Are macroinvertebrate communities influenced by seagrass structural complexity?

A study was undertaken within a sub-tidal Zostera marina seagrass bed (Devon, U.K.), with the aim of elucidating the relationship between seagrass structural complexity and the size and composition of the associated macroinvertebrate community. Samples of macroinvertebrates were recovered from three designated areas of shoot density. Various physical characteristics were measured for individual plants, and an a priori complexity index was determined relevant to the associated target organisms. Resulting data were analysed using linear regression and multivariate techniques. Significant relationships were found between shoot density and number of leaves/shoot, leaf length, stem length and algal epiphyte biomass. Neither the number of species nor abundance of macroinvertebrates was significantly related with the derived complexity index. Multivariate analysis indicated that macroinvertebrate communities from the three areas of shoot density were significantly different, the pattern of macroinvertebrate community composition being best explained by sea-grass biomass. Linear regression of seagrass biomass with macroinvertebrate number of species and abundance revealed significant positive relationships. Regression also indicated that there was no significant increase in complexity with increasing seagrass biomass. The results suggest that within a seagrass bed the size and composition of the associated macroinvertebrate community is not determined by the structural complexity of the plants, but by the amount of plant available. This finding indicates a simple species-area relationship, and arguably one brought about as a result of a sampling artefact. Thus, the current paradigm that structural complexity of seagrass is responsible for increased species diversity, can only be justifiably applied to comparisons between seagrass and other habitats, and not within a seagrass bed itself.     

Low-amplitude, low-frequency electric field-stimulated bone cell proliferation may in part be mediated by increased IGF-II release.

We have developed an in vitro model incorporating a low-amplitude (10(-7) V/cm), low frequency (f less than 100 Hz), capacitively coupled electric field in order to study the mechanism through which an electric field may increase bone cell proliferation. Utilizing this model we have previously shown that electric field-stimulated bone cell proliferation was dependent on release of mitogen activity into the culture medium from exposed cells. The current studies were intended to characterize this mitogen activity. In these studies we found that electric field-stimulated human bone cell proliferation was associated with increased IGF-II mRNA accumulation and IGF-II secretion suggesting that IGF-II may in part mediate the increase in bone cell proliferation following electric field exposure.     

Siderocalin (Lcn 2) also binds carboxymycobactins, potentially defending against mycobacterial infections through iron sequestration

Siderocalin, a member of the lipocalin family of binding proteins, is found in neutrophil granules, uterine secretions, and at markedly elevated levels in serum and synovium during bacterial infection; it is also secreted from epithelial cells in response to inflammation or tumorigenesis. Identification of high-affinity ligands, bacterial catecholate-type siderophores (such as enterochelin), suggested a possible function for siderocalin: an antibacterial agent, complementing the general antimicrobial innate immune system iron-depletion strategy, sequestering iron as ferric siderophore complexes. Supporting this hypothesis, siderocalin is a potent bacteriostatic agent in vitro under iron-limiting conditions and, when knocked out, renders mice remarkably susceptible to bacterial infection. Here we show that siderocalin also binds soluble siderophores of mycobacteria, including M. tuberculosis: carboxymycobactins. Siderocalin employs a degenerate recognition mechanism to cross react with these dissimilar types of siderophores, broadening the potential utility of this innate immune defense.     

Mutant copper-zinc superoxide dismutase binds to and destabilizes human low molecular weight neurofilament mRNA

The mechanism by which mutated copper-zinc superoxide dismutase (SOD1) causes familial amyotrophic lateral sclerosis is believed to involve an adverse gain of function, independent of the physiological antioxidant enzymatic properties of SOD1. In this study, we have observed that mutant SOD1 (G41S, G85A, and G93A) but not the wild type significantly reduced the stability of the low molecular weight neurofilament mRNA in a dosage-dependent manner. We have also demonstrated that mutant SOD1 but not the wild type bound directly to the neurofilament mRNA 3'-untranslated region and that the binding was necessary to induce mRNA destabilization. These observations provide an explanation for a novel gain of function in which mutant SOD1 expression in motor neurons alters an intermediate filament protein expression.     

Tidal and seasonal effects on survival rates of the endangered California clapper rail: does invasive Spartina facilitate greater survival in a dynamic environment?

Invasive species frequently degrade habitats, disturb ecosystem processes, and can increase the likelihood of extinction of imperiled populations. However, novel or enhanced functions provided by invading species may reduce the impact of processes that limit populations. It is important to recognize how invasive species benefit endangered species to determine overall effects on sensitive ecosystems. For example, since the 1990s, hybrid Spartina (Spartina foliosa × alterniflora) has expanded throughout South San Francisco Bay, USA, supplanting native vegetation and invading mudflats. The endangered California clapper rail (Rallus longirostris obsoletus) uses the tall, dense hybrid Spartina for cover and nesting, but the effects of hybrid Spartina on clapper rail survival was unknown. We estimated survival rates of 108 radio-marked California clapper rails in South San Francisco Bay from January 2007 to March 2010, a period of extensive hybrid Spartina eradication, with Kaplan–Meier product limit estimators. Clapper rail survival patterns were consistent with hybrid Spartina providing increased refuge cover from predators during tidal extremes which flood native vegetation, particularly during the winter when the vegetation senesces. Model averaged annual survival rates within hybrid Spartina dominated marshes before eradication (? = 0.466) were greater than the same marshes posttreatment (? = 0.275) and a marsh dominated by native vegetation (? = 0.272). However, models with and without marsh treatment as explanatory factor for survival rates had nearly equivalent support in the observed data, lending ambiguity as to whether hybrid Spartina facilitated greater survival rates than native marshland. Conservation actions to aid in recovery of this endangered species should recognize the importance of available of high tide refugia, particularly in light of invasive species eradication programs and projections of future sea-level rise.     

