Multi-scale phylogenetic structure in coastal dune plant communities across the globe

Aims Studies integrating phylogenetic history and large-scale community assembly are few, and many questions remain unanswered. Here, we use a global coastal dune plant data set to uncover the important factors in community assembly across scales from the local filtering processes to the global long-term diversification and dispersal dynamics. Coastal dune plant communities occur worldwide under a wide range of climatic and geologic conditions as well as in all biogeographic regions. However, global patterns in the phylogenetic composition of coastal dune plant communities have not previously been studied.Methods The data set comprised vegetation data from 18463 plots in New Zealand, South Africa, South America, North America and Europe. The phylogenetic tree comprised 2241 plant species from 149 families. We calculated phylogenetic clustering (Net Relatedness Index, NRI, and Nearest Taxon Index, NTI) of regional dune floras to estimate the amount of in situ diversification relative to the global dune species pool and evaluated the relative importance of land and climate barriers for these diversification patterns by geographic analyses of phylogenetic similarity. We then tested whether dune plant communities exhibit similar patterns of phylogenetic structure within regions. Finally, we calculated NRI for local communities relative to the regional species pool and tested for an association with functional traits (plant height and seed mass) thought to vary along sea–inland gradients.Important findings Regional species pools were phylogenetically clustered relative to the global pool, indicating regional diversification. NTI showed stronger clustering than NRI pointing to the importance of especially recent diversifications within regions. The species pools grouped phylogenetically into two clusters on either side of the tropics suggesting greater dispersal rates within hemispheres than between hemispheres. Local NRI plot values confirmed that most communities were also phylogenetically clustered within regions. NRI values decreased with increasing plant height and seed mass, indicating greater phylogenetic clustering in communities with short maximum height and good dispersers prone to wind and tidal disturbance as well as salt spray, consistent with environmental filtering along sea–inland gradients. Height and seed mass both showed significant phylogenetic signal, and NRI tended to correlate negatively with both at the plot level. Low NRI plots tended to represent coastal scrub and forest, whereas high NRI plots tended to represent herb-dominated vegetation. We conclude that regional diversification processes play a role in dune plant community assembly, with convergence in local phylogenetic community structure and local variation in community structure probably reflecting consistent coastal-inland gradients. Our study contributes to a better understanding of the globally distributed dynamic coastal ecosystems and the structuring factors working on dune plant communities across spatial scales and regions.     

Mutation-selection models of codon substitution and their use to estimate selective strengths on codon usage

Current models of codon substitution are formulated at the levels of nucleotide substitution and do not explicitly consider the separate effects of mutation and selection. They are thus incapable of inferring whether mutation or selection is responsible for evolution at silent sites. Here we implement a few population genetics models of codon substitution that explicitly consider mutation bias and natural selection at the DNA level. Selection on codon usage is modeled by introducing codon-fitness parameters, which together with mutation-bias parameters, predict optimal codon frequencies for the gene. The selective pressure may be for translational efficiency and accuracy or for fine-tuning translational kinetics to produce correct protein folding. We apply the models to compare mitochondrial and nuclear genes from several mammalian species. Model assumptions concerning codon usage are found to affect the estimation of sequence distances (such as the synonymous rate d(S), the nonsynonymous rate d(N), and the rate at the 4-fold degenerate sites d(4)), as found in previous studies, but the new models produced very similar estimates to some old ones. We also develop a likelihood ratio test to examine the null hypothesis that codon usage is due to mutation bias alone, not influenced by natural selection. Application of the test to the mammalian data led to rejection of the null hypothesis in most genes, suggesting that natural selection may be a driving force in the evolution of synonymous codon usage in mammals. Estimates of selection coefficients nevertheless suggest that selection on codon usage is weak and most mutations are nearly neutral. The sensitivity of the analysis on the assumed mutation model is discussed.     

The 20S Proteasome as an Assembly Platform for the 19S Regulatory Complex

26S proteasomes consist of cylindrical 20S proteasomes with 19S regulatory complexes attached to the ends. Treatment with high concentrations of salt causes the regulatory complexes to separate into two sub-complexes, the base, which is in contact with the 20S proteasome, and the lid, which is the distal part of the 19S complex. Here, we describe two assembly intermediates of the human regulatory complex. One is a dimer of the two ATPase subunits, Rpt3 and Rpt6. The other is a complex of nascent Rpn2, Rpn10, Rpn11, Rpn13, and Txnl1, attached to preexisting 20S proteasomes. This early assembly complex does not yet contain Rpn1 or any of the ATPase subunits of the base. Thus, assembly of 19S regulatory complexes takes place on preexisting 20S proteasomes, and part of the lid is assembled before the base.     

