scholarly journals Transient opening of tricellular vertices controls paracellular transport through the follicle epithelium during Drosophila oogenesis

2021 ◽  
Vol 56 (8) ◽  
pp. 1083-1099.e5 ◽  
Author(s):  
Jone Isasti-Sanchez ◽  
Fenja Münz-Zeise ◽  
Mylène Lancino ◽  
Stefan Luschnig
Keyword(s):  
Paracellular Transport ◽  
Drosophila Oogenesis

Claudin Tight Junction Proteins: Novel Aspects in Paracellular Transport

2008 ◽  
Vol 28 (6) ◽  
pp. 577-584 ◽  
Author(s):  
Constanze Will ◽  
Michael Fromm ◽  
Dominik Müller
Keyword(s):  
Tight Junction ◽  
Solute Transport ◽  
Molecular Mechanisms ◽  
Family Members ◽  
Transport Processes ◽  
Paracellular Transport ◽  
Solute Flux ◽  
Solute Fluxes ◽  
Essential Components ◽  
Renal Tubular

Claudins are essential components of the intercellular tight junction and major determinants of paracellular solute fluxes across epithelia and endothelia. Many members of this family display a distinct charge or size specificity, whereas others render the epithelium impermeable to transport. Due to intercellular localization, claudin-mediated transport processes are passive and driven by an electrochemical gradient. In epithelial tissues, claudins exhibit a temporal–spatial expression pattern corresponding with regional and local solute transport profiles. Whereas paracellular transport mechanisms in organs such as intestine and kidney have been extensively investigated, little is known about the molecular mechanisms determining solute transport in the peritoneum, and thus the determinants of peritoneal dialysis. Given the ubiquitous expression of claudins in endothelia and epithelia, it is predictable that claudins also contribute to pore formation and determination in the peritoneum, and that they are involved in solute flux. Therefore, we review the basic characteristics of claudin family members and their function as exemplified in renal tubular transport and give an outlook to what extent claudin family members might be of importance for solute reabsorption across the peritoneal membrane.

scholarly journals Claudin-4 augments alveolar epithelial barrier function and is induced in acute lung injury

2009 ◽  
Vol 297 (2) ◽  
pp. L219-L227 ◽  
Author(s):  
Charlie Wray ◽  
Ying Mao ◽  
Jue Pan ◽  
Anita Chandrasena ◽  
Frank Piasta ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Tight Junction ◽  
Pulmonary Edema ◽  
Barrier Function ◽  
Mapk Pathway ◽  
Paracellular Transport ◽  
Epithelial Barrier ◽  
Altered Expression ◽  
Alveolar Epithelial

Intact alveolar barrier function is associated with better outcomes in acute lung injury patients; however, the regulation of alveolar epithelial paracellular transport during lung injury has not been extensively investigated. This study was undertaken to determine whether changes in tight junction claudin expression affect alveolar epithelial barrier properties and to determine the mechanisms of altered expression. In anesthetized mice exposed to ventilator-induced lung injury, claudin-4 was specifically induced among tight junction structural proteins. Real-time PCR showed an eightfold increase in claudin-4 expression in the lung injury model. To examine the role of this protein in barrier regulation, claudin-4 function was inhibited with small interfering RNA (siRNA) and a blocking peptide derived from the binding domain of Clostridium perfringens enterotoxin (CPEBD). Inhibition of claudin-4 decreased transepithelial electrical resistance but did not alter macromolecule permeability in primary rat and human epithelial cells. In mice, CPEBD decreased air space fluid clearance >33% and resulted in pulmonary edema during moderate tidal volume ventilation that did not induce edema in control peptide-treated mice. In vitro phorbol ester induced a ninefold increase in claudin-4 expression that was dependent on PKC activation and the JNK MAPK pathway. These data establish that changes in alveolar epithelial claudin expression influence paracellular transport, alveolar fluid clearance rates, and susceptibility to pulmonary edema. We hypothesize that increased claudin-4 expression early in acute lung injury represents a mechanism to limit pulmonary edema and that the regulation of alveolar epithelial claudin expression may be a novel target for acute lung injury therapy.

scholarly journals A late phase of germ plasm accumulation during Drosophila oogenesis requires Lost and Rumpelstiltskin

