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MICAL, the Flavoenzyme Participating in Cytoskeleton Dynamics  [PDF]
Maria A. Vanoni,Teresa Vitali,Daniela Zucchini
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms14046920
Abstract: MICAL (from the Molecule Interacting with CasL) indicates a family of recently discovered cytosolic, multidomain proteins, which uniquely couple an N-terminal FAD-containing monooxygenase-like domain to typical calponine homology, LIM and coiled-coil protein-interaction modules. Genetic and cell biology approaches have demonstrated an essential role of the catalytic activity of the monooxygenase-like domain in transducing the signal initiated by semaphorins interaction with their plexin receptors, which results in local actin cytoskeleton disassembly as part of fundamental processes that include differentiation, migration and cell-cell contacts in neuronal and non-neuronal cell types. This review focuses on the structure-function relations of the MICAL monooxygenase-like domain as they are emerging from the available in vitro studies on mouse, human and Drosophila MICAL forms that demonstrated a NADPH-dependent actin depolymerizing activity of MICAL. With Drosophila MICAL forms, actin depolymerization was demonstrated to be associated to conversion of Met44 to methionine sulfone through a postulated hydroxylating reaction. Arguments supporting the concept that MICAL effect on F-actin may be reversible will be discussed.
EHD1 Functions in Endosomal Recycling and Confers Salt Tolerance  [PDF]
Maya Bar, Meirav Leibman, Silvia Schuster, Hilla Pitzhadza, Adi Avni
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0054533
Abstract: Endocytosis is a crucial process in all eukaryotic organisms including plants. We have previously shown that two Arabidopsis proteins, AtEHD1 and AtEHD2, are involved in endocytosis in plant systems. Knock-down of EHD1 was shown to have a delayed recycling phenotype in mammalians. There are many works in mammalian systems detailing the importance of the various domains in EHDs but, to date, the domains of plant EHD1 that are required for its activity have not been characterized. In this work we demonstrate that knock-down of EHD1 causes a delayed recycling phenotype and reduces Brefeldin A sensitivity in Arabidopsis seedlings. The EH domain of EHD1 was found to be crucial for the localization of EHD1 to endosomal structures. Mutant EHD1 lacking the EH domain did not localize to endosomal structures and showed a phenotype similar to that of EHD1 knock-down seedlings. Mutants lacking the coiled-coil domain, however, showed a phenotype similar to wild-type or EHD1 overexpression seedlings. Salinity stress is a major problem in current agriculture. Microarray data demonstrated that salinity stress enhances the expression of EHD1, and this was confirmed by semi quantitative RT-PCR. We demonstrate herein that transgenic plants over expressing EHD1 possess enhanced tolerance to salt stress, a property which also requires an intact EH domain.
Budding and vesiculation induced by conical membrane inclusions  [PDF]
Thorsten Auth,Gerhard Gompper
Physics , 2009, DOI: 10.1103/PhysRevE.80.031901
Abstract: Conical inclusions in a lipid bilayer generate an overall spontaneous curvature of the membrane that depends on concentration and geometry of the inclusions. Examples are integral and attached membrane proteins, viruses, and lipid domains. We propose an analytical model to study budding and vesiculation of the lipid bilayer membrane, which is based on the membrane bending energy and the translational entropy of the inclusions. If the inclusions are placed on a membrane with similar curvature radius, their repulsive membrane-mediated interaction is screened. Therefore, for high inclusion density the inclusions aggregate, induce bud formation, and finally vesiculation. Already with the bending energy alone our model allows the prediction of bud radii. However, in case the inclusions induce a single large vesicle to split into two smaller vesicles, bending energy alone predicts that the smaller vesicles have different sizes whereas the translational entropy favors the formation of equal-sized vesicles. Our results agree well with those of recent computer simulations.
