A globally consistent richness-climate relationship for angiosperms

Species richness, the simplest index of biodiversity, varies greatly over broad spatial scales. Richness-climate relationships often account for >80% of the spatial variance in richness. However, it has been suggested that richness-climate relationships differ significantly among geographic regions and that there is no globally consistent relationship. This study investigated the global patterns of species and family richness of angiosperms in relation to climate. We found that models relating angiosperm richness to mean annual temperature, annual water deficit, and their interaction or models relating richness to annual potential evapotranspiration and water deficit are both globally consistent and very strong and are independent of the diverse evolutionary histories and functional assemblages of plants in different parts of the world. Thus, effects of other factors such as evolutionary history, postglacial dispersal, soil nutrients, topography, or other climatic variables either must be quite minor over broad scales (because there is little residual variation left to explain) or they must be strongly collinear with global patterns of climate. The correlations shown here must be predicted by any successful hypothesis of mechanisms controlling richness patterns.     

Natural selection on the erythrocyte surface

Surface glycoproteins are principal receptors used by pathogens to invade target cells. It has been suggested that mammalian erythrocyte surface glycoproteins function as decoy receptors attracting pathogens to the anucleated erythrocyte and away from their target tissues. Glycophorin A (GYPA) is solely expressed on the erythrocyte surface where it is the most abundant sialoglycoprotein, although its function is unknown. The pathogen decoy hypothesis may be relevant here, as GYPA has been shown in vitro to bind numerous viruses and bacteria, which do not infect erythrocytes. However, it is also a receptor for erythrocyte invasion by the malarial parasite Plasmodium falciparum. Analyses of gypa sequence variation among six higher primates and within a human population show that there is a large excess of replacement (nonsynonymous) substitutions along each primate lineage (particularly on exons 2-4 encoding the extracellular glycosylated domain of GYPA) and a significant excess of polymorphisms in exon 2 (encoding the terminal portion of the extracellular domain) within humans. These two signatures suggest that there has been exceptionally strong positive selection on this receptor driving GYPA divergence during primate evolution and balancing selection maintaining allelic variation within human populations. The pathogen decoy hypothesis alone is adequate to explain both these signatures of between-species and within-species diversifying selection. This has implications for understanding the functions of erythrocyte surface components and their roles in health and disease.     

TAPAS-1, a novel microdomain within the unique N-terminal region of the PDE4A1 cAMP-specific phosphodiesterase that allows rapid, Ca2+-triggered membrane association with selectivity for interaction with phosphatidic acid

Here we identify an 11-residue helical module in the unique N-terminal region of the cyclic AMP-specific phosphodiesterase PDE4A1 that determines association with phospholipid bilayers and shows a profound selectivity for interaction with phosphatidic acid (PA). This module contains a core bilayer insertion unit that is formed by two tryptophan residues, Trp(19) and Trp(20), whose orientation is optimized for bilayer insertion by the Leu(16):Val(17) pairing. Ca(2+), at submicromolar levels, interacts with Asp(21) in this module and serves to gate bilayer insertion, which is completed within 10 ms. Selectivity for interaction with PA is suggested to be achieved primarily through the formation of a charge network of the form (Asp(21-):Ca(2+):PA(2-):Lys(24+)) with overall neutrality at the bilayer surface. This novel phospholipid-binding domain, which we call TAPAS-1 (tryptophan anchoring phosphatidic acid selective-binding domain 1), is here identified as being responsible for membrane association of the PDE4A1 cAMP-specific phosphodiesterase. TAPAS-1 may not only serve as a paradigm for other PA-binding domains but also aid in detecting related phospholipid-binding domains and in generating simple chimeras for conferring membrane association and intracellular targeting on defined proteins.     

Isolation of three zebrafish dachshund homologues and their expression in sensory organs, the central nervous system and pectoral fin buds

Drosophila dachshund (dac) interacts with sine oculis (so), eyes absent (eya) and eyeless (ey) to control compound eye development. We have cloned three zebrafish dac homologues, dachA, dachB and dachC, which are expressed widely, in distinct but overlapping patterns. Expression of all three is found in sensory organs, the central nervous system and pectoral fin buds. dachA is also expressed strongly in the somites and dachC in the neural crest and pronephros. These expression domains overlap extensively with those of zebrafish pax, eya and six family members, the homologues of Drosophila ey, eya and so, respectively. This is consistent with the proposal that Dach, Eya, Six and Pax family members may form networks, similar to that found in the fly eye, in the development of many vertebrate organs.     

The scourge of scabies

Scabies ('Itch Mite') is truly a Great Neglected Disease that inflicts misery on millions. Molecular approaches, while still in their infancy, are providing a better understanding of the parasite and will have important implications for control and prevention. It has long been thought that dogs may act as a reservoir for human infections. However, genetic studies cast doubt over this supposition.     

Verotoxin 1 binding to intestinal crypt epithelial cells results in localization to lysosomes and abrogation of toxicity

Verotoxins (VTs) are important virulence factors of enterohaemorrhagic Escherichia coli (EHEC), a group of bacteria associated with severe disease sequelae in humans. The potent cytotoxic activity of VTs is important in pathogenicity, resulting in the death of cells expressing receptor Gb3 (globotriaosylceramide). EHEC, particularly serotype O157:H7, frequently colonize reservoir hosts (such as cattle) in the absence of disease, however, the basis to avirulence in this host has been unclear. The objective of this study was assessment of interaction between VT and intestinal epithelium, which represents the major interface between the host and enteric organisms. Bovine intestinal epithelial cells expressed Gb3 in vitro in primary cell cultures, localizing specifically to proliferating crypt cells in corroboration with in situ immunohistological observations on intestinal mucosa. Expression of receptor by these cells contrasts with the absence of Gb3 on human intestinal epithelium in vivo. Despite receptor expression, VT exhibited no cytotoxic activity against bovine epithelial cells. Sub-cellular localization of VT indicated that this toxin was excluded from endoplasmic reticulum but localized to lysosomes, corresponding with abrogation of cytotoxicity. VT intracellular trafficking was unaffected by treatment of primary cell cultures with methyl-beta-cyclodextrin, indicating that Gb3 in these cells is not associated with lipid rafts but is randomly distributed in the membrane. The combination of Gb3 isoform, membrane distribution and VT trafficking correlate with observations of other receptor-positive cells that resist verocytotoxicity. These studies demonstrate that intestinal epithelium is an important determinant in VT interaction with major implications for the differential consequences of EHEC infection in reservoir hosts and humans.     

Myotome meanderings. Cellular morphogenesis and the making of muscle

The formation of muscles within the vertebrate embryo is a tightly orchestrated and complex undertaking. Beyond the initial specification of cells to become muscle are several complex cellular movements and migrations, which lead to the positioning of muscle precursors at specific locations within the embryo. The consequent differentiation, elongation and striation of these cells results in the formation of individual muscles. Investigation of the in vivo morphogenesis of individual vertebrate muscle cells has only recently begun, and is being approached through the use of sophisticated cell labelling and lineage analysis techniques. However, a consensus about the mechanisms involved has yet to be achieved. This review outlines vertebrate embryonic muscle formation in chick, fish and mice, focusing on the embryonic myotome, which generates both the axial musculature and the appendicular muscle of the fins and limbs. We highlight the points of consensus about, and the complexity of, this developmental system, and propose an evolutionary context for the basis of these understandings.     

Developmental diorama

Spring meeting of the British Society for Developmental Biology, held April 2003 at the University of Warwick, UK.