Departures from neutrality induced by niche and relative fitness differences

© The Author(s), 2015. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Theoretical Ecology 8 (2015): 449-465, doi:10.1007/s12080-015-0261-0.Breaking the core assumption of ecological equivalence in Hubbell’s “neutral theory of biodiversity” requires a theory of species differences. In one framework for characterizing differences between competing species, non-neutral interactions are said to involve both niche differences, which promote stable coexistence, and relative fitness differences, which promote competitive exclusion. We include both in a stochastic community model in order to determine if relative fitness differences compensate for changes in community structure and dynamics induced by niche differences, possibly explaining neutral theory’s apparent success. We show that species abundance distributions are sensitive to both niche and relative fitness differences, but that certain combinations of differences result in abundance distributions that are indistinguishable from the neutral case. In contrast, the distribution of species’ lifetimes, or the time between speciation and extinction, differs under all combinations of niche and relative fitness differences. The results from our model experiment are inconsistent with the hypothesis of “emergent neutrality” and support instead a hypothesis that relative fitness differences counteract effects of niche differences on distributions of abundance. However, an even more developed theory of interspecific variation appears necessary to explain the diversity and structure of non-neutral communities.The research was funded by NSF grant ECCS-0835847 and a postdoctoral scholarship from the Woods Hole Oceanographic Institution

Niche and fitness differences relate the maintenance of diversity to ecosystem function: reply

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134128/1/ecy20129361487.pd

Niche and fitness differences relate the maintenance of diversity to ecosystem function

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/116920/1/ecy20119251157.pd

Pathways to Accelerated Carbon Mineralization in Mine Tailings

Alkaline waste generated from mining of magnesium silicate rocks reacts spontaneously with atmospheric carbon dioxide (CO2) to precipitate carbon in solid mineral form. The total capacity of these mine tailings to sequester carbon is about ten times greater than greenhouse gas emissions of associated mining and mineral processing. Waste from mining activity globally has capacity to sequester 100-200 Mt of CO2 per year. However passive, or unintentional, CO2 mineralization at individual mine sites is modest (1-50 kt/yr), and typically limited by CO2 supply. Acceleration of these reactions represents an opportunity to generate considerable greenhouse gas offsets for the industry, and to develop expertise in carbon mineralization that is relevant to accelerated weathering at Earth’s surface and mineral trapping in low temperature aquifers and reservoirs. Experimental acceleration of carbon mineralization is readily achieved through enhanced delivery of CO2, wherein reaction rates are limited by rates of cation (e.g., Mg2+) supply from mineral dissolution. Further acceleration requires optimization of mineral dissolution processes. Continuous-flow dissolution experiments on minerals and mine tailings exhibit rapid, transient cation release rates that decay to slower rates indicative of conventional steady-state bulk mineral dissolution processes (Fig. 1A). The transient initial phase of the experiments can release a significant amount (5-10%) of the total cation content of the material. It reflects the dissolution of highly soluble trace minerals, and surface processes in sheet silicate minerals which together we take to represent the labile cation capacity of the material. Longer-term steady-state cation release is much slower and represents recalcitrant cation capacity indicative of bulk mineral dissolution. The labile cation content represents the carbon mineralization capacity of alkaline mine wastes accessible with existing low-cost technologies while recalcitrant cation content is unlikely to be tapped at existing carbon prices (Fig. 1B). Measured labile cation content of mine tailings varies substantially between and within deposits, with implications for how carbon mineralization capacity should be characterized and how carbonation intervention would be incorporated into mine operations. Specific mines and specific alteration types with high labile cation content, which for some mines is sufficient to offset total mine greenhouse gas emissions, should be the focus of pilot scale carbon mineralization projects. Please click Additional Files below to see the full abstract

Post-translational modifications near the quinone binding site of mammalian complex I.

Complex I (NADH:ubiquinone oxidoreductase) in mammalian mitochondria is an L-shaped assembly of 44 protein subunits with one arm buried in the inner membrane of the mitochondrion and the orthogonal arm protruding about 100 Å into the matrix. The protruding arm contains the binding sites for NADH, the primary acceptor of electrons flavin mononucleotide (FMN), and a chain of seven iron-sulfur clusters that carries the electrons one at a time from FMN to a coenzyme Q molecule bound in the vicinity of the junction between the two arms. In the structure of the closely related bacterial enzyme from Thermus thermophilus, the quinone is thought to bind in a tunnel that spans the interface between the two arms, with the quinone head group close to the terminal iron-sulfur cluster, N2. The tail of the bound quinone is thought to extend from the tunnel into the lipid bilayer. In the mammalian enzyme, it is likely that this tunnel involves three of the subunits of the complex, ND1, PSST, and the 49-kDa subunit. An arginine residue in the 49-kDa subunit is symmetrically dimethylated on the ω-N(G) and ω-N(G') nitrogen atoms of the guanidino group and is likely to be close to cluster N2 and to influence its properties. Another arginine residue in the PSST subunit is hydroxylated and probably lies near to the quinone. Both modifications are conserved in mammalian enzymes, and the former is additionally conserved in Pichia pastoris and Paracoccus denitrificans, suggesting that they are functionally significant

Enteric bacterial proteases in inflammatory bowel disease- pathophysiology and clinical implications