A neurotoxic peripherin splice variant in a mouse model of ALS

Peripherin, a neuronal intermediate filament (nIF) protein found associated with pathological aggregates in motor neurons of patients with amyotrophic lateral sclerosis (ALS) and of transgenic mice overexpressing mutant superoxide dismutase-1 (SOD1G37R), induces the selective degeneration of motor neurons when overexpressed in transgenic mice. Mouse peripherin is unique compared with other nIF proteins in that three peripherin isoforms are generated by alternative splicing. Here, the properties of the peripherin splice variants Per 58, Per 56, and Per 61 have been investigated in transfected cell lines, in primary motor neurons, and in transgenic mice overexpressing peripherin or overexpressing SOD1G37R. Of the three isoforms, Per 61 proved to be distinctly neurotoxic, being assembly incompetent and inducing degeneration of motor neurons in culture. Using isoform-specific antibodies, Per 61 expression was detected in motor neurons of SOD1G37R transgenic mice but not of control or peripherin transgenic mice. The Per 61 antibody also selectively labeled motor neurons and axonal spheroids in two cases of familial ALS and immunoprecipitated a higher molecular mass peripherin species from disease tissue. This evidence suggests that expression of neurotoxic splice variants of peripherin may contribute to the neurodegenerative mechanism in ALS.     

Inhibitory insulin-like growth factor-binding protein: cloning, complete sequence, and physiological regulation.

In this study we report the preparation of a human osteosarcoma cell cDNA library and describe the isolation and sequence determination of a clone encoding the complete sequence of a novel human insulin-like growth factor (IGF)-binding protein (hIGFBP-4). Previous work indicated that hIGFBP-4 is the predominant IGFBP expressed by human osteoblast-like cells, and that IGFBP-4 binds and inhibits the mitogenic activities of IGF-I and IGF-II. Sequence determination revealed that hIGFBP-4 is a unique gene product with significant amino- and carboxy-terminal sequence similarity to three other known IGFBPs. Identical alignment of 18 cysteines in IGFBP-4 and the three other IGFBPs is a key structural feature of this protein family. In vitro studies of human osteoblast-like cells suggest that PTH regulates the expression of hIGFBP-4 and that the PTH effect is mediated through a cAMP mechanism. hIGFBP-4 mRNA was also expressed in skin fibroblasts, and thus, this inhibitory IGFBP could be an important physiological regulator of IGF actions in bone cells and other cell types as well.     

Antigenic characterization of a T-CLL with heteroantisera and monoclonal antibodies: evidence for the T cell lineage of an Ia-positive, Fc-IgG--positive, suppressor-cell subpopulation

In a previous report, peripheral blood mononuclear T cells from a patient with T-chronic lymphocytic leukemia (T-CLL) were shown to bear receptors for the Fc portion of IgG (T gamma). Moreover, the ability of these cells to rosette with sheep erythrocytes was strongly inhibited by a preincubation of the cells with theophylline. These data indicated that they represent a highly purified subpopulation of Fc-IgG receptor-positive, low-affinity rosetting cells with in vitro suppressor activity on lectin-induced proliferation of normal lymphocytes. They also were reactive in antibody-dependent cell-mediated cytotoxicity but had no reactivity in natural killer cell assays. These cells were studied in this report with several heteroantisera and monoclonal antibodies. Results indicate that these T-CLL cells express a T cell antigenic pattern (OKT-3+) and the majority are Ia positive. They also react with the OKT-8 reagent (a reagent detecting the subset of T cells that contains the cytotoxic/suppressor cells), whereas they are negative with OKT-4 (which reacts with the subset of T cells that contains helper cells) and OKT-6 (thymocyte) antibodies. Heteroantisera also support the results obtained with monoclonal reagents. Despite some recent evidence showing that a high percentage of T gamma cells may belong to the monocyte-myeloid lineage, these T-CLL cells were negative with OKM-1, a monoclonal antibody reported to detect a monomyeloid antigen. These results suggest that a distinct subpopulation of suppressor T cells can be identified by membrane-marker phenotyping.     

Evidence for WT1 as a Wilms tumor (WT) gene: intragenic germinal deletion in bilateral WT.

The inactivation of two alleles at a locus on the short arm of chromosome 11 (band 11p13) has been suggested to be critical steps in the development of Wilms tumor (WT), a childhood kidney tumor. Two similar candidate WT cDNA clones (WT33 and LK15) have recently been identified on the basis of both their expression in fetal kidney and their location within the smallest region of overlap of somatic 11p13 deletions in some tumors. These homozygous deletions, however, are large and potentially affect more than one gene. Using a cDNA probe to the candidate gene, we have analyzed DNA from both normal and tumor tissue from WT patients, in an effort to detect rearrangements at this locus. We report here a patient with bilateral WT who is heterozygous for a small (less than 11 kb) germinal deletion within this candidate gene. DNA from both tumors is homozygous for this intragenic deletion allele, which, by RNA-PRC sequence analysis, is predicted to encode a protein truncated by 180 amino acids. These data support the identification of this locus as an 11p13 WT gene (WT1) and provide direct molecular data supporting the two-hit mutational model for WT.