Development ◽  
2011 ◽  
Vol 138 (16) ◽  
pp. 3431-3440 ◽  
Author(s):  
Kristina S. Sinsimer ◽  
Roshan A. Jain ◽  
Seema Chatterjee ◽  
Elizabeth R. Gavis
Keyword(s):  
Germ Plasm ◽  
Late Phase ◽  
Drosophila Oogenesis

fringeandNotchspecify polar cell fate duringDrosophilaoogenesis

Development ◽  
2001 ◽  
Vol 128 (12) ◽  
pp. 2243-2253 ◽  
Author(s):  
Muriel Grammont ◽  
Kenneth D. Irvine
Keyword(s):  
Cell Fate ◽  
Null Allele ◽  
Somatic Cells ◽  
Ectopic Expression ◽  
Notch Receptor ◽  
Drosophila Oogenesis ◽  
Early Stages ◽  
Polar Cell ◽  
Hypomorphic Alleles ◽  
Notch Activation

fringe encodes a glycosyltransferase that modulates the ability of the Notch receptor to be activated by its ligands. We describe studies of fringe function during early stages of Drosophila oogenesis. Animals mutant for hypomorphic alleles of fringe contain follicles with an incorrect number of germline cells, which are separated by abnormally long and disorganized stalks. Analysis of clones of somatic cells mutant for a null allele of fringe localizes the requirement for fringe in follicle formation to the polar cells, and demonstrates that fringe is required for polar cell fate. Clones of cells mutant for Notch also lack polar cells and the requirement for Notch in follicle formation appears to map to the polar cells. Ectopic expression of fringe or of an activated form of Notch can generate an extra polar cell. Our results indicate that fringe plays a key role in positioning Notch activation during early oogenesis, and establish a function for the polar cells in separating germline cysts into individual follicles.

scholarly journals Corrigendum to “JAK/STAT signaling prevents excessive apoptosis to ensure maintenance of the interfollicular stalk critical for Drosophila oogenesis” [Dev. Biol. 438 (2018) 1–9]

2018 ◽  
Vol 444 (1) ◽  
pp. 41
Author(s):  
Antoine Borensztejn ◽  
Alexandra Mascaro ◽  
Kristi A. Wharton
Keyword(s):  
Drosophila Oogenesis ◽  
Stat Signaling

scholarly journals Extracellular spreading of Wingless is required for Drosophila oogenesis

PLoS Genetics ◽  
2021 ◽  
Vol 17 (4) ◽  
pp. e1009469
Author(s):  
Xiaoxi Wang ◽  
Kimberly S. LaFever ◽  
Indrayani Waghmare ◽  
Andrea Page-McCaw
Keyword(s):  
Stem Cells ◽  
Wnt Signaling ◽  
Long Range ◽  
Wing Disc ◽  
Secreted Protein ◽  
Loss Of Function ◽  
Drosophila Oogenesis ◽  
Central Source ◽  
Follicle Stem Cells

Recent studies have investigated whether the Wnt family of extracellular ligands can signal at long range, spreading from their source and acting as morphogens, or whether they signal only in a juxtacrine manner to neighboring cells. The original evidence for long-range Wnt signaling arose from studies of Wg, a Drosophila Wnt protein, which patterns the wing disc over several cell diameters from a central source of Wg ligand. However, the requirement of long-range Wg for patterning was called into question when it was reported that replacing the secreted protein Wg with a membrane-tethered version, NRT-Wg, results in flies with normally patterned wings. We and others previously reported that Wg spreads in the ovary about 50 μm or 5 cell diameters, from the cap cells to the follicle stem cells (FSCs) and that Wg stimulates FSC proliferation. We used the NRT-wg flies to analyze the consequence of tethering Wg to the cap cells. NRT-wg homozygous flies are sickly, but we found that hemizygous NRT-wg/null flies, carrying only one copy of tethered Wingless, were significantly healthier. Despite their overall improved health, these hemizygous flies displayed dramatic reductions in fertility and in FSC proliferation. Further, FSC proliferation was nearly undetectable when the wg locus was converted to NRT-wg only in adults, and the resulting germarium phenotype was consistent with a previously reported wg loss-of-function phenotype. We conclude that Wg protein spreads from its source cells in the germarium to promote FSC proliferation.

scholarly journals A two-step Notch-dependant mechanism controls the selection of the polar cell pair in Drosophila oogenesis

Development ◽  
2010 ◽  
Vol 137 (16) ◽  
pp. 2703-2711 ◽  
Author(s):  
C. Vachias ◽  
J.-L. Couderc ◽  
M. Grammont
Keyword(s):  
Drosophila Oogenesis ◽  
Cell Pair ◽  
Polar Cell ◽  
Selection Of

Drosophila Oogenesis

2015 ◽  
Keyword(s):  
Drosophila Oogenesis
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