Important relationships between Rab and MICAL proteins in endocytic trafficking  [cached]
Juliati Rahajeng,Sai Srinivas Panapakkam Giridharan,Bishuang Cai,Naava Naslavsky
World Journal of Biological Chemistry , 2010,
Abstract: The internalization of essential nutrients, lipids and receptors is a crucial process for all eukaryotic cells. Accordingly, endocytosis is highly conserved across cell types and species. Once internalized, small cargo-containing vesicles fuse with early endosomes (also known as sorting endosomes), where they undergo segregation to distinct membrane regions and are sorted and transported on through the endocytic pathway. Although the mechanisms that regulate this sorting are still poorly understood, some receptors are directed to late endosomes and lysosomes for degradation, whereas other receptors are recycled back to the plasma membrane; either directly or through recycling endosomes. The Rab family of small GTP-binding proteins plays crucial roles in regulating these trafficking pathways. Rabs cycle from inactive GDP-bound cytoplasmic proteins to active GTP-bound membrane-associated proteins, as a consequence of the activity of multiple specific GTPase-activating proteins (GAPs) and GTP exchange factors (GEFs). Once bound to GTP, Rabs interact with a multitude of effector proteins that carry out Rab-specific functions. Recent studies have shown that some of these effectors are also interaction partners for the C-terminal Eps15 homology (EHD) proteins, which are also intimately involved in endocytic regulation. A particularly interesting example of common Rab-EHD interaction partners is the MICAL-like protein, MICAL-L1. MICAL-L1 and its homolog, MICAL-L2, belong to the larger MICAL family of proteins, and both have been directly implicated in regulating endocytic recycling of cell surface receptors and junctional proteins, as well as controlling cytoskeletal rearrangement and neurite outgrowth. In this review, we summarize the functional roles of MICAL and Rab proteins, and focus on the significance of their interactions and the implications for endocytic transport.
The endocytic recycling regulator EHD1 is essential for spermatogenesis and male fertility in mice
Mark A Rainey, Manju George, GuoGuang Ying, Reiko Akakura, Daniel J Burgess, Ed Siefker, Tom Bargar, Lynn Doglio, Susan E Crawford, Gordon L Todd, Venkatesh Govindarajan, Rex A Hess, Vimla Band, Mayumi Naramura, Hamid Band
BMC Developmental Biology , 2010, DOI: 10.1186/1471-213x-10-37
Abstract: Both male and female Ehd1-/- mice survived at sub-Mendelian ratios. A proportion of Ehd1-/- mice were viable and showed smaller size at birth, which continued into adulthood. Ehd1-/- adult males were infertile and displayed decreased testis size, whereas Ehd1-/- females were fertile. In situ hybridization and immunohistochemistry of developing wildtype mouse testes revealed EHD1 expression in most cells of the seminiferous epithelia. Histopathology revealed abnormal spermatogenesis in the seminiferous tubules and the absence of mature spermatozoa in the epididymides of Ehd1-/- males. Seminiferous tubules showed disruption of the normal spermatogenic cycle with abnormal acrosomal development on round spermatids, clumping of acrosomes, misaligned spermatids and the absence of normal elongated spermatids in Ehd1-/- males. Light and electron microscopy analyses indicated that elongated spermatids were abnormally phagocytosed by Sertoli cells in Ehd1-/- mice.Contrary to a previous report, these results demonstrate an important role for EHD1 in pre- and post-natal development with a specific role in spermatogenesis.The C-terminal Eps15 homology domain-containing (EHD) proteins regulate endocytic recycling of membrane and associated cell surface receptors [1]. The founding EHD family member, the single C. elegans ortholog RME-1 (Receptor-Mediated Endocytosis-1), was identified in a screen for mutants defective in yolk protein endocytosis, and is required for yolk receptor and basolateral fluid recycling in the worm [2]. Mutations of the single Drosophila EHD protein ortholog Past1 decreased fertility and germline development in the fly [3]. Mammals express four highly homologous EHD proteins (EHD1-4) each containing an N-terminal ATPase domain [4,5], a central coiled-coil region that facilitates homo- and hetero-oligomerization [6-8], and a single C-terminal Eps15 homology (EH) domain that mediates interactions with proteins containing Asn-Pro-Phe motifs [9,10]. Ectopic ex
