Zeta potential in ceramic industry

Deflocculation, electrical conductivity and zeta potential (ZP) are studied for the addition of 0 to 10000 ppm Na2SiO3 deflocculator to slips obtained from three argillaceous materials (kaolin d'Arvor, ball clay Hyplas 64, and/or Granger Clay No. 10). The quantity of Na2SO3 required to deflocculate a slip is independent of the density but differes for each clay. The ZP is directly related to the density of the slip. The higher the ZP the more stable a slip is; the value of the ZP of a mixture does not follow a simple law but the electrical resistance of a mixture does follow a simple additive law. The ZP appears to have linear relation with the specific surface of the argillaceous material

Cell adhesion and cortex contractility determine cell patterning in the Drosophila retina

Hayashi and Carthew (Nature 431 [2004], 647) have shown that the packing of cone cells in the Drosophila retina resembles soap bubble packing, and that changing E- and N-cadherin expression can change this packing, as well as cell shape. The analogy with bubbles suggests that cell packing is driven by surface minimization. We find that this assumption is insufficient to model the experimentally observed shapes and packing of the cells based on their cadherin expression. We then consider a model in which adhesion leads to a surface increase, balanced by cell cortex contraction. Using the experimentally observed distributions of E- and N-cadherin, we simulate the packing and cell shapes in the wildtype eye. Furthermore, by changing only the corresponding parameters, this model can describe the mutants with different numbers of cells, or changes in cadherin expression.Comment: revised manuscript; 8 pages, 6 figures; supplementary information not include

Trafficking through Rab11 Endosomes Is Required for Cellularization during Drosophila Embryogenesis

AbstractBackground: Embryonic cleavage leads to the formation of an epithelial layer during development. In Drosophila, the process is specialized and called cellularization. The trafficking pathways that underlie this process and that are responsible for the mobilization of membrane pools, however, remain poorly understood.Results: We provide functional evidence for the role of endocytic trafficking through Rab11 endosomes in remobilizing vesicular membrane pools to ensure lateral membrane growth. Part of the membrane stems from endocytosed apical material. Mutants in the endocytic regulators rab5 and shibire/dynamin inhibit basal-lateral membrane growth, and apical endocytosis is blocked in shibire mutants. In addition, shibire controls vesicular trafficking through Rab11-positive endosomes. In shibire mutants, the transmembrane protein Neurotactin follows the secretory pathway normally but is not properly inserted in the plasma membrane and accumulates instead in Rab11 subapical endosomes. Consistent with a direct role of shibire in vesicular trafficking through Rab11 endosomes, Shibire is enriched in this compartment. Moreover, we show by electron microscopy the large accumulation of intracellular coated pits on subapical endocytic structures in shibire mutants. Finally, we show that Rab11 is essential for membrane growth and invagination during cellularization.Conclusion: Together, the data show that endocytic trafficking is required for basal-lateral membrane growth during cellularization. We identify Rab11 endosomes as key trafficking intermediates that control vesicle exocytosis and membrane growth during cellularization. This pathway may be required in other morphogenetic processes characterized by the growth of a membrane domain

Dynamiques du vivant

Enseignement Cours – Mécanique de la morphogenèse : principes fondamentaux Introduction générale Le cours 2017-2018, « Mécanique de la morphogenèse », initie le thème des bases moléculaires, cellulaires et biophysiques des formes tissulaires chez les animaux et les plantes, qui sera poursuivi l’an prochain. En s’inscrivant dans une démarche historique des concepts clés, il rendra compte des avancées scientifiques décisives permettant de comprendre le paradoxe apparent de structures tissulaire..

The Unfolded Protein Response: A Key Player in Zika Virus-Associated Congenital Microcephaly

Zika virus (ZIKV) is a mosquito-borne virus that belongs to the Flaviviridae family, together with dengue, yellow fever, and West Nile viruses. In the wake of its emergence in the French Polynesia and in the Americas, ZIKV has been shown to cause congenital microcephaly. It is the first arbovirus which has been proven to be teratogenic and sexually transmissible. Confronted with this major public health challenge, the scientific and medical communities teamed up to precisely characterize the clinical features of congenital ZIKV syndrome and its underlying pathophysiological mechanisms. This review focuses on the critical impact of the unfolded protein response (UPR) on ZIKV-associated congenital microcephaly. ZIKV infection of cortical neuron progenitors leads to high endoplasmic reticulum (ER) stress. This results in both the stalling of indirect neurogenesis, and UPR-dependent neuronal apoptotic death, and leads to cortical microcephaly. In line with these results, the administration of molecules inhibiting UPR prevents ZIKV-induced cortical microcephaly. The discovery of the link between ZIKV infection and UPR activation has a broader relevance, since this pathway plays a crucial role in many distinct cellular processes and its induction by ZIKV may account for several reported ZIKV-associated defects

A human genome-wide loss-of-function screen identifies effective chikungunya antiviral drugs

Chikungunya virus (CHIKV) is a globally spreading alphavirus against which there is no commercially available vaccine or therapy. Here we use a genome-wide siRNA screen to identify 156 proviral and 41 antiviral host factors affecting CHIKV replication. We analyse the cellular pathways in which human proviral genes are involved and identify druggable targets. Twenty-one small-molecule inhibitors, some of which are FDA approved, targeting six proviral factors or pathways, have high antiviral activity in vitro, with low toxicity. Three identified inhibitors have prophylactic antiviral effects in mouse models of chikungunya infection. Two of them, the calmodulin inhibitor pimozide and the fatty acid synthesis inhibitor TOFA, have a therapeutic effect in vivo when combined. These results demonstrate the value of loss-of-function screening and pathway analysis for the rational identification of small molecules with therapeutic potential and pave the way for the development of new, host-directed, antiviral agents

The <em>Drosophila</em> MAST kinase Drop out is required to initiate membrane compartmentalisation during cellularisation and regulates dynein-based transport

Cellularisation of the Drosophila syncytial blastoderm embryo into the polarised blastoderm epithelium provides an excellent model with which to determine how cortical plasma membrane asymmetry is generated during development. Many components of the molecular machinery driving cellularisation have been identified, but cell signalling events acting at the onset of membrane asymmetry are poorly understood. Here we show that mutations in drop out (dop) disturb the segregation of membrane cortical compartments and the clustering of E-cadherin into basal adherens junctions in early cellularisation. dop is required for normal furrow formation and controls the tight localisation of furrow canal proteins and the formation of F-actin foci at the incipient furrows. We show that dop encodes the single Drosophila homologue of microtubule-associated Ser/Thr (MAST) kinases. dop interacts genetically with components of the dynein/dynactin complex and promotes dynein-dependent transport in the embryo. Loss of dop function reduces phosphorylation of Dynein intermediate chain, suggesting that dop is involved in regulating cytoplasmic dynein activity through direct or indirect mechanisms. These data suggest that Dop impinges upon the initiation of furrow formation through developmental regulation of cytoplasmic dynein