Predictable ecological response to rising CO2 of a community of marine phytoplankton

Rising atmospheric CO₂ and ocean acidification are fundamentally altering conditions for life of all marine organisms, including phytoplankton. Differences in CO₂ related physiology between major phytoplankton taxa lead to differences in their ability to take up and utilize CO₂. These differences may cause predictable shifts in the composition of marine phytoplankton communities in response to rising atmospheric CO₂. We report an experiment in which seven species of marine phytoplankton, belonging to four major taxonomic groups (cyanobacteria, chlorophytes, diatoms, and coccolithophores), were grown at both ambient (500 μatm) and future (1,000 μatm) CO₂ levels. These phytoplankton were grown as individual species, as cultures of pairs of species and as a community assemblage of all seven species in two culture regimes (high‐nitrogen batch cultures and lower‐nitrogen semicontinuous cultures, although not under nitrogen limitation). All phytoplankton species tested in this study increased their growth rates under elevated CO₂ independent of the culture regime. We also find that, despite species‐specific variation in growth response to high CO₂, the identity of major taxonomic groups provides a good prediction of changes in population growth and competitive ability under high CO₂. The CO₂‐induced growth response is a good predictor of CO₂‐induced changes in competition (R² > .93) and community composition (R² > .73). This study suggests that it may be possible to infer how marine phytoplankton communities respond to rising CO₂ levels from the knowledge of the physiology of major taxonomic groups, but that these predictions may require further characterization of these traits across a diversity of growth conditions. These findings must be validated in the context of limitation by other nutrients. Also, in natural communities of phytoplankton, numerous other factors that may all respond to changes in CO2, including nitrogen fixation, grazing, and variation in the limiting resource will likely complicate this prediction.     

Localisation of Formyl-Peptide Receptor 2 in the Rat Central Nervous System and Its Role in Axonal and Dendritic Outgrowth

Arachidonic acid and docosahexaenoic acid (DHA) released by the action of phospholipases A₂ (PLA₂) on membrane phospholipids may be metabolized by lipoxygenases to the anti-inflammatory mediators lipoxin A4 (LXA4) and resolvin D1 (RvD1), and these can bind to a common receptor, formyl-peptide receptor 2 (FPR2). The contribution of this receptor to axonal or dendritic outgrowth is unknown. The present study was carried out to elucidate the distribution of FPR2 in the rat CNS and its role in outgrowth of neuronal processes. FPR2 mRNA expression was greatest in the brainstem, followed by the spinal cord, thalamus/hypothalamus, cerebral neocortex, hippocampus, cerebellum and striatum. The brainstem and spinal cord also contained high levels of FPR2 protein. The cerebral neocortex was moderately immunolabelled for FPR2, with staining mostly present as puncta in the neuropil. Dentate granule neurons and their axons (mossy fibres) in the hippocampus were very densely labelled. The cerebellar cortex was lightly stained, but the deep cerebellar nuclei, inferior olivary nucleus, vestibular nuclei, spinal trigeminal nucleus and dorsal horn of the spinal cord were densely labelled. Electron microscopy of the prefrontal cortex showed FPR2 immunolabel mostly in immature axon terminals or ‘pre-terminals’, that did not form synapses with dendrites. Treatment of primary hippocampal neurons with the FPR2 inhibitors, PBP10 or WRW4, resulted in reduced lengths of axons and dendrites. The CNS distribution of FPR2 suggests important functions in learning and memory, balance and nociception. This might be due to an effect of FPR2 in mediating arachidonic acid/LXA4 or DHA/RvD1-induced axonal or dendritic outgrowth.     

Conjugative plasmids of enteric bacteria from many different incompatibility groups have similar genes for single-stranded DNA-binding proteins.

Among 30 conjugative plasmids of enteric bacteria from 23 incompatibility (Inc) groups, we found 19 (from 12 Inc groups) which can complement defects caused by a defective single-stranded DNA-binding protein of Escherichia coli K-12. The genes which are responsible for the complementation from three of these plasmids (Inc groups I1, Y, and 9) were cloned. These genes showed extensive homology with each other and with the E. coli F factor ssb gene (formerly denoted ssf), which codes for a single-stranded DNA binding protein. The proteins coded for by the cloned genes bound tightly to single-stranded DNA. Six other ssb- -complementing plasmids were tested for homology to the F factor ssb gene, and all of these showed homology, as did one of the ssb- -noncomplementing plasmids. Plasmids from a total of 13 different Inc groups of enteric bacteria were found to be likely to have genes with some homology to the ssb gene of the F factor. For plasmids from several different Inc groups, we found no evidence for strong homology with ssb of the F factor.     