Impact vesiculation – a new trigger for volcanic bubble growth and degassing  [PDF]
D. A. Rothery,J. M. Sumner,O. Spieler,D. B. Dingwell
eEarth Discussions , 2007,
Abstract: We highlight a potentially important trigger for bubble growth and degassing in volcanic bombs. We have successfully triggered bubble growth in previously unvesiculated samples of silicate melt during experiments to simulate volcanic bomb impact, by firing pellets at, and dropping weights onto, melt samples. We call this phenomenon "impact vesiculation". Further work is required on real volcanic bombs to establish the extent to which impact vesiculation occurs in nature. However, our experiments are sufficient to demonstrate that impact vesiculation is a viable processes and should be borne in mind in analysis of bubble populations and degassing histories of bombs and spatter-fed lava flows. Degassing caused by impact vesiculation can occur only at ground-level, so any attempt to calculate the amount of erupted gas available for transport high into the atmosphere by convection above the source of a fountain-fed lava flow that is based on subtracting the volatile content of fluid inclusions from the volatile content of the resulting lava flow would be an overestimate if significant impact vesiculation has occurred.
Allelic expression analysis of the osteoarthritis susceptibility locus that maps to MICAL3
Madhushika Ratnayake, Louise N Reynard, Emma VA Raine, Mauro Santibanez-Koref, John Loughlin
BMC Medical Genetics , 2012, DOI: 10.1186/1471-2350-13-12
Abstract: We used total and allelic expression analysis to assess whether the OA association to rs2277831 is mediated by an influence on MICAL3, BCL2L13 or BID expression. Using RNA extracted from joint tissues of 60 patients who had undergone elective joint replacement surgery, we assessed whether rs2277831 correlated with allelic expression of either of the three genes by: 1) measuring the expression of each gene by quantitative PCR and then stratifying the data by genotype at rs2277831 and 2) accurately discriminating and quantifying the mRNA synthesised from the alleles of OA patients using allelic-quantitative PCR.We found no evidence for a correlation between gene expression and genotype at rs2277831, with P-values of 0.09 for BCL2L13, 0.07 for BID and 0.33 for MICAL3. In the allelic expression analysis we observed several examples of significant (p < 0.05) allelic imbalances, with an allelic expression ratio of 2.82 observed in BCL2L13 (P = 0.004), 2.09 at BID (P = 0.001) and the most extreme case being at MICAL3, with an allelic expression ratio of 5.47 (P = 0.001). However, there was no correlation observed between the pattern of allelic expression and the genotype at rs2277831.In the tissues that we have studied, our data do not support our hypothesis that the association between rs2277831 and OA is due to the effect this SNP has on MICAL3, BCL2L13 or BID gene expression. Instead, our data point towards other functional effects accounting for the OA associated signal.Osteoarthritis (OA) is a common disease of the synovial joint characterized by cartilage loss and is often accompanied by alteration in the normal function of other tissues of the articulating joint [1]. Based on epidemiological studies, the disease is known to have a major genetic component, although elucidating this has proven challenging [2]. This is a reflection of the heterogeneity associated with the disease, with severe OA being a clinical end-point reached from a multitude of starting points. Ge
Margaretha Stéen; Elaphystrongylosis. A clinical, pathological and taxono-mical study with special emphasis on the infection in moose
Sven Skjenneberg (ed.)
Rangifer , 1992,
Abstract: Margareta Steen defended her PhD thesis Elaphystrongylosis. A clinical, pathological and taxono-mical study with special emphasis on the infection in moose at the Swedish University of Agriculture, Uppsala, Sweden on December 13, 1991.
