‘Who’s in the Network?’ When Stakeholders Influence Data Analysis

Environmental applications of social network analysis (SNA) are just beginning to emerge, and so far have focussed on understanding the characteristics of social networks that increase the likelihood of collective action and successful natural resource management. We move beyond this discussion to demonstrate how knowledge gained from analysing the social networks of stakeholders can be harnessed for selecting stakeholders, and further, how these analyses can be influenced by the expressed wishes and concerns of stakeholders. Although we began our SNA using concepts derived from the resource-management literature, stakeholder involvement in the interpretation of the results led to the use of SNA techniques that had not previously been applied in the context of resource management. We thus re-analysed our data and modified our selection of research participants. Re-analysis led to the selection of research participants who (1) had unique positions in the network, thus occupying non-redundant communication roles in the network, (2) came from different stakeholder categories and (3) were relatively well-connected to others and tended to broker across different segments of the network. By combining insights from researchers and stakeholders in this way, it was possible to use SNA in an innovative and sensitive way to better meet the needs of the stakeholders and the research project.

Humanin peptide suppresses apoptosis by interfering with Bax activation

Bax (Bcl2-associated X protein) is an apoptosis-inducing protein that participates in cell death during normal development and in various diseases. Bax resides in an inactive state in the cytosol of many cells. In response to death stimuli, Bax protein undergoes conformational changes that expose membrane-targeting domains, resulting in its translocation to mitochondrial membranes, where Bax inserts and causes release of cytochrome c and other apoptogenic proteins. It is unknown what controls conversion of Bax from the inactive to active conformation. Here we show that Bax interacts with humanin (HN), an anti-apoptotic peptide of 24 amino acids encoded in mammalian genomes. HN prevents the translocation of Bax from cytosol to mitochondria. Conversely, reducing HN expression by small interfering RNAs sensitizes cells to Bax and increases Bax translocation to membranes. HN peptides also block Bax association with isolated mitochondria, and suppress cytochrome c release in vitro. Notably, the mitochondrial genome contains an identical open reading frame, and the mitochondrial version of HN can also bind and suppress Bax. We speculate therefore that HN arose from mitochondria and transferred to the nuclear genome, providing a mechanism for protecting these organelles from Bax.     

Non-apoptotic role of BID in inflammation and innate immunity

Innate immunity is a fundamental defence response that depends on evolutionarily conserved pattern recognition receptors for sensing infections or danger signals. Nucleotide-binding and oligomerization domain (NOD) proteins are cytosolic pattern-recognition receptors of paramount importance in the intestine, and their dysregulation is associated with inflammatory bowel disease. They sense peptidoglycans from commensal microorganisms and pathogens and coordinate signalling events that culminate in the induction of inflammation and anti-microbial responses. However, the signalling mechanisms involved in this process are not fully understood. Here, using genome-wide RNA interference, we identify candidate genes that modulate the NOD1 inflammatory response in intestinal epithelial cells. Our results reveal a significant crosstalk between innate immunity and apoptosis and identify BID, a BCL2 family protein, as a critical component of the inflammatory response. Colonocytes depleted of BID or macrophages from Bid(-/-) mice are markedly defective in cytokine production in response to NOD activation. Furthermore, Bid(-/-) mice are unresponsive to local or systemic exposure to NOD agonists or their protective effect in experimental colitis. Mechanistically, BID interacts with NOD1, NOD2 and the IκB kinase (IKK) complex, impacting NF-κB and extracellular signal-regulated kinase (ERK) signalling. Our results define a novel role of BID in inflammation and immunity independent of its apoptotic function, furthering the mounting evidence of evolutionary conservation between the mechanisms of apoptosis and immunity.     

