Managing the middle: A shift in conservation priorities based on the global human modification gradient

An increasing number of international initiatives aim to reconcile development with conservation. Crucial to successful implementation of these initiatives is a comprehensive understanding of the current ecological condition of landscapes and their spatial distributions. Here, we provide a cumulative measure of human modification of terrestrial lands based on modeling the physical extents of 13 anthropogenic stressors and their estimated impacts using spatially explicit global datasets with a median year of 2016. We quantified the degree of land modification and the amount and spatial configuration of low modified lands (i.e., natural areas relatively free from human alteration) across all ecoregions and biomes. We identified that fewer unmodified lands remain than previously reported and that most of the world is in a state of intermediate modification, with 52% of ecoregions classified as moderately modified. Given that these moderately modified ecoregions fall within critical land use thresholds, we propose that they warrant elevated attention and require proactive spatial planning to maintain biodiversity and ecosystem function before important environmental values are lost.     

Passive and facilitated transport in nuclear pore complexes is largely uncoupled

Nuclear pore complexes provide the sole gateway for the exchange of material between nucleus and cytoplasm of interphase eukaryotic cells. They support two modes of transport: passive diffusion of ions, metabolites, and intermediate-sized macromolecules and facilitated, receptor-mediated translocation of proteins, RNA, and ribonucleoprotein complexes. It is generally assumed that both modes of transport occur through a single diffusion channel located within the central pore of the nuclear pore complex. To test this hypothesis, we studied the mutual effects between transporting molecules utilizing either the same or different modes of translocation. We find that the two modes of transport do not interfere with each other, but molecules utilizing a particular mode of transport do hinder motion of others utilizing the same pathway. We therefore conclude that the two modes of transport are largely segregated.     

How plastic can phenotypic plasticity be? The branching coral Stylophora pistillata as a model system

Phenotypic plasticity enables multicellular organisms to adjust morphologies and various life history traits to variable environmental challenges. Here, we elucidate fixed and plastic architectural rules for colony astogeny in multiple types of colonial ramets, propagated by cutting from genets of the branching coral Stylophora pistillata from Eilat, the Red Sea. We examined 16 morphometric parameters on 136 one-year old S. pistillata colonies (of seven genotypes), originating from small fragments belonging, each, to one of three single-branch types (single tips, start-up, and advanced bifurcating tips) or to structural preparative manipulations (representing a single or two growth axes). Experiments were guided by the rationale that in colonial forms, complexity of evolving phenotypic plasticity can be associated with a degree of structural modularity, where shapes are approached by erecting iterative growth patterns at different levels of coral-colony organization. Analyses revealed plastic morphometric characters at branch level, and predetermined morphometric traits at colony level (only single trait exhibited plasticity under extreme manipulation state). Therefore, under the experimental manipulations of this study, phenotypic plasticity in S. pistillata appears to be related to branch level of organization, whereas colony traits are controlled by predetermined genetic architectural rules. Each level of organization undergoes its own mode of astogeny. However, depending on the original ramet structure, the spherical 3-D colonial architecture in this species is orchestrated and assembled by both developmental trajectories at the branch level, and traits at the colony level of organization. In nature, branching colonial forms are often subjected to harsh environmental conditions that cause fragmentation of colony into ramets of different sizes and structures. Developmental traits that are plastic, responding to fragment structure and are not predetermine in controlling astogeny, allow formation of species-specific architecture product through integrated but variable developmental routes. This adaptive plasticity or regeneration is an efficient mechanism by which isolated fragments of branching coral species cope with external environmental forces.     

Semaphorins as Mediators of Neuronal Apoptosis

Shrinkage and collapse of the neuritic network are often observed during the process of neuronal apoptosis. However, the molecular and biochemical basis for the axonal damage associated with neuronal cell death is still unclear. We present evidence for the involvement of axon guidance molecules with repulsive cues in neuronal cell death. Using the differential display approach, an up-regulation of collapsin response mediator protein was detected in sympathetic neurons undergoing dopamine-induced apoptosis. A synchronized induction of mRNA of the secreted collapsin-1 and the intracellular collapsin response mediator protein that preceded commitment of neurons to apoptosis was detected. Antibodies directed against a conserved collapsin-derived peptide provided marked and prolonged protection of several neuronal cell types from dopamine-induced apoptosis. Moreover, neuronal apoptosis was inhibited by antibodies against neuropilin-1, a putative component of the semaphorin III/collapsin-1 receptor. Induction of neuronal apoptosis was also caused by exposure of neurons to semaphorin III-alkaline phosphatase secreted from 293EBNA cells. Anti-collapsin-1 antibodies were effective in blocking the semaphorin III-induced death process. We therefore suggest that, before their death, apoptosis-destined neurons may produce and secrete destructive axon guidance molecules that can affect their neighboring cells and thus transfer a "death signal" across specific and susceptible neuronal populations.     