Genetic variability within the innate immune system influences personality traits in women

Raised levels of inflammation markers have been associated with several mental disorders; however, studies regarding the relationship between inflammation or the immune system and various aspects of human behaviour are not numerous. The aim of the present study was to investigate whether an association exists between personality traits and two single nucleotide polymorphisms located in genes that are associated with the innate immune system. The studied population consisted of 42-year-old women recruited from the population registry that had been assessed by means of Karolinska Scales of Personality, a self-reported inventory. The first polymorphism, +1444C>T (rs1130864), is located in the gene coding for C-reactive protein (CRP), a marker of low-grade inflammation. The T-allele has previously been suggested to be linked to raised serum levels of CRP. The second polymorphism, Y402H (1277T>C, rs1061170), is located in the gene coding for complement factor H, an important regulator of the complement system. The C-allele has consistently been associated with age-related macular degeneration. While the +1444T allele was associated with higher scores in the personality traits impulsiveness, monotony avoidance and social desirability, the 1277C polymorphism was associated with higher scores in verbal aggression and lower scores in social desirability. In conclusion, the associations between the personality traits and the studied polymorphisms further support the possible influence of the immune system on mental functions.     

A trypsin-like protease with apparent dual function in early Lepeophtheirus salmonis (Kr?yer) development

Background  

Trypsin-like serine proteases are involved in a large number of processes including digestive degradation, regulation of developmental processes, yolk degradation and yolk degradome activation. Trypsin like peptidases considered to be involved in digestion have been characterized in Lepeophtheirus salmonis. During these studies a trypsin-like peptidase which differed in a number of traits were identified.     

Dimerisation and an increase in active site aromatic groups as adaptations to high temperatures: X-ray solution scattering and substrate-bound crystal structures of Rhodothermus marinus endoglucanase Cel12A

Cellulose, a polysaccharide consisting of beta-1,4-linked glucose, is the major component of plant cell walls and consequently one of the most abundant biopolymers on earth. Carbohydrate polymers such as cellulose are molecules with vast diversity in structure and function, and a multiplicity of hydrolases operating in concert are required for depolymerisation. The bacterium Rhodothermus marinus, isolated from shallow water marine hot springs, produces a number of carbohydrate-degrading enzymes including a family 12 cellulase Cel12A. The structure of R.marinus Cel12A in the ligand-free form (at 1.54 angstroms) and structures of RmCel12A after crystals were soaked in cellopentaose for two different lengths of time, have been determined. The shorter soaked complex revealed the conformation of unhydrolysed cellotetraose, while cellopentaose had been degraded more completely during the longer soak. Comparison of these structures with those of mesophilic family 12 cellulases in complex with inhibitors and substrate revealed that RmCel12A has a more extensive aromatic network in the active site cleft which ejects products after hydrolysis. The substrate structure confirms that during hydrolysis by family 12 cellulases glucose does not pass through a (2,5)B conformation. Small-angle X-ray scattering analysis of RmCel12A showed that the enzyme forms a loosely associated antiparallel dimer in solution, which may target the enzyme to the antiparallel polymer strands in cellulose.     

Adrm1, a putative cell adhesion regulating protein, is a novel proteasome-associated factor

