Spatial aspects of nest defence by pumpkinseed sunfish (Lepomis gibbosus): Stimulus features and an application of catastrophe theory

Using fixed stimulus dummies as territory intruders, we studied the spatial distributions of the aggressive responses made by nesting male pumpkinseed sunfish. Results replicated over three field seasons indicate that males defend two territory boundaries concurrently, depending on whether an intruder is approaching (“the defence perimeter’) or withdrawing (‘the attack perimeter’). This finding supports Zeeman's (1976) ‘cusp catastrophe model’ of nest defence. In addition, the defence perimeter remains constant over the breeding cycle while the attack perimeter varies. We discuss the ecological costs and benefits of this variation and present a motivational interpretation of the cusp catastrophe model. By varying the speed at which dummies intruded into nests, we determined that males react with a fixed latency to intruders at a fixed distance from the nest. Finally, the spatial distributions of male defence responses were partially determined by the location of the nest rim, but were unaffected by dummy size (contrary to Zeeman's model) or posture.     

High-voltage electron microscope study of the release of vaccinia virus from whole cells.

High-voltage (1,000-kV) electron microscope examination of whole BSC-1 cells infected with vaccinia virus at different times after infection revealed the presence of increasing numbers of virions no longer confined to factories but situated along the cell periphery of monolayer cells. Stereoscopic images showed each virus enclosed within a membrane-like component of the host cell cytoplasm. Viruses within factories appeared to lack similar enclosures. Cytochalasin B, but not vinblastine, caused the enclosures to disrupt. Vaccinia viruses were observed to escape the host cell individually from the tips of microvillie and within packets of cytoplasm. Observations suggest that the intracellular movement and release of vaccinia virus utilize a host cell cytoplasmic network that involves microfilaments for stability.     

Strain distribution during anchorage failure of Pinus pinaster Ait. at different ages and tree growth response to wind-induced root movement

Winching tests were carried out on 5- 13- and 17-year-old tap rooted Maritime pine (Pinus pinaster Ait.) in order to determine how the mode of anchorage failure changes throughout the life of a tree. As trees were pulled sideways, strain along the lateral roots was recorded using strain gauges attached to a strain indicator. Measurements of strain in the root system, taken during winching, provide information about root movement when loaded by wind. The mode of mechanical failure appeared to depend on tree age. The youngest trees bent over completely during winching, but did not break due to the plasticity of their trunks. The 13-year-old trees either broke at the base of the tree (due to the presence of grafting scar tissue) or at the base of the tap-root. The oldest trees broke at the base of the tap-root and sounds of roots breaking were also heard. Strain was twice as great in the trunk compared to the roots in the 5- and 13-year-old trees and was three times greater in the compression roots of 17-year–old trees compared to that in the trunk. In one 17-year-old tree, strain was found to increase at a distance of 35 cm in tension roots before decreasing again. Although the mode of failure changed with tree size, anchorage strength increased proportionally with the third power of trunk diameter, therefore another reason why failure differs with tree age must exist. In order to determine if different types of wood were being laid down in the lateral roots in response to wind loading, maturation strains, indicating the existence of mechanical stress in developing wood cells, were measured at different points along the roots. A high correlation was found between maturation strain and strain measured during winching, in roots that lay in the wind direction only. Therefore, trees appear to be able to respond to external loading stress, even at a local level within a root. This revised version was published online in June 2006 with corrections to the Cover Date.     

Mammalian SIRT1 limits replicative life span in response to chronic genotoxic stress

The Saccharomyces cerevisiae chromatin silencing factor Sir2 suppresses genomic instability and extends replicative life span. In contrast, we find that mouse embryonic fibroblasts (MEFs) deficient for SIRT1, a mammalian Sir2 homolog, have dramatically increased resistance to replicative senescence. Extended replicative life span of SIRT1-deficient MEFs correlates with enhanced proliferative capacity under conditions of chronic, sublethal oxidative stress. In this context, SIRT1-deficient cells fail to normally upregulate either the p19(ARF) senescence regulator or its downstream target p53. However, upon acute DNA damage or oncogene expression, SIRT1-deficient cells show normal p19(ARF) induction and cell cycle arrest. Together, our findings demonstrate an unexpected SIRT1 function in promoting replicative senescence in response to chronic cellular stress and implicate p19(ARF) as a downstream effector in this pathway.     