Vesiculation of biological membrane driven by curvature induced frustrations in membrane orientational ordering  [cached]
Jesenek D,Perutková S,Gó?d? W,Kralj-Igli? V
International Journal of Nanomedicine , 2013,
Abstract: Dalija Jesenek,1 arká Perutková,2 Wojciech Gó d ,3 Veronika Kralj-Igli ,4 Ale Igli ,2,5 Samo Kralj1,61Condensed Matter Physics Department, Jo ef Stefan Institute, Ljubljana, Slovenia; 2Laboratory of Biophysics, Faculty of Electrical Engineering, University of Ljubljana, Ljubljana, Slovenia; 3Department of Complex Systems and Chemical Processing of Information, Institute of Physical Chemistry, Polish Academy of Sciences, Warsaw, Poland; 4Laboratory of Clinical Biophysics, Faculty of Health Studies, University of Ljubljana, Ljubljana, Slovenia; 5Laboratory of Clinical Biophysics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia; 6Department of Physics, Faculty of Natural Sciences and Mathematics, University of Maribor, Maribor, SloveniaAbstract: Membrane budding often leads to the formation and release of microvesicles. The latter might play an important role in long distance cell-to-cell communication, owing to their ability to move with body fluids. Several mechanisms exist which might trigger the pinching off of globular buds from the parent membrane (vesiculation). In this paper, we consider the theoretical impacts of topological defects (frustrations) on this process in the membranes that exhibit global in-plane orientational order. A Landau–de Gennes theoretical approach is used in terms of tensor orientational order parameters. The impact of membrane shapes on position and the number of defects is analyzed. In studied cases, only defects with winding numbers m = ±1/2 appear, where we refer to the number of defects with m = 1/2 as defects, and with m = –1/2 as anti-defects. It is demonstrated that defects are attracted to regions with maximal positive Gaussian curvature, K. On the contrary, anti-defects are attracted to membrane regions exhibiting minimal negative values of K. We show on membrane structures exhibiting spherical topology that the coexistence of regions with K > 0 and K < 0 might trigger formation of defect–anti-defect pairs for strong enough local membrane curvatures. Critical conditions for triggering pairs are determined in several demonstrative cases. Then the additionally appeared anti-defects are assembled at the membrane neck, where K < 0. Consequent strong local fluctuations of membrane constituent anisotropic molecules might trigger membrane fission neck rupture, enabling a membrane fission process and the release of membrane daughter microvesicles (ie, vesiculation).Keywords: structural transitions, topological defects, membrane microvesicles, membrane curvature, membrane fission, vesiculation
Enhancement of Cell Membrane Invaginations, Vesiculation and Uptake of Macromolecules by Protonation of the Cell Surface  [PDF]
Nadav Ben-Dov, Rafi Korenstein
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035204
Abstract: The different pathways of endocytosis share an initial step involving local inward curvature of the cell’s lipid bilayer. It has been shown that to generate membrane curvature, proteins or lipids enforce transversal asymmetry of the plasma membrane. Thus it emerges as a general phenomenon that transversal membrane asymmetry is the common required element for the formation of membrane curvature. The present study demonstrates that elevating proton concentration at the cell surface stimulates the formation of membrane invaginations and vesiculation accompanied by efficient uptake of macromolecules (Dextran-FITC, 70 kD), relative to the constitutive one. The insensitivity of proton induced uptake to inhibiting treatments and agents of the known endocytic pathways suggests the entry of macromolecules to proceeds via a yet undefined route. This is in line with the fact that neither ATP depletion, nor the lowering of temperature, abolishes the uptake process. In addition, fusion mechanism such as associated with low pH uptake of toxins and viral proteins can be disregarded by employing the polysaccharide dextran as the uptake molecule. The proton induced uptake increases linearly in the extracellular pH range of 6.5 to 4.5, and possesses a steep increase at the range of 4> pH>3, reaching a plateau at pH≤3. The kinetics of the uptake implies that the induced vesicles release their content to the cytosol and undergo rapid recycling to the plasma membrane. We suggest that protonation of the cell’s surface induces local charge asymmetries across the cell membrane bilayer, inducing inward curvature of the cell membrane and consequent vesiculation and uptake.
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