Anton Karabinos et al. (2002) European Worm Meeting "Essential roles for four cytoplasmic intermediate filament proteins in Caenorhabditis elegans development"

Ralf Schnabel, Anton Karabinos, Klaus Weber, Henning Schmidt, Jens Harborth

[European Worm Meeting, 2002]

The structural proteins of the cytoplasmic intermediate filaments (IF) arise in the nematode C. elegans from eight previously reported genes and an additional three genes now identified in the complete genome. Using double stranded RNA interference (RNAi) for all 11 C. elegans genes encoding cytoplasmic IF proteins we observe phenotypes for the five genes A1, A2, A3, B1 and C2. These range from embryonic lethality (B1) and embryonic/larval lethality (A3) to larval lethality (A1 and A2) and to a mild dumpy phenotype of adults (C2). Phenotypes A2 and A3 involve displaced body muscles and paralysis. They probably arise by reduction of hypodermal IF which participate in the transmission of force from the muscle cells to the cuticle. The B1 phenotype has multiple morphogenetic defects while the A1 phenotype arrested at the L1 stage. Thus, at least four IF genes are essential for C. elegans development. Their RNAi phenotypes describe the first lethal defects due to silencing of single IF genes. In contrast to C. elegans no IF genes have been identified in the complete Drosophila genome, posing the question of how Drosophila can compensate for the lack of these proteins which are essential in mammals and C. elegans. We speculate that the lack of IF proteins in Drosophila can be viewed as cytoskeletal alteration in which, for instance, stable microtubules, often arranged as bundles, substitute for cytoplasmic IF.

Morten K. Larsen et al. (2006) European Worm Meeting "MAA-1, A Novel Acyl-CoA Binding Protein Involved in Endosomal Vesicle Transport in C. elegans"

Morten K. Larsen, Simon Tuck, Jens K. Knudsen, Nils J. Faergeman

[European Worm Meeting, 2006]

Morten K. Larsen1, Simon Tuck1, Nils J. Faergeman2 and Jens K. Knudsen2. The formation of transport vesicles during membrane trafficking requires an intricate interplay between many proteins including those coating the vesicles, adaptor proteins that recruit components of the coat, and small GTPases involved in initiation of vesicle formation. In addition to the protein factors, membrane bilayer lipids are increasingly being recognised as molecules participating actively during vesicle formation. For example, formation of transport carriers is promoted by the hydrolysis of acyl-CoA lipid esters in vitro. The mechanisms by which these lipid esters are directed to the appropriate membranes during vesicle biogenesis is not yet understood. Here we present the first study of MAA-1, a novel member of the acyl-CoA-binding protein family. We show that in C. elegans, MAA-1 is membrane associated and localizes to intracellular membrane organelles in several polarised tissues in C. elegans. MAA-1 binds fatty acyl-CoA in vitro and the ability to form high affinity ligand-protein complexes is necessary for function. Lack of maa-1 reduces the rate of endosomal recycling and enhances phenotypes caused by rme-1, an EH domain protein involved in endosomal recycling. Our results are consistent with a role for acyl-CoA and MAA-1 during endosomal recycling in vivo.

Jacques Pecreaux et al. (2006) European Worm Meeting "Mechanical Oscillations during Asymmetric Spindle Positioning Require a Threshold Number of Active Cortical Force Generators"

Jonathon Howard, Frank Julicher, Stephan W. Grill, Anthony A. Hyman, Karsten Kruse, Jens-Christian Roper, Jacques Pecreaux

[European Worm Meeting, 2006]

Jacques Pecreaux1, Jens-Christian Rper2, Karsten Kruse3, Frank Julicher3, Anthony A. Hyman1, Stephan W. Grill, Jonathon Howard1 Background. Asymmetric division of the C. elegans zygote is due to the posterior-directed movement of the mitotic spindle during metaphase and anaphase. During this movement along the anterior-posterior axis, the spindle oscillates transversely. A theoretical analysis indicates that oscillations might occur as a result of the concerted action of many cortical force generators that pull on astral microtubules in a tug-of-war situation. This model predicts a threshold of motor activity below which no oscillations occur. Results: We have tested the existence of a threshold by using RNA interference to gradually reduce the levels of GPR-1 and GPR-2 that are involved in the G-protein-mediated regulation of the force generators. We found an abrupt cessation of oscillations as expected if the activity drops below a threshold. Furthermore, we could account for the complex choreography of the mitotic spindle - the precise temporal coordination of the build-up and die-down of the transverse oscillations with the posterior displacement - by a gradual increase in the processivity of the force generators during metaphase and anaphase. Conclusions: The agreement between our results and modeling suggests that the same motor machinery underlies two different spindle motions in the embryo: the equal and opposite motors on each side of the AP axis drive oscillations whereas the imbalanced motors in the two halves of the embryo drive posterior displacement.