We have identified Adrm1 as a novel component of the regulatory ATPase complex of the 26 S proteasome: Adrm1 was precipitated with an antibody to proteasomes and vice versa. Adrm1 co-migrated with proteasomes on gel-filtration chromatography and non-denaturing polyacrylamide gel electrophoresis. Adrm1 has been described as an interferon-gamma-inducible, heavily glycosylated membrane protein of 110 kDa. However, we found Adrm1 in mouse tissues only as a 42 kDa peptide, corresponding to the mass of the non-glycosylated peptide chain, and it could not be induced in HeLa cells with interferon. Adrm1 was present almost exclusively in soluble 26 S proteasomes, albeit a small fraction was membrane-associated, like proteasomes. Adrm1 was found in cells in amounts equimolar with S6a, a 26 S proteasome subunit. HeLa cells contain no pool of free Adrm1 but recombinant Adrm1 could bind to pre-existing 26 S proteasomes in cell extracts. Adrm1 may be distantly related to the yeast proteasome subunit Rpn13, mutants of which are reported to display no obvious phenotype. Accordingly, knock-down of Adrm1 in HeLa cells had no effect on the amount of proteasomes, or on degradation of bulk cell protein, or accumulation of polyubiquitinylated proteins. This indicates that Adrm1 has a specialised role in proteasome function.     

The disordered PCI‐binding human proteins CSNAP and DSS1 have diverged in structure and function

Intrinsically disordered proteins (IDPs) regularly constitute components of larger protein assemblies contributing to architectural stability. Two small, highly acidic IDPs have been linked to the so‐called PCI complexes carrying PCI‐domain subunits, including the proteasome lid and the COP9 signalosome. These two IDPs, DSS1 and CSNAP, have been proposed to have similar structural propensities and functions, but they display differences in their interactions and interactome sizes. Here we characterized the structural properties of human DSS1 and CSNAP at the residue level using NMR spectroscopy and probed their propensities to bind ubiquitin. We find that distinct structural features present in DSS1 are completely absent in CSNAP, and vice versa, with lack of relevant ubiquitin binding to CSNAP, suggesting the two proteins to have diverged in both structure and function. Our work additionally highlights that different local features of seemingly similar IDPs, even subtle sequence variance, may endow them with different functional traits. Such traits may underlie their potential to engage in multiple interactions thereby impacting their interactome sizes.     

Contrasting demographic histories of the neighboring bonobo and chimpanzee

The Pleistocene epoch was a period of dramatic climate change that had profound impacts on the population sizes of many animal species. How these species were shaped by past events is often unclear, hindering our understanding of the population dynamics resulting in present day populations. We analyzed complete mitochondrial genomes representing all four recognized chimpanzee subspecies and the bonobo to infer the recent demographic history and used simulations to exclude a confounding effect of population structure. Our genus-wide Bayesian coalescent-based analysis revealed surprisingly dissimilar demographic histories of the chimpanzee subspecies and the bonobo, despite their overlapping habitat requirements. Whereas the central and eastern chimpanzee subspecies were inferred to have expanded tenfold between around 50,000 and 80,000 years ago and today, the population size of the neighboring bonobo remained constant. The changes in population size are likely linked to changes in habitat area due to climate oscillations during the late Pleistocene. Furthermore, the timing of population expansion for the rainforest-adapted chimpanzee is concurrent with the expansion of the savanna-adapted human, which could suggest a common response to changed climate conditions around 50,000–80,000 years ago.     

Herp regulates Hrd1-mediated ubiquitylation in a ubiquitin-like domain-dependent manner

Accumulation of aberrant proteins in the endoplasmic reticulum (ER) triggers the unfolded protein response pathway that helps the cell to survive under these stress conditions. Herp is a mammalian ubiquitin domain protein, which is strongly induced by the unfolded protein response. It is involved in ER-associated protein degradation (ERAD) and interacts directly with the ubiquitin ligase Hrd1, which is found in high molecular mass complexes of the ER membrane. Here we present the first evidence that Herp regulates Hrd1-mediated ubiquitylation in a ubiquitin-like (UBL) domain-dependent manner. We found that upon exposure of cells to ER stress, elevation of Herp steady state levels is accompanied by an enhanced association of Herp with pre-existing Hrd1. Hrd1-associated Herp is rapidly degraded and substituted by de novo synthesized Herp, suggesting a continuous turnover of the protein at Hrd1 complexes. Further analysis revealed the presence of multiple Hrd1 copies in a single complex enabling binding of a variable number of Herp molecules. Efficient ubiquitylation of the Hrd1-specific ERAD substrate α1-antitrypsin null Hong Kong (NHK) required the presence of the Herp UBL domain, which was also necessary for NHK degradation. In summary, we propose that binding of Herp to Hrd1-containing ERAD complexes positively regulates the ubiquitylation activity of these complexes, thus permitting survival of the cell during ER stress.