Growth and architecture of small honey mesquites under jackrabbit browsing: overcoming the disadvantage of being eaten

Browsing is an important mortality factor in seedlings and small plants. However, the induced changes in the architecture of plant survivors may influence subsequent browsing, opening the possibility of compensating for the damage done. How jackrabbit (Lepus californicus) browsing affects the growth and architecture of small individuals of honey mesquite, Prosopis glandulosa var. torreyana, a tree/shrub that produces spines at every node, was explored. Naturally established mesquites of unknown age were selected in one site, and 2-year-old mesquites were transplanted in another site. In both cases, half of them were exposed to jackrabbits and the other half were excluded as controls. After 4 years, shoot production (height, length and number of derived shoots) and plant growth (height and cover) increased 1.4-2.5-fold in naturally established controls relative to exposed plants, depending on the measured variable. In the transplant experiment, the increases were 2.8-7.1-fold in controls relative to exposed plants 2 years after initiation of the experiment. The net loss of biomass in treatment vs. control plants in these experiments suggests a negative response to browsing which has been defined as under-compensation. Alternative architectures in honey mesquites were evident at the end of the exclusion experiments: controls had long branches and an extended crown cover, while exposed plants had short branches and a compact crown cover. Results indicated that mesquites were able to grow under browser pressure by packing many stems in a compact matrix armed with spines and producing one or more shoots tall and wide enough to escape from jackrabbits.     

Modeling of a bipedal locomotor using coupled nonlinear oscillators of Van der Pol

 Research to date points to an understanding of human biped locomotion that has been primarily experimental in nature largely due to the complexity of the process. In view of the new, exciting possibilities of programmed electrostimulation of artificial muscles to generate motion (locomotion), a critical study at the theoretical level is greatly warranted. There is strong evidence that many biological clocks consist of a population of mutually coupled oscillators [Pavlidis T (1973) Biological oscillators, Academic; Johnsson A (1978) Zur Biophysik biologischer Oszillatoren. In: Biophisik, Springer]. In this work, a form of bipedal locomotion is simulated by using mutually coupled nonlinear oscillators. A planar model, which includes three out of the six determinants of gait that characterize the human locomotion, was adopted. Received: 4 August 2002 / Accepted: 12 November 2002 / Published online: 7 March 2003 Correspondence to: M. S. Dutra (e-mail: max@serv.com.ufrj.br) Acknowledgements. The authors would like to express their gratitude to CNPq, CAPES, and FAPERJ for the financial support provided during the course of this research.     

Patterns of morphological integration in marine modular organisms: supra-module organization in branching octocoral colonies

Despite the relative simplicity of their modular growth, marine invertebrates such as arborescent gorgonian octocorals (Octocorallia: Cnidaria) generate complex colonial forms. Colony form in these taxa is a consequence of modular (polyp) replication, and if there is a tight integration among modular and supramodular traits (e.g. polyp aperture, inter-polyp spacing, branch thickness, internode and branch length), then changes at the module level may lead to changes in colony architecture. Alternatively, different groups of traits may evolve semi-independently (or conditionally independent). To examine the patterns of integration among morphological traits in Caribbean octocorals, we compared five morphological traits across 21 species, correcting for the effects of phylogenetic relationships among the taxa. Graphical modelling and phylogenetic independence contrasts among the five morphological characters indicate two groups of integrated traits based on whether they were polyp- or colony-level traits. Although all characters exhibited bivariate associations, multivariate analyses (partial correlation coefficients) showed the strongest integration among the colony-level characters (internode distance and branch length). It is a quantitative demonstration that branching characters within the octocorals studied are independent of characters of the polyps. Despite the universally recognized modularity of octocorals at the level of polyps, branching during colony development may represent an emergent level of integration and modularity.     

Altered adhesion features and signal transduction in NRK-49F cells transformed by down-regulation of lysyl oxidase

Lysyl oxidase (LOX) down-regulation induced an oncogenic phenotype in NRK-49F. This event was accompanied by a constitutive activation of ras oncogene and down-regulation of PDGF beta receptor, among other important phenotypic and molecular modifications. In the present paper we show that ras activation is not accompanied by a constitutive activation of the MAP kinases as expected. Surprisingly, even if MAPK-independent, ras activation was accompanied by a constitutive Ser(63) and Ser(73) phosphorylation of c-jun, a further downstream target of ras. Although rare, this ras alternative pathway has been described. Since ras alone is seldom able to trigger cell transformation and the transformed phenotype showed clearly an abnormal adhesion pattern, we investigated the main molecules involved in cell-cell adhesion. In fact, we found that beta-catenin was up-regulated, escaping the glycogen synthase kinase-3 beta (GSK-3 beta) control, through unclear mechanisms. Its nuclear accumulation was accompanied by an up-regulation of cyclin D1, as classically described in the activation of the Wnt/beta-catenin signal pathway. We believe that the resulting up-regulation of cyclin D1 acted in synergy with ras to induce the cell transformation.     