Numerous reports have identified a dysbiosis in the intestinal microbiota in patients suffering from inflammatory bowel diseases (IBD), yet the mechanism(s) in which this complex microbial community initiates or perpetuates inflammation remains unclear. The purpose of this review is to present evidence for one such mechanism that implicates enteric microbial derived proteases in the pathogenesis of IBD. We highlight and discuss studies demonstrating that proteases and protease receptors are abundant in the digestive system. Additionally, we investigate studies demonstrating an association between increased luminal protease activity and activation of protease receptors, ultimately resulting in increased intestinal permeability and exacerbation of colitis in animal models as well as in human IBD. Proteases are essential for the normal functioning of bacteria and in some cases can serve as virulence factors for pathogenic bacteria. Although not classified as traditional virulence factors, proteases originating from commensal enteric bacteria also have a potential association with intestinal inflammation via increased enteric permeability. Reports of increased protease activity in stools from IBD patients support a possible mechanism for a dysbiotic enteric microbiota in IBD. A better understanding of these pathways and characterization of the enteric bacteria involved, their proteases, and protease receptors may pave the way for new therapeutic approaches for these diseases

Striving for safety: communicating and deciding in sociotechnical systems

How do communications and decisions impact the safety of sociotechnical systems? This paper frames this question in the context of a dynamic system of nested sub-systems. Communications are related to the construct of observability (i.e. how components integrate information to assess the state with respect to local and global constraints). Decisions are related to the construct of controllability (i.e. how component sub-systems act to meet local and global safety goals). The safety dynamics of sociotechnical systems are evaluated as a function of the coupling between observability and controllability across multiple closed-loop components. Two very different domains (nuclear power and the limited service food industry) provide examples to illustrate how this framework might be applied. While the dynamical systems framework does not offer simple prescriptions for achieving safety, it does provide guides for exploring specific systems to consider the potential fit between organisational structures and work demands, and for generalising across different systems regarding how safety can be managed

NDUFAF7 methylates arginine 85 in the NDUFS2 subunit of human complex I.

Complex I (NADH ubiquinone oxidoreductase) in mammalian mitochondria is an L-shaped assembly of 44 subunits. One arm is embedded in the inner membrane with the other protruding ∼100 Å into the matrix of the organelle. The extrinsic arm contains binding sites for NADH and the primary electron acceptor FMN, and it provides a scaffold for seven iron-sulfur clusters that form an electron pathway linking FMN to the terminal electron acceptor, ubiquinone, which is bound in the region of the junction between the arms. The membrane arm contains four antiporter-like domains, probably energetically coupled to the quinone site and involved in pumping protons from the matrix into the intermembrane space contributing to the proton motive force. Complex I is put together from preassembled subcomplexes. Their compositions have been characterized partially, and at least 12 extrinsic assembly factor proteins are required for the assembly of the complex. One such factor, NDUFAF7, is predicted to belong to the family of S-adenosylmethionine-dependent methyltransferases characterized by the presence in their structures of a seven-β-strand protein fold. In the present study, the presence of NDUFAF7 in the mitochondrial matrix has been confirmed, and it has been demonstrated that it is a protein methylase that symmetrically dimethylates the ω-N(G),N(G') atoms of residue Arg-85 in the NDUFS2 subunit of complex I. This methylation step occurs early in the assembly of complex I and probably stabilizes a 400-kDa subcomplex that forms the initial nucleus of the peripheral arm and its juncture with the membrane arm

Can attention to the intestinal microbiota improve understanding and treatment of anorexia nervosa?

Anorexia nervosa (AN) is characterized by severe dietary restriction or other weight loss behaviors and exhibits the highest mortality rate of any psychiatric disorder. Therapeutic renourishment in AN is founded primarily on clinical opinion and guidelines, with a weak evidence base. Genetic factors do not fully account for the etiology of AN, and non-genetic factors that contribute to the onset and persistence of this disease warrant investigation. Compelling evidence that the intestinal microbiota regulates adiposity and metabolism, and more recently, anxiety behavior, provides a strong rationale for exploring the role of this complex microbial community in the onset, maintenance of, and recovery from AN. This review explores the relationship between the intestinal microbiota and AN and a potential role for this enteric microbial community as a therapy for this severe illness

Assembly of the peripheral stalk of ATP synthase in human mitochondria.

The adenosine triphosphate (ATP) synthase in human mitochondria is a membrane bound assembly of 29 proteins of 18 kinds organized into F1-catalytic, peripheral stalk (PS), and c8-rotor ring modules. All but two membrane components are encoded in nuclear genes, synthesized on cytoplasmic ribosomes, imported into the mitochondrial matrix, and assembled into the complex with the mitochondrial gene products ATP6 and ATP8. Intermediate vestigial ATPase complexes formed by disruption of nuclear genes for individual subunits provide a description of how the various domains are introduced into the enzyme. From this approach, it is evident that three alternative pathways operate to introduce the PS module (including associated membrane subunits e, f, and g). In one pathway, the PS is built up by addition to the core subunit b of membrane subunits e and g together, followed by membrane subunit f. Then this b-e-g-f complex is bound to the preformed F1-c8 module by subunits OSCP and F6 The final component of the PS, subunit d, is added subsequently to form a key intermediate that accepts the two mitochondrially encoded subunits. In another route to this key intermediate, first e and g together and then f are added to a preformed F1-c8-OSCP-F6-b-d complex. A third route involves the addition of the c8-ring module to the complete F1-PS complex. The key intermediate then accepts the two mitochondrially encoded subunits, stabilized by the addition of subunit j, leading to an ATP synthase complex that is coupled to the proton motive force and capable of making ATP