Whitening,thallus decay and fragmentation in Gracilaria chilensis associated with an endophytic amoeba

Whitening of Gracilaria chilensis, accompanied by tissue softening and thallus fragmentation, was found to be associated with the presence of an endophytic amoeba. Although the symptoms developed originally in green mutant thalli, subsequent infections in the laboratory also affected normal, wild-type G. chilensis. Ultrastructural evidence indicates that the amoebae perforate the host cell walls of both cortical and medullary cells and digest their protoplasm. Feeding by the amoeba appears to involve both phagocytosis and enzymatic digestion of the host tissue. Destruction of the host tissue resulted in large cavities first, followed by thallus fragmentation. No other organism was found during the early stages of thallus invasion by the amoeba, although bacteria may appear once the amoeba reaches the inner tissues of the host.     

Chondrodysplasias due to proteoglycan defects

The proteoglycans, especially the large chondroitin sulfate proteoglycan aggrecan, have long been viewed as important components of the extracellular matrix of cartilage. The drastic change in expression during differentiation from mesenchyme to cartilage, the loss of tissue integrity associated with proteoglycan degradation in several disease processes and, most important, the demonstration of abnormalities in proteoglycan production concomitant with the aberrant growth patterns exhibited by the brachymorphic mouse, the cartilage matrix deficient mouse, and the nanomelic chick provide the strongest evidence that the proteoglycan aggrecan is essential during differentiation and for maintenance of the skeletal elements. More recently, mutations associated with proteoglycans other than aggrecan, especially the heparan sulfate proteoglycans, glypican and perlecan, suggest an important role for these molecules in skeletal development as well. This review focuses on the molecular bases of the hereditary proteoglycan defects in animal models, as well as of some human chondrodysplasias, that collectively are providing a better understanding of the role of proteoglycans in the development and maintenance of the skeletal elements.     

Temperature-dependent sex determination in reptiles: Proximate mechanisms,ultimate outcomes,and practical applications

In many egg-laying reptiles, the incubation temperature of the egg determines the sex of the offspring, a process known as temperature-dependent sex determination (TSD). In TSD sex determination is an “all or none” process and intersexes are rarely formed. How is the external signal of temperature transduced into a genetic signal that determines gonadal sex and channels sexual development? Studies with the red-eared slider turtle have focused on the physiological, biochemical, and molecular cascades initiated by the temperature signal. Both male and female development are active processes—rather than the crganized/default system characteristic of vertebrates with genotypic sex determination—that require simultaneous activation and suppression of testis- and ovary-determining cascades for normal sex determination. It appears that temperature accomplishes this end by acting on genes encoaing for steroidogenic enzymes and steroid hormone receptors and modifying the endocrine microenvironment in the embryo. The temperature experienced in development also has long-term functional outcomes in addition to sex determination. Research with the leopard gecko indicates that incubation temperature as well as steroid hormones serve as organizers in shaping the adult phenotype, with temperature modulating sex hormone action in sexual differentiation. Finally, practical applications of this research have emerged for the conservation and restoration of endangered egg-laying reptiles as well as the embryonic development of reptiles as biomarkers to monitor the estrogenic effects of common environmental contaminants. © 1994 Wiley-Liss, Inc.     

Evolution of post-weaning skull ontogeny in New World opossums (Didelphidae)

Quantification of mammalian skull development has received much attention in the recent literature. Previous results in different lineages have shown an effect of historical legacy on patterns of skull growth. In marsupials, the skull of adults exhibits high variation across species, principally along a size axis. The development keys of the marsupial skull are fundamental to understanding the evolution of skull function in this clade. Its generally well-resolved phylogeny makes the group ideal for studying macroevolution of skull ontogeny. Here, we tested the hypothesis that ontogenetic similarity is correlated with phylogeny in New World marsupials, so that developmental patterns are expected to be conserved from ancestral opossums. We concatenated our previously published ontogenetic cranial data from several opossum species with new ontogenetic sequences and constructed an allometric space on the basis of a set of comparable cranial linear measurements. In this ontogenetic space, we determined the degree of correspondence of developmental patterns and the phylogeny of the group. In addition, we mapped ontogenetic trajectories onto the opossum phylogeny, treating the trajectories as composite, continuously varying characters. Didelphids differed widely in the magnitude of skull allometry across species. Splanchnocranial components exhibited all possible patterns of inter-specific variation, whereas mandibular variables were predominantly allometrically “positive” and neurocranial components were predominantly allometrically “negative.” The distribution of species in allometric space reflected the compounded effect of phylogeny and size variation characteristic of didelphids. The terminal morphology of related species differed in shape, so their ontogenetic trajectories deviated with respect to that of reconstructed common ancestors in varying degree. Phylogeny was the main factor structuring the allometric space of New World marsupials. Didelphids inherited an ancestral constellation of allometry coefficients without change and retained much of it throughout their lineage history. Conserved allometric values on the nodes splitting placental outgroups and marsupials suggest a developmental basis common to all therians.     

Cranial ontogeny of<Emphasis Type="Italic">Lutreolina crassicaudata</Emphasis> (Didelphidae): a comparison with<Emphasis Type="Italic">Didelphis albiventris</Emphasis>

Metatherians experience the greatest developmental changes during extrauterine life. Following previous studies onDidelphis albiventris Lund, 1840, we examined the postweaning cranial allometry of size of the Neotropical marsupialLutreolina crassicaudata (Desmerest, 1804). Our aim was to compare growth patterns of both species to identify traits particular to each species and traits common to both species. This may contribute toward identifying a common developmental plan for didelphids. We measured 15 cranial variables in 32–43 specimens from just-weaned young to old adult. Total length of the skull was the estimator of overall size in least squares and reduced major axis regressions. The skull ofLutreolina crassicaudata grows at a rate slower than the overall change in size in its neurocranial components, palate, and postcanine rows, and it grows relatively faster in the rest of the splanchnocranium. This pattern closely resembles that ofDidelphis albiventris, from which it differs mainly in the allometry of the muzzle. In both species, allometry explains most postweaning changes of the trophic apparatus on functional grounds, in relation to interspecific differences in diet. We hypothesize that most local allometric departures from a generalized didelphid plan would relate to main dietary trends.     

The Actin Filament-Binding Protein Coronin Regulates Motility in Plasmodium Sporozoites

Parasites causing malaria need to migrate in order to penetrate tissue barriers and enter host cells. Here we show that the actin filament-binding protein coronin regulates gliding motility in Plasmodium berghei sporozoites, the highly motile forms of a rodent malaria-causing parasite transmitted by mosquitoes. Parasites lacking coronin show motility defects that impair colonization of the mosquito salivary glands but not migration in the skin, yet result in decreased transmission efficiency. In non-motile sporozoites low calcium concentrations mediate actin-independent coronin localization to the periphery. Engagement of extracellular ligands triggers an intracellular calcium release followed by the actin-dependent relocalization of coronin to the rear and initiation of motility. Mutational analysis and imaging suggest that coronin organizes actin filaments for productive motility. Using coronin-mCherry as a marker for the presence of actin filaments we found that protein kinase A contributes to actin filament disassembly. We finally speculate that calcium and cAMP-mediated signaling regulate a switch from rapid parasite motility to host cell invasion by differentially influencing actin dynamics.