Merging aquatic and terrestrial perspectives of nutrient biogeochemistry

Although biogeochemistry is an integrative discipline, terrestrial and aquatic subdisciplines have developed somewhat independently of each other. Physical and biological differences between aquatic and terrestrial ecosystems explain this history. In both aquatic and terrestrial biogeochemistry, key questions and concepts arise from a focus on nutrient limitation, ecosystem nutrient retention, and controls of nutrient transformations. Current understanding is captured in conceptual models for different ecosystem types, which share some features and diverge in other ways. Distinctiveness of subdisciplines has been appropriate in some respects and has fostered important advances in theory. On the other hand, lack of integration between aquatic and terrestrial biogeochemistry limits our ability to deal with biogeochemical phenomena across large landscapes in which connections between terrestrial and aquatic elements are important. Separation of the two approaches also has not served attempts to scale up or to estimate fluxes from large areas based on plot measurements. Understanding connectivity between the two system types and scaling up biogeochemical information will rely on coupled hydrologic and ecological models, and may be critical for addressing environmental problems associated with locally, regionally, and globally altered biogeochemical cycles.We dedicate this paper to the memory of Catherine Lisa Dent, a member of our working group who contributed much to the ideas presented herein, and to the joy of developing them together.Due to an error in the citation line, this revised PDF (published in December 2003) deviates from the printed version, and is the correct and authoritative version of the paper.     

Studying the global distribution of infectious diseases using GIS and RS

West Nile virus, severe acute respiratory syndrome and monkeypox are infectious diseases that have recently been introduced into areas far from their region of origin. The greatest risk of new diseases comes from zoonoses--pathogens that circulate among wild animals and are occasionally transferred to humans by intermediate invertebrate hosts or vectors that are sensitive to climatic conditions. Analytical tools that are based on geographical information systems and that can incorporate remotely sensed information about the environment offer the potential to define the limiting conditions for any disease in its native region for which there are at least some distribution data. The direction, intensity or likelihood of its spread to new regions could then be predicted, potentially allowing disease early-warning systems to be developed.     

Granulocyte-dendritic cell unbalance in the non-obese diabetic mice

Several investigators, including ourselves, have reported lower yield of GM-CSF bone marrow-derived dendritic cells (DC) with altered MHC class II and co-stimulatory molecules expression in the non-obese diabetic (NOD) mice. However, whether this defect was intrinsic to the DC lineage and/or related to abnormal expansion of other cell types responding to GM-CSF remained an opened issue. We performed phenotypical and morphological analysis of cells from GM-CSF-supplemented-bone marrow-cultures and of freshly isolated bone marrow and blood cells from unmanipulated prediabetic NOD mice. The results show a heretofore undescribed bias towards generation of granulocytes in NOD mice, concomitant with quantitative and qualitative alterations of the DC lineage in both the bone marrow and the blood of this mouse strain. We propose that increased generation of granulocytes in NOD mice might contribute to autoimmunity. First, high numbers of granulocytes per se might favor inflammatory environment. Second, granulocytes, by interfering with DC development, might favor unbalanced antigen presenting cell function leading to T cell autoimmunity.     

Microarray analysis of murine palatogenesis: temporal expression of genes during normal palate development

The mammalian face is assembled in utero in a series of complex and interdependent molecular, cell and tissue processes. The orofacial complex appears to be exquisitely sensitive to genetic and environmental influence and this explains why clefts of the lip and palate are the most common congenital anomaly in humans (one in 700 live births). In this study, microarray technology was used to identify genes that may play pivotal roles in normal murine palatogenesis. mRNA was isolated from murine embryonic palatal shelves oriented vertically (before elevation), horizontally (following elevation, before contact), and following fusion. Changes in gene expression between the three different stages were analyzed with GeneChip microarrays. A number of genes were upregulated or downregulated, and large changes were seen in the expression of loricrin, glutamate decarboxylase, gamma-amino butyric acid type A receptor beta3 subunit, frizzled, Wnt-5a, metallothionein, annexin VIII, LIM proteins, Sox1, plakophilin1, cathepsin K and creatine kinase. In this paper, the changes in genetic profile of the developing murine palate are presented, and the possible role individual genes/proteins may play during normal palate development are discussed. Candidate genes with a putative role in cleft palate are also highlighted.     

Forced activation of Wnt signaling alters morphogenesis and sensory organ identity in the chicken inner ear

Components of the Wnt signaling pathway are expressed in the developing inner ear. To explore their role in ear patterning, we used retroviral gene transfer to force the expression of an activated form of beta-catenin that should constitutively activate targets of the canonical Wnt signaling pathway. At embryonic day 9 (E9) and beyond, morphological defects were apparent in the otic capsule and the membranous labyrinth, including ectopic and fused sensory patches. Most notably, the basilar papilla, an auditory organ, contained infected sensory patches with a vestibular phenotype. Vestibular identity was based on: (1) stereociliary bundle morphology; (2) spacing of hair cells and supporting cells; (3) the presence of otoliths; (4) immunolabeling indicative of vestibular supporting cells; and (5) expression of Msx1, a marker of certain vestibular sensory organs. Retrovirus-mediated misexpression of Wnt3a also gave rise to ectopic vestibular patches in the cochlear duct. In situ hybridization revealed that genes for three Frizzled receptors, c-Fz1, c-Fz7, and c-Fz10, are expressed in and adjacent to sensory primordia, while Wnt4 is expressed in adjacent, nonsensory regions of the cochlear duct. We hypothesize that Wnt/beta-catenin signaling specifies otic epithelium as macular and helps to define and maintain sensory/nonsensory boundaries in the cochlear duct.     

C-value estimates for 31 species of ladybird beetles (Coleoptera: Coccinellidae)

This study provides C-value (haploid nuclear DNA content) estimates for 31 species of ladybird beetles (representing 6 subfamilies and 8 tribes), the first such data for the family Coccinellidae. Despite their unparalleled diversity, the Coleoptera have been very poorly studied in terms of genome size variation, such that even this relatively modest sample of species makes the Coccinellidae the third best studied family of beetles, behind the Tenebrionidae and Chrysomelidae. The present study provides a comparison of patterns of genome size variation with these two relatively well-studied families. No correlation was found between genome size and body size in the ladybirds, in contrast to some other invertebrate groups but in keeping with findings for other beetle families. However, there is some indication that developmental time and/or feeding ecology is related to genome size in this group. Some phylogenetic patterns and possible associations with subgenomic features are also discussed.     

Loss of G protein gamma 7 alters behavior and reduces striatal alpha(olf) level and cAMP production

The G protein beta gamma-dimer is required for receptor interaction and effector regulation. However, previous approaches have not identified the physiologic roles of individual subtypes in these processes. We used a gene knockout approach to demonstrate a unique role for the G protein gamma(7)-subunit in mice. Notably, deletion of Gng7 caused behavioral changes that were associated with reductions in the alpha(olf)-subunit content and adenylyl cyclase activity of the striatum. These data demonstrate that an individual gamma-subunit contributes to the specificity of a given signaling pathway and controls the formation or stability of a particular G protein heterotrimer.