The life cycle of Hydroperla crosbyi (Plecoptera: Perlodidae)

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Relative vulnerability to extirpation of montane breeding birds in the Great Basin

Seventy-four species of montane breeding birds were evaluated for their vulnerability to extirpation in the Great Basin. Although none of these species are endemic to the Great Basin, the montane island system results in a unique pattern of species associations. Loss of species from these montane communities could be indicative of region wide habitat degradation. I ranked susceptibility to extirpation based on seven biological variables: geographic range, population size, reproductive potential, susceptibility to cowbird parasitism, migratory status, and diet specialization. Each variable was weighted equally in its contribution to vulnerability, and scores were the sum of trait scores for each species. Different suites of life-history traits led to similar vulnerabilities. The following 10 montane bird species were categorized as most vulnerable to extirpation from the Great Basin, listed as most to least vulnerable: Olive-sided Flycatcher ( Contopus borealis ), Painted Redstart ( Myioborus pictus ), Hammond's Flycatcher ( Empidonax hammondii ), Veery ( Catharus fuscescens ), Whip-poor-will ( Caprimulgus vociferus ), Lincoln's Sparrow ( Melospiza lincolnii ), Black-backed woodpecker ( Picoides arcicus ), Three-toed Woodpecker ( P. tridactylus ), Himalayan Snowcock ( Tetraogallus himalayensis ), and Nashville Warbler ( Verminvora ruficapilla ). Species of similar vulnerability scores often were dissimilar in threats related to their vulnerability. No taxonomic patterns in vulnerability were found. This type of analysis should be used proactively to identify vulnerable species or populations and to set priorities for research management.     

Effects of habitat type and degradation on avian species richness in Great Basin riparian habitats

The overwhelming majority of bird species in the Great Basin region are found in riparian habitats. However, most previous research on the impact of change in habitat condition through degradation on these bird communities failed to account for the large intersite differences, in both habitat type and extent of degradation. We examined songbird communities in 4 riparian habitat types (meadows, willow-birch-, and aspen-dominated forest stands) during summers 1994 (last year of a 7-yr drought) and 1995 (following the 6th wettest winter recorded) in the Toiyabe Mountain Range of central Nevada. Habitat degradation significantly influenced bird species richness in riparian areas, but the impact was dependent upon habitat type. While meadow bird communities were affected adversely by habitat degradation, with significant drops in species richness on degraded sites, bird species richness in forested riparian habitats was consistently greater on degraded sites. Data for the 6 most common species seen during our study indicated that degradation may have influenced distribution of American Robins ( Turdus migratorius ) and Yellow Warblers ( Dendroica petechia ), but habitat type was the best predictor of abundance for House Wrens ( Troglodytes aedon ), Red-naped Sapsuckers ( Sphyrapicus nuchalis ), Warbling Vircos ( Vireo gilvus ), and Brewer's Blackbirds ( Euphagus cyanocephalus ). Avian species diversity in meadow habitats may be linked to moisture levels during specific times of the year. Diversity increased during the pre-migratory period of the dry year (1994) when compared with that of the breeding season, but was unchanged in the wet year (1995).     

Maternal imprinting of the mouse Snrpn gene and conserved linkage homology with the human Prader-Willi syndrome region.

Prader-Willi syndrome (PWS) is associated with paternal gene deficiencies in human chromosome 15q11-13, suggesting that PWS is caused by a deficiency in one or more maternally imprinted genes. We have now mapped a gene, Snrpn, encoding a brain-enriched small nuclear ribonucleoprotein (snRNP)-associated polypeptide SmN, to mouse chromosome 7 in a region of homology with human chromosome 15q11-13 and demonstrated that Snrpn is a maternally imprinted gene in mouse. These studies, in combination with the accompanying human mapping studies showing that SNRPN maps in the Prader-Willi critical region, identify SNRPN as a candidate gene involved in PWS and suggest that PWS may be caused, in part, by defects in mRNA processing.     

The M-superfamily of conotoxins: a review

The focus of this review is the M-superfamily of Conus venom peptides. Disulfide rich peptides belonging to the M-superfamily have three loop regions and the cysteine arrangement: CC–C–C–CC, where the dashes represent loops one, two, and three, respectively. Characterization of M-superfamily peptides has demonstrated that diversity in cystine connectivity occurs between different branches of peptides even though the cysteine pattern remains consistent. This superfamily is subdivided into five branches, M-1 through M-5, based on the number of residues in the third loop region, between the fourth and fifth cysteine residues. M-superfamily peptides appear to be ubiquitous in Conus venom. They are largely unexplained in indigenous biological function, and they represent an active area of research within the scientific community.