Amino acid sequence versus morphological data and the interordinal relationships of mammals

To a large extent, the mutual affinities of the mammalian orders continue to puzzle systematists, even though comparative anatomy and amino acid sequencing offer a massive data base from which these relationships could potentially be adduced. In the present paper the consistency index--the number of character states less the number of characters in a data set, divided by the total number of changes in the character states on a cladogram--was used to examine the relative resolving powers of recently published morphological and molecular- sequence data. Consistency indices were calculated for previously published alpha crystallin A chain and myoglobin amino acid-sequence cladograms and for four original amino acid-sequence cladograms (alpha crystallin A, myoglobin, and alpha and beta hemoglobin); these were found to be comparable to the consistency indices of morphologically based cladograms. Qualitative comparisons between the morphologically based and molecularly based trees were also made; only moderate congruence between the two was observed. Moreover, there was a general lack of congruence between the cladograms specified by each of the four proteins. Amino acid-sequence and morphological data agreed on the placement of edentates as an early eutherian offshoot and on the grouping of hyracoids, proboscideans, and sirenians. Otherwise there was only limited congruence: morphology strongly supported the grouping of lagomorphs and rodents and the alliance of pholidotes and edentates, but sequence analyses did not. The placement of tubulidentates differed widely among proteins. Morphology indicated the close association of sirenians with proboscideans; proteins suggested a pairing of sirenians with hyracoids. Sequence data did not identify many (morphologically well-diagnosed) orders as monophyletic (e.g., Lagomorpha).(ABSTRACT TRUNCATED AT 250 WORDS)      

A single gene encodes soluble and membrane-bound forms of the major histocompatibility Qa-2 antigen: anchoring of the product by a phospholipid tail

The H-2, Qa, and Tla genes of the murine major histocompatibility complex are related to each other by DNA sequence homology. The H-2 genes encode ubiquitously expressed transplantation antigens that serve as recognition structures for cytotoxic T cells. The identities of the Qa and Tla products, their sites of expression, and their functions are largely unknown. We report here that the Qa region gene Q7 encodes a membrane-bound as well as a secreted form of the serologically defined antigen Qa-2. The Q7 gene introduced into liver-derived cells is expressed as a membrane-bound and as a secreted molecule. In transfected L cells it is expressed only as a soluble protein. Biochemical analysis suggests that the Q7 product is anchored to the liver cell membranes by a phospholipid tail. This feature may be responsible for cell type-specific expression of the two forms of the Qa-2 molecules.     

Cell-specific processing of preprosomatostatin in cultured neuroendocrine cells

We have previously found that preprosomatostatin is processed accurately to both somatostatin-14 and somatostatin-28 in pituitary gonadotrophs of transgenic mice. The foreign somatostatin peptides have been shown to enter the regulated secretory pathway of these cells. To determine whether accurate preprosomatostatin processing can occur in any neuroendocrine cell, we introduced preprosomatostatin cDNA expression vectors into several different neuroendocrine cell lines. We found that prosomatostatin was cleaved efficiently to somatostatin-14 and somatostatin-28 in RIN 5F and AtT20 cells, but not in GH4 or PC12 cells. The ability of a particular cell type to process prosomatostatin did not correlate with cellular storage capacity and was independent of the level of biosynthesis of the precursor. These data suggest that prosomatostatin processing requires specific pathways which are present in some neuroendocrine cells, but not in others.     

Removal of covalently bound inositol from Torpedo acetylcholinesterase and mammalian alkaline phosphatases by deamination with nitrous acid. Evidence for a common membrane-anchoring structure.

Our earlier evidence suggested that both acetylcholinesterase and alkaline phosphatase are anchored to the cell surface via covalently-attached phosphatidylinositol [Low, Futerman, Ferguson & Silman (1986) Trends Biochem. Sci. 11, 212-215]. We now present chemical data, based upon a nitrous acid deamination reaction, showing that in both proteins the phosphatidylinositol moiety is attached through a glycosidic linkage to a sugar residue bearing a free amino group.     

Direct measurement of inositol in bovine myelin basic protein.

Myelin basic protein has been isolated from bovine central-nervous-system myelin by four methods, none of which exposes the protein to acid. After purification the inositol content of both hydrolysed and unhydrolysed protein was quantified by g.c.-m.s. Basic protein prepared by all methods contained less than 4 mol % of inositol. It is concluded, contrary to a previous proposal, that covalent binding to phosphoinositides does not represent a general mechanism for attachment of this cytoplasmically-oriented protein to its membrane.     

Renal dipeptidase is one of the membrane proteins released by phosphatidylinositol-specific phospholipase C.

4,4-Di-isothiocyanostilbene-2,2'-disulphonic acid inhibition of taurocholate efflux from canalicular vesicles was used to demonstrate that potential driven and 'carrier'-mediated canalicular excretion of taurocholate occur via a common, rather than two separate, pathways. This electrogenic canalicular bile acid 'carrier' preferentially transports trihydroxylated and conjugated dihydroxylated bile acids, but not the unphysiological oxo bile acids, and possibly extends its substrate specificity to other amphipathic molecules such as sulphobromophthalein.