hyphal body adjacent to the fat body of the mosquito had occasional involutions of the plasma membrane sheathed by cisternae of endoplasmic reticulum. In contrast with these hyphal bodies, cytoplasmic protuberances were spaced at wide intervals along filamentous hyphae. Aborting thalli were contorted and deeply lobed. The plasma membrane was smooth, and cytoplasmic protuberances were absent on other hyphae and hyphal bodies, particularly at advanced stages of infection. Instead unattached vesicles, morphologically similar to the protuberances found on some thalli, were embedded in granular material clustered around the smooth plasma membrane of these thalli. Mosquito hemocytes appeared to engulf these vesicles and granular material. As the vegetative stage was transformed into the reproductive stage, a newly formed, compact extracellular layer surrounded the sporangial initial. Later, a darkly staining wall appeared around the resting sporangium. Cisternae of endoplasmic reticulum consistently subtended thin areas in this pitted wall.

scholarly journals CD13 tethers the IQGAP1-ARF6-EFA6 complex to the plasma membrane to promote ARF6 activation, β1 integrin recycling, and cell migration

2019 ◽  
Vol 12 (579) ◽  
pp. eaav5938 ◽  
Author(s):  
Mallika Ghosh ◽  
Robin Lo ◽  
Ivan Ivic ◽  
Brian Aguilera ◽  
Veneta Qendro ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cell Migration ◽  
Cell Adhesion ◽  
Cell Attachment ◽  
Leading Edge ◽  
Small Gtpase ◽  
Β1 Integrin ◽  
Recycling Endosomes ◽  
Cellular Processes ◽  
Early Endosomes

Cell attachment to the extracellular matrix (ECM) requires a balance between integrin internalization and recycling to the surface that is mediated by numerous proteins, emphasizing the complexity of these processes. Upon ligand binding in various cells, the β1 integrin is internalized, traffics to early endosomes, and is returned to the plasma membrane through recycling endosomes. This trafficking process depends on the cyclical activation and inactivation of small guanosine triphosphatases (GTPases) by their specific guanine exchange factors (GEFs) and their GTPase-activating proteins (GAPs). In this study, we found that the cell surface antigen CD13, a multifunctional transmembrane molecule that regulates cell-cell adhesion and receptor-mediated endocytosis, also promoted cell migration and colocalized with β1 integrin at sites of cell adhesion and at the leading edge. A lack of CD13 resulted in aberrant trafficking of internalized β1 integrin to late endosomes and its ultimate degradation. Our data indicate that CD13 promoted ARF6 GTPase activity by positioning the ARF6-GEF EFA6 at the cell membrane. In migrating cells, a complex containing phosphorylated CD13, IQGAP1, GTP-bound (active) ARF6, and EFA6 at the leading edge promoted the ARF6 GTPase cycling and cell migration. Together, our findings uncover a role for CD13 in the fundamental cellular processes of receptor recycling, regulation of small GTPase activities, cell-ECM interactions, and cell migration.

Phosphoinositide lipids and cell polarity: linking the plasma membrane to the cytocortex

2012 ◽  
Vol 53 ◽  
pp. 15-27 ◽  
Author(s):  
Michael P. Krahn ◽  
Andreas Wodarz
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Membrane Lipids ◽  
Leading Edge ◽  
Cell Types ◽  
Specific Protein ◽  
Molecular Organization ◽  
Apical Side ◽  
Cell Substrate ◽  
Basolateral Side

Many cell types in animals and plants are polarized, which means that the cell is subdivided into functionally and structurally distinct compartments. Epithelial cells, for example, possess an apical side facing a lumen or the outside environment and a basolateral side facing adjacent epithelial cells and the basement membrane. Neurons possess distinct axonal and dendritic compartments with specific functions in sending and receiving signals. Migrating cells form a leading edge that actively engages in pathfinding and cell-substrate attachment, and a trailing edge where such attachments are abandoned. In all of these cases, both the plasma membrane and the cytocortex directly underneath the plasma membrane show differences in their molecular composition and structural organization. In this chapter we will focus on a specific type of membrane lipids, the phosphoinositides, because in polarized cells they show a polarized distribution in the plasma membrane. They furthermore influence the molecular organization of the cytocortex by recruiting specific protein binding partners which are involved in the regulation of the cytoskeleton and in signal transduction cascades that control polarity, growth and cell migration.

Ultrastructural changes induced in zoospores of Lagenidium callinectes by exposure to Captan

1979 ◽  
Vol 57 (20) ◽  
pp. 2116-2121 ◽  
Author(s):  
D. G. Ruch ◽  
C. E. Bland
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Fine Structure ◽  
Nuclear Matrix ◽  
Active Component ◽  
Marine Fungus ◽  
Toxic Action ◽  
Ultrastructural Changes ◽  
Mitochondrial Matrix ◽  
Growth Development

The effects of the fungicide Captan on growth, development, and fine structure of the marine fungus Lagenidium callinectes Couch are studied. At the minimum lethal concentration (LC100) of Captan for L. callinectes (3.2 ppm active component), zoospores exposed for 30 min failed to encyst or germinate. Ultrastructural changes caused by exposure to Captan included "washing-out" of the mitochondrial matrix and disappearance of many of the cristae, clumping of the chromatin and disappearance of the nuclear matrix, and swelling of the cisternae of the endoplasmic reticulum. Longer exposure of zoospores to Captan resulted ultimately in breakdown of the plasma membrane. These observations were in agreement with those of previous studies which indicated that the toxic action of Captan occurs primarily in mitochondria.

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