Heme transport exhibits polarity in Caco-2 cells: evidence for an active and membrane protein-mediated process

Heme prosthetic groups are vital for all living organisms, but they can also promote cellular injury by generating reactive oxygen species. Therefore, intestinal heme absorption and distribution should be carefully regulated. Although a human intestine brush-border heme receptor/transporter has been suggested, the mechanism by which heme crosses the apical membrane is unknown. After it enters the cell, heme is degraded by heme oxygenase-1 (HO-1), and iron is released. We hypothesized that heme transport is actively regulated in Caco-2 cells. Cells exposed to hemin from the basolateral side demonstrated a higher HO-1 induction than cells exposed to hemin from the apical surface. Hemin secretion was more rapid than absorption, and net secretion occurred against a concentration gradient. Treatment of the apical membrane with trypsin increased hemin absorption by threefold, but basolateral treatment with trypsin had no effect on hemin secretion. Neither apical nor basolateral trypsin changed the paracellular pathway. We conclude that heme is acquired and transported in both absorptive and secretory directions in polarized Caco-2 cells. Secretion is via an active metabolic/transport process. Trypsin applied to the apical surface increased hemin absorption, suggesting that protease activity can uncover a process for heme uptake that is otherwise quiescent. These processes may be involved in preventing iron overload in humans.     

Single mucosal, but not parenteral, immunization with recombinant adenoviral-based vaccine provides potent protection from pulmonary tuberculosis

Bacillus Calmette-Guerin (BCG) vaccine has failed to control the global tuberculosis (TB) epidemic, and there is a lack of safe and effective mucosal vaccines capable of potent protection against pulmonary TB. A recombinant replication-deficient adenoviral-based vaccine expressing an immunogenic Mycobacterium tuberculosis Ag Ag85A (AdAg85A) was engineered and evaluated for its potential to be used as a respiratory mucosal TB vaccine in a murine model of pulmonary TB. A single intranasal, but not i.m., immunization with AdAg85A provided potent protection against airway Mycobacterium tuberculosis challenge at an improved level over that by cutaneous BCG vaccination. Systemic priming with an Ag85A DNA vaccine and mucosal boosting with AdAg85A conferred a further enhanced immune protection which was remarkably better than BCG vaccination. Such superior protection triggered by AdAg85 mucosal immunization was correlated with much greater retention of Ag-specific T cells, particularly CD4 T cells, in the lung and was shown to be mediated by both CD4 and CD8 T cells. Thus, adenoviral TB vaccine represents a promising novel vaccine platform capable of potent mucosal immune protection against TB. Our study also lends strong evidence that respiratory mucosal vaccination is critically advantageous over systemic routes of vaccination against TB.     

Chloroplast division and morphology are differentially affected by overexpression of FtsZ1 and FtsZ2 genes in Arabidopsis

In higher plants, two nuclear gene families, FtsZ1 and FtsZ2, encode homologs of the bacterial protein FtsZ, a key component of the prokaryotic cell division machinery. We previously demonstrated that members of both gene families are essential for plastid division, but are functionally distinct. To further explore differences between FtsZ1 and FtsZ2 proteins we investigated the phenotypes of transgenic plants overexpressing AtFtsZ1-1 or AtFtsZ2-1, Arabidopsis members of the FtsZ1 and FtsZ2 families, respectively. Increasing the level of AtFtsZ1-1 protein as little as 3-fold inhibited chloroplast division. Plants with the most severe plastid division defects had 13- to 26-fold increases in AtFtsZ1-1 levels over wild type, and some of these also exhibited a novel chloroplast morphology. Quantitative immunoblotting revealed a correlation between the degree of plastid division inhibition and the extent to which the AtFtsZ1-1 protein level was elevated. In contrast, expression of an AtFtsZ2-1 sense transgene had no obvious effect on plastid division or morphology, though AtFtsZ2-1 protein levels were elevated only slightly over wild-type levels. This may indicate that AtFtsZ2-1 accumulation is more tightly regulated than that of AtFtsZ1-1. Plants expressing the AtFtsZ2-1 transgene did accumulate a form of the protein smaller than those detected in wild-type plants. AtFtsZ2-1 levels were unaffected by increased or decreased accumulation of AtFtsZ1-1 and vice versa, suggesting that the levels of these two plastid division proteins are regulated independently. Taken together, our results provide additional evidence for the functional divergence of the FtsZ1 and FtsZ2 plant gene families.