Hormonal control of inflorescence development in plantlets of calla lily (Zantedeschia spp.) grown in vitro

Hormonal control of flower induction and inflorescence development in vitro was investigated in photoperiodically day-neutral calla lily (Zantedeschia spp., colored cultivars). The effects of gibberellins (GAs, 5.8–2900 M) and the cytokinin benzyl adenine (BA, 0.4–13.3 M) on inflorescence development were studied in plantlets regenerated in tissue culture. Plantlets were dipped in GA and BA solutions prior to replanting in new media. GA was mandatory for the shift from the vegetative to the reproductive stage. GA3, GA1 and GA4 had the same florigenic effect. Inflorescence development in the apical bud was observed after 30–50 days in GA-treated plantlets grown in vitro and resembled the pattern occurring under natural conditions. The transition from the vegetative to the reproductive phase was characterized by a swollen, dome-shaped apex that transformed into a smooth elongated apex surrounded by the spathe primordium, at the tip of the elongating peduncle primordium. Floret primordia developed in inflorescences at a more advanced stage. The female florets located at the base of the primordial spadix, could be clearly distinguished from male florets located above them. BA did not have an effect on flower induction but, in the presence of GA, BA at concentrations up to 4.4 M enhanced inflorescence differentiation. The results indicate that inflorescence development in Zantedeschia plantlets in tissue culture can serve as a potential model to study the role of GAs and other factors in the flowering process of day-neutral plants that do not require external signals for flower induction.     

'Cup cell disease' in the colonial tunicate Botryllus schlosseri

A new progressive, fatal disease called 'cup cell disease' was characterized in ex situ cultures of Botryllus schlosseri, a colonial tunicate. The disease originated as a few dark spots growing within zooids. The infected colonies then started to deteriorate, morphologically diagnosed by ampullar retraction, lethargic blood circulation and by a swollen and soft tunic matrix. In later stages of the disease, developed buds were also affected. Many large black dots were scattered within the tunic matrix, and zooids were transformed to opaque, dilated, sac-like structures, signaling impending death. Colonies were infected periodically, even without direct tissue contact. The time course from first appearance to colony death ranged between 30 and 45 d. Histological studies, in vitro culturing of blood cells and blood smears revealed the existence of numerous cup-like cells (up to 4.8 microm diameter on average) with a yellowish cell wall and transparent cytoplasm that was not stained by various dyes (except azocarmine-G). Cells were refractive under bright-field illumination and revealed a flattened wall with flanges, characteristic of species of the phylum Haplosporidia. Cup cells aggregated in blood vessels and in internal parts of zooids and buds and were phagocytosed by blood cells. In a single case, plasmodia-like structures were found only in the tunic matrix of an infected colony. This is the first record in botryllid ascidians of an infectious lethal disease associated with haplosporidian protists.     

Analyzing time series gene expression data

MOTIVATION: Time series expression experiments are an increasingly popular method for studying a wide range of biological systems. However, when analyzing these experiments researchers face many new computational challenges. Algorithms that are specifically designed for time series experiments are required so that we can take advantage of their unique features (such as the ability to infer causality from the temporal response pattern) and address the unique problems they raise (e.g. handling the different non-uniform sampling rates). RESULTS: We present a comprehensive review of the current research in time series expression data analysis. We divide the computational challenges into four analysis levels: experimental design, data analysis, pattern recognition and networks. For each of these levels, we discuss computational and biological problems at that level and point out some of the methods that have been proposed to deal with these issues. Many open problems in all these levels are discussed. This review is intended to serve as both, a point of reference for experimental biologists looking for practical solutions for analyzing their data, and a starting point for computer scientists interested in working on the computational problems related to time series expression analysis.     

Enzyme activity--it's all about image

Unraveling the functional roles of proteins is a major challenge facing the postgenome researcher. Advances towards this goal have been made through the development of both chemical and biochemical tools for monitoring protein activity. Recently, a myriad of fluorescence-based imaging tools have emerged for in vitro, in vivo and whole animal applications. These tools have provided methods to monitor the spatial and temporal distribution of proteins and bioorganic molecules dynamically. Here, recent advances in chemical and biochemical techniques that allow the detection of enzymatic activity within intact cells and in vivo are reviewed. Such technologies have the potential to be integrated into drug-development programs to facilitate both the functional validation of pharmaceutical targets and the treatment of human disease.     

VEGF162, a new heparin-binding vascular endothelial growth factor splice form that is expressed in transformed human cells

The splice forms of vascular endothelial growth factor (VEGF) differ in biological properties such as the receptor types that they recognize and their interaction with heparan sulfate proteoglycans. We have identified a new VEGF mRNA splice form encoding a VEGF species containing 162 amino acids (VEGF(162)) in human A431 ovarian carcinoma cells. This novel mRNA contains the peptides encoded by exons 1-5, 6A, 6B, and 8 of the VEGF gene. Recombinant VEGF(162) is biologically active. It induces proliferation of endothelial cells in vitro and angiogenesis in vivo as determined by the alginate bead assay. VEGF(162) binds less efficiently than VEGF(145) but more efficiently than VEGF(165) to a natural basement membrane produced by corneal endothelial cells. VEGF(138), an artificial VEGF form that contains exon 6B but lacks exons 6A and 7, did not bind to this basement membrane at all, indicating that exon 6B probably interferes with the interaction of exon 6A with heparin and heparan sulfate proteoglycans.