A first molecular phylogenetic analysis of Passiflora (Passifloraceae)

Passiflora, a genus with more than 400 species, exhibits a high diversity of floral and vegetative structures and a complex taxonomy, which includes 23 subgenera and many sections and series. To better understand Passiflora's variability and interspecific relationships, the phylogeny of 61 species, classified in 11 of 23 suggested subgenera, was investigated. Three molecular markers were used, the nuclear ribosomal internal transcribed spacers (nrITS), the plastid trnL-trnF spacer regions (～1000 bp), and the rps4 plastid gene (～570 bp). Three major clades were highly supported, independent of the marker and phylogenetic method used; one included the subgenera Distephana, Dysosmia, Dysosmioides, Passiflora, and Tacsonioides, a second, the subgenera Adopogyne, Decaloba, Murucuja, and Pseudomurucuja, and a third, the subgenus Astrophea. We call these the Passiflora, Decaloba, and Astrophea clades, respectively. The position of subgenus Deidamioides is undefined. The monophyly of Passiflora could not be statistically corroborated, and the relationships among the major clades and of these clades with the related genera remain unresolved. Our results indicate that a reevaluation of the monophyly of Passiflora and its infrageneric classification is necessary.     

Structured HCV nucleocapsids composed of P21 core protein assemble primary in the nucleus of Pichia pastoris yeast

The relationship between HCV core protein (HCcAg) processing and the structural composition and morphogenesis of nucleocapsid-like particles (NLPs) produced in Pichia pastoris cells was studied. At early stages of heterologous expression, data suggest that HCcAg (in the P21 form) was transported soon after its synthesis in the cytoplasm into the nucleus. HCcAg assembly into nucleocapsid-like particles with 20-30 nm in diameter took place primary in the cell nucleus. However, at later stages, when P21 and P23 forms were co-detected, data suggest that new assembly of nucleocapsid particles containing P21 possibly occurs at ER membranes and in the cytoplasm. This is the first report showing that structured HCV NLPs composed of P21 core protein assemble primary in the nucleus of P. pastoris yeast.     

Proline oxidase induces apoptosis in tumor cells,and its expression is frequently absent or reduced in renal carcinomas

Proline oxidase is a p53-induced gene that can mediate apoptosis in lung carcinoma cells. Here, we provide evidence implicating a role for proline oxidase in renal carcinoma. We observed absent or reduced expression of proline oxidase in 8 of 12 primary renal cell carcinomas, with respect to their normal tissue counterparts. Two renal cell carcinomas, which displayed little or no expression of proline oxidase, expressed p53s that were less capable of inducing proline oxidase than p53 isolated from normal renal tissue. One of those tumor-derived p53s contained a double transition mutation at amino acid residues 125 (Ala to Thr) and 193 (Arg to His), and the other exhibited a single transition mutation at amino acid 149 (Ser to Phe). Forced up-regulation of proline oxidase induced the formation of reactive oxygen species and mediated apoptosis in the 786-0 renal cell carcinoma cell line. A proline oxidase antisense vector repressed p53-induced up-regulation of proline oxidase, release of cytochrome c from mitochondria, and apoptosis in 786-0 renal carcinoma cells. Taken together, these findings support a role for proline oxidase as a downstream effector in p53-mediated apoptosis. We hypothesize that its altered expression can contribute to the development of renal carcinomas. The presence of proline oxidase in mitochondria, a primary organelle that regulates apoptosis, places this molecule in a subcellular localization that can directly influence the apoptotic pathway and thus tumorigenesis.     

Naturally occurring mutations in the largest extracellular loops of ABCA1 can disrupt its direct interaction with apolipoprotein A-I

The ABCA1 transporter contains two large domains into which many of the genetic mutations in individuals with Tangier disease fall. To investigate the structural requirements for the cellular cholesterol efflux mediated by ABCA1, we have determined the topology of these two domains and generated transporters harboring five naturally occurring missense mutations in them. These mutants, unlike wild type ABCA1, produced little or no apoA-I-stimulated cholesterol efflux when transfected into 293 cells, establishing their causality in Tangier disease. Because all five mutant proteins were well expressed and detectable on the plasma membrane, their interaction with the ABCA1 ligand, apolipoprotein (apo) A-I, was measured using bifunctional cross-linking agents. Four of five mutants had a marked decline in cross-linking to apoA-I, whereas one (W590S) retained full cross-linking activity. Cross-linking of apoA-I was temperature-dependent, rapid in onset, and detectable with both lipid- and water-soluble cross-linking agents. These results suggest that apoA-I-stimulated cholesterol efflux cannot occur without a direct interaction between the apoprotein and critical residues in two extracellular loops of ABCA1. The behavior of the W590S mutant indicates that although binding of apoA-I by ABCA1 may be necessary, it is not sufficient for stimulation of cholesterol efflux.