Biodiversity and ecosystem multifunctionality

Biodiversity loss can affect ecosystem functions and services. Individual ecosystem functions generally show a positive asymptotic relationship with increasing biodiversity, suggesting that some species are redundant. However, ecosystems are managed and conserved for multiple functions, which may require greater biodiversity. Here we present an analysis of published data from grassland biodiversity experiments, and show that ecosystem multifunctionality does require greater numbers of species. We analysed each ecosystem function alone to identify species with desirable effects. We then calculated the number of species with positive effects for all possible combinations of functions. Our results show appreciable differences in the sets of species influencing different ecosystem functions, with average proportional overlap of about 0.2 to 0.5. Consequently, as more ecosystem processes were included in our analysis, more species were found to affect overall functioning. Specifically, for all of the analysed experiments, there was a positive saturating relationship between the number of ecosystem processes considered and the number of species influencing overall functioning. We conclude that because different species often influence different functions, studies focusing on individual processes in isolation will underestimate levels of biodiversity required to maintain multifunctional ecosystems.     

Catastrophic flooding origin of shelf valley systems in the English Channel

Megaflood events involving sudden discharges of exceptionally large volumes of water are rare, but can significantly affect landscape evolution, continental-scale drainage patterns and climate change. It has been proposed that a significant flood event eroded a network of large ancient valleys on the floor of the English Channel-the narrow seaway between England and France. This hypothesis has remained untested through lack of direct evidence, and alternative non-catastrophist ideas have been entertained for valley formation. Here we analyse a new regional bathymetric map of part of the English Channel derived from high-resolution sonar data, which shows the morphology of the valley in unprecedented detail. We observe a large bedrock-floored valley that contains a distinct assemblage of landforms, including streamlined islands and longitudinal erosional grooves, which are indicative of large-scale subaerial erosion by high-magnitude water discharges. Our observations support the megaflood model, in which breaching of a rock dam at the Dover Strait instigated catastrophic drainage of a large pro-glacial lake in the southern North Sea basin. We suggest that megaflooding provides an explanation for the permanent isolation of Britain from mainland Europe during interglacial high-sea-level stands, and consequently for patterns of early human colonisation of Britain together with the large-scale reorganization of palaeodrainage in northwest Europe.     

FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation

Intestinal immune homeostasis depends on a tightly regulated cross talk between commensal bacteria, mucosal immune cells and intestinal epithelial cells (IECs). Epithelial barrier disruption is considered to be a potential cause of inflammatory bowel disease; however, the mechanisms regulating intestinal epithelial integrity are poorly understood. Here we show that mice with IEC-specific knockout of FADD (FADD(IEC-KO)), an adaptor protein required for death-receptor-induced apoptosis, spontaneously developed epithelial cell necrosis, loss of Paneth cells, enteritis and severe erosive colitis. Genetic deficiency in RIP3, a critical regulator of programmed necrosis, prevented the development of spontaneous pathology in both the small intestine and colon of FADD(IEC-KO) mice, demonstrating that intestinal inflammation is triggered by RIP3-dependent death of FADD-deficient IECs. Epithelial-specific inhibition of CYLD, a deubiquitinase that regulates cellular necrosis, prevented colitis development in FADD(IEC-KO) but not in NEMO(IEC-KO) mice, showing that different mechanisms mediated death of colonic epithelial cells in these two models. In FADD(IEC-KO) mice, TNF deficiency ameliorated colon inflammation, whereas MYD88 deficiency and also elimination of the microbiota prevented colon inflammation, indicating that bacteria-mediated Toll-like-receptor signalling drives colitis by inducing the expression of TNF and other cytokines. However, neither CYLD, TNF or MYD88 deficiency nor elimination of the microbiota could prevent Paneth cell loss and enteritis in FADD(IEC-KO) mice, showing that different mechanisms drive RIP3-dependent necrosis of FADD-deficient IECs in the small and large bowel. Therefore, by inhibiting RIP3-mediated IEC necrosis, FADD preserves epithelial barrier integrity and antibacterial defence, maintains homeostasis and prevents chronic intestinal inflammation. Collectively, these results show that mechanisms preventing RIP3-mediated epithelial cell death are critical for the maintenance of intestinal homeostasis and indicate that programmed necrosis of IECs might be implicated in the pathogenesis of inflammatory bowel disease, in which Paneth cell and barrier defects are thought to contribute to intestinal inflammation.     

