Decrease in Cryptosporidium parvum Oocyst Infectivity In Vitro by Using the Membrane Filter Dissolution Method for Recovering Oocysts from Water Samples

Exposure of Cryptosporidium parvum oocysts to solutions used for cellulose acetate membrane (CAM) dissolution filtration reduced their infectivity in HCT-8 cells. Ethanol (95% [vol/vol] and 70% [vol/vol]) alone and short exposure times to acetone decreased infectivity. These findings contrast with similar experiments using excystation assays and infectivity in mice.     

Route of Passive Ion Permeation in Epithelia

“Tight junctions” between cells in some epithelia actually provide the main route of passive ion permeation. The degree of junctional tightness may underlie important functional differences between different epithelia.     

Surface-bound Immunoglobulin as a Marker of B Lymphocytes in Man

IMMUNOLOGICAL reactions in many species depend on two functionally different types of small lymphocytes, thymus-derived T lymphocytes and bone marrow-derived B lymphocytes¹. In the mouse, the θ antigen is a marker for T lymphocytes, while membrane-bound Ig is found on θ-negative lymphocytes². This has raised the question whether the presence of surface-bound Ig³ may be regarded as a marker for B lymphocytes. We have obtained data indicating that this is the case with human lymphocytes.     

A re-evaluation of the phylogeny of Parelaphostrongylus Boev & Schulz, 1950 (Nematoda: Protostrongylidae)

The phylogeny of the genus Parelaphostrongylus was reconstructed using Elaphostrongylus rangiferi as an outgroup. Parelaphostrongylus is monophyletic and divided into two clades, one containing the meningeal worm, P. tenuis of white-tailed deer, and the other consisting of two muscle-inhabiting forms, P. andersoni and P. odocoilei of white-tailed and mule deer, respectively. Differences in biological features, including tissue migration route and prepatent period, are mapped onto the cladogram and discussed. Phylogenetic relationships among the host group, the Cervidae, are reviewed. It is suggested that E. rangiferi evolved in a Palaearctic cervid. Parelaphostrongylus probably co-speciated with Nearctic deer, Odocoileus spp. Host-switching from O. virginianus may explain the widespread occurrence of P. andersoni in Rangifer in North America.     

Evolution of ontogenetic allometry shaping giant species: a case study from the damselfish genus Dascyllus (Pomacentridae)

The evolution of body size, the paired phenomena of giantism and dwarfism, has long been studied by biologists and paleontologists. However, detailed investigations devoted to the study of the evolution of ontogenetic patterns shaping giant species are scarce. The damselfishes of the genus Dascyllus appear as an excellent model for such a study. Their well understood phylogeny reveals that large‐bodied species have evolved in two different clades. Geometric morphometric methods were used to compare the ontogenetic trajectories of the neurocranium and the mandible in both small‐bodied (Dascyllus aruanus and Dascyllus carneus; maximum size: 50–65 mm standard length) and giant (Dascyllus trimaculatus and Dascyllus flavicaudus; maximum size: 90–110 mm standard length) Dascyllus species. At their respective maximum body size, the neurocranium of the giant species is significantly shorter and have a higher supraoccipital crest relative to the small‐bodied species, whereas mandible shape variation is more limited and is not related to the ‘giant’ trait. The hypothesis of ontogenetic scaling whereby the giant species evolved by extending the allometric trajectory of the small‐bodied ones (i.e. hypermorphosis) is rejected. Instead, the allometric trajectories vary among species by lateral transpositions. The rate of shape changes and the type of lateral transposition also differ according to the skeletal unit among Dascyllus species. Differences seen between the two giant species in the present study demonstrate that giant species may appear by varied alterations of the ancestor allometric pattern. © 2010 The Linnean Society of London, Biological Journal of the Linnean Society, 2010, 99 , 99–117.     