Cryptic and non-cryptic diversity in New Guinea ground snakes of the genus Stegonotus Duméril,Bibron and Duméril, 1854: a description of four new species (Squamata: Colubridae)

ABSTRACT

The island of New Guinea has been identified as biologically megadiverse but many taxa are still poorly known. This is especially the case for many of the island’s snakes, which by their very nature can be difficult to collect and study. Here we examine the phylogenetic and phylogeographic structure of a poorly studied snake genus, Stegonotus, focusing on the species of New Guinea; until now, Stegonotus has never been examined using modern phylogenetic methods. Using molecular data from 49 individuals representing eight of the ten described species, and including all New Guinea taxa, we estimate a multilocus phylogeny and examine population structure to help identify undescribed taxa. We use morphological data from the corresponding museum vouchered specimens (where available) and also examine additional specimens for taxa not included in the molecular data set to determine morphological differences among putative taxa. We find molecular evidence for four new species of Stegonotus, both morphologically obvious and cryptic, and describe them herein. The recognition of these four species indicates that Stegonotus diversity has been previously underestimated and also suggests that there are likely additional undescribed taxa within the genus. These four taxa increase the number of described species by 40% and further confirm New Guinea as the centre of diversity for the genus.

www.zoobank.org/urn:lsid:zoobank.org:pub:9E21390E-3FD4-40EB-9442-31BC92A76B4F     

Evolution: how do characters evolve?

Ricklefs claims to show that morphological evolution in birds is associated with speciation events--that is, it is punctuational--by inference from data on only species number, clade age and character variance from a range of passerine clades. He suggests that variance increases in proportion with clade age under gradual change, but in proportion to the logarithm of species number if change is punctuational. Here I show that both clade age and the logarithm of species number independently predict variance under both gradual and punctuational change, rendering Ricklefs' results uninformative about his central hypothesis.     

Small area population estimates project: data quality of administrative datasets

The Office for National Statistics (ONS) has set up a project to investigate the feasibility of producing postcensal small area population estimates on a nationally consistent basis for England and Wales. Research has taken place to identify datasets that could potentially be used within a method to produce small area population estimates. Following an evaluation of a number of different administrative datasets, the most suitable have been short-listed for further consideration. This article presents the findings of the evaluation, based on 2001 data, and summarises the characteristics of these short-listed data sources. This article does not cover the methods that are being evaluated as part of the feasibility assessment.     

Loss-of-function mutations in LEMD3 result in osteopoikilosis, Buschke-Ollendorff syndrome and melorheostosis

Osteopoikilosis, Buschke-Ollendorff syndrome (BOS) and melorheostosis are disorders characterized by increased bone density. The occurrence of one or more of these phenotypes in the same individual or family suggests that these entities might be allelic. We collected data from three families in which affected individuals had osteopoikilosis with or without manifestations of BOS or melorheostosis. A genome-wide linkage analysis in these families, followed by the identification of a microdeletion in an unrelated individual with these diseases, allowed us to map the gene that is mutated in osteopoikilosis. All the affected individuals that we investigated were heterozygous with respect to a loss-of-function mutation in LEMD3 (also called MAN1), which encodes an inner nuclear membrane protein. A somatic mutation in the second allele of LEMD3 could not be identified in fibroblasts from affected skin of an individual with BOS and an individual with melorheostosis. XMAN1, the Xenopus laevis ortholog, antagonizes BMP signaling during embryogenesis. In this study, LEMD3 interacted with BMP and activin-TGFbeta receptor-activated Smads and antagonized both signaling pathways in human cells.     

The knockout mouse project

Mouse knockout technology provides a powerful means of elucidating gene function in vivo, and a publicly available genome-wide collection of mouse knockouts would be significantly enabling for biomedical discovery. To date, published knockouts exist for only about 10% of mouse genes. Furthermore, many of these are limited in utility because they have not been made or phenotyped in standardized ways, and many are not freely available to researchers. It is time to harness new technologies and efficiencies of production to mount a high-throughput international effort to produce and phenotype knockouts for all mouse genes, and place these resources into the public domain.     

A 5-bp deletion in ELOVL4 is associated with two related forms of autosomal dominant macular dystrophy

Stargardt-like macular dystrophy (STGD3, MIM 600110) and autosomal dominant macular dystrophy (adMD) are inherited forms of macular degeneration characterized by decreased visual acuity, macular atrophy and extensive fundus flecks. Genetic mapping data suggest that mutations in a single gene may be responsible for both conditions, already known to bear clinical resemblance. Here we limit the minimum genetic region for STGD3 and adMD to a 0.6-cM interval by recombination breakpoint mapping and identify a single 5-bp deletion within the protein-coding region of a new retinal photoreceptor-specific gene, ELOVL4, in all affected members of STGD3 and adMD families. Bioinformatic analysis of ELOVL4 revealed that it has homology to a group of yeast proteins that function in the biosynthesis of very long chain fatty acids. Our results are therefore the first to implicate the biosynthesis of fatty acids in the pathogenesis of inherited macular degeneration.