Description of Babesia duncani n.sp. (Apicomplexa: Babesiidae) from humans and its differentiation from other piroplasms

The morphologic, ultrastructural and genotypic characteristics of Babesia duncani n.sp. are described based on the characterization of two isolates (WA1, CA5) obtained from infected human patients in Washington and California. The intraerythrocytic stages of the parasite are morphologically indistinguishable from Babesia microti, which is the most commonly identified cause of human babesiosis in the USA. Intraerythrocytic trophozoites of B. duncani n.sp. are round to oval, with some piriform, ring and ameboid forms. Division occurs by intraerythrocytic schizogony, which results in the formation of merozoites in tetrads (syn. Maltese cross or quadruplet forms). The ultrastructural features of trophozoites and merozoites are similar to those described for B. microti and Theileria spp. However, intralymphocytic schizont stages characteristic of Theileria spp. have not been observed in infected humans. In phylogenetic analyses based on sequence data for the complete18S ribosomal RNA gene, B. duncani n.sp. lies in a distinct clade that includes isolates from humans, dogs and wildlife in the western United States but separate from Babesia sensu stricto, Theileria spp. and B. microti. ITS2 sequence analysis of the B. duncani n.sp. isolates (WA1, CA5) show that they are phylogenetically indistinguishable from each other and from two other human B. duncani-type parasites (CA6, WA2 clone1) but distinct from other Babesia and Theileria species sequenced. This analysis provides robust molecular support that the B. duncani n.sp. isolates are monophyletic and the same species. The morphologic characteristics together with the phylogenetic analysis of two genetic loci support the assertion that B. duncani n.sp. is a distinct species from other known Babesia spp. for which morphologic and sequence information are available.     

The actin-binding ERM protein Moesin binds to and stabilizes microtubules at the cell cortex

Ezrin, Radixin, and Moesin (ERM) proteins play important roles in many cellular processes including cell division. Recent studies have highlighted the implications of their metastatic potential in cancers. ERM’s role in these processes is largely attributed to their ability to link actin filaments to the plasma membrane. In this paper, we show that the ERM protein Moesin directly binds to microtubules in vitro and stabilizes microtubules at the cell cortex in vivo. We identified two evolutionarily conserved residues in the FERM (4.1 protein and ERM) domains of ERMs that mediated the association with microtubules. This ERM–microtubule interaction was required for regulating spindle organization in metaphase and cell shape transformation after anaphase onset but was dispensable for bridging actin filaments to the metaphase cortex. These findings provide a molecular framework for understanding the complex functional interplay between the microtubule and actin cytoskeletons mediated by ERM proteins in mitosis and have broad implications in both physiological and pathological processes that require ERMs.     

Molecular networks linked by Moesin drive remodeling of the cell cortex during mitosis

The cortical mechanisms that drive the series of mitotic cell shape transformations remain elusive. In this paper, we identify two novel networks that collectively control the dynamic reorganization of the mitotic cortex. We demonstrate that Moesin, an actin/membrane linker, integrates these two networks to synergize the cortical forces that drive mitotic cell shape transformations. We find that the Pp1-87B phosphatase restricts high Moesin activity to early mitosis and down-regulates Moesin at the polar cortex, after anaphase onset. Overactivation of Moesin at the polar cortex impairs cell elongation and thus cytokinesis, whereas a transient recruitment of Moesin is required to retract polar blebs that allow cortical relaxation and dissipation of intracellular pressure. This fine balance of Moesin activity is further adjusted by Skittles and Pten, two enzymes that locally produce phosphoinositol 4,5-bisphosphate and thereby, regulate Moesin cortical association. These complementary pathways provide a spatiotemporal framework to explain how the cell cortex is remodeled throughout cell division.     

Moesin and its activating kinase Slik are required for cortical stability and microtubule organization in mitotic cells

Cell division requires cell shape changes involving the localized reorganization of cortical actin, which must be tightly linked with chromosome segregation operated by the mitotic spindle. How this multistep process is coordinated remains poorly understood. In this study, we show that the actin/membrane linker moesin, the single ERM (ezrin, radixin, and moesin) protein in Drosophila melanogaster, is required to maintain cortical stability during mitosis. Mitosis onset is characterized by a burst of moesin activation mediated by a Slik kinase-dependent phosphorylation. Activated moesin homogenously localizes at the cortex in prometaphase and is progressively restricted at the equator in later stages. Lack of moesin or inhibition of its activation destabilized the cortex throughout mitosis, resulting in severe cortical deformations and abnormal distribution of actomyosin regulators. Inhibiting moesin activation also impaired microtubule organization and precluded stable positioning of the mitotic spindle. We propose that the spatiotemporal control of moesin activation at the mitotic cortex provides localized cues to coordinate cortical contractility and microtubule interactions during cell division.