Root architecture governs plasticity in response to drought

Aims

Fine root morphological traits are generally changed under soil nitrogen (N) enrichment, however, the underlying mechanism and functional significance are still not well understood. Our aims were to investigate the linkage of root morphology to anatomy, and its implication for root function at elevated soil N availability.

Methods

Ingrowth cores were used to sample root tips (0–20 cm soil depth) from six temperate tree species growing in monoculture plantations at a common site in northeastern China. Root morphological and anatomical traits were concurrently measured, and their relationships were determined within and among species in both control and N fertilization (10 g N m^?2y^?1) plots.

Results

Root diameter generally increased in all six species (non-significant for Phellodendron amurense) following N fertilization, which was caused by the increased root stele radius rather than cortical thickness. Congruently, N fertilization significantly decreased the ratio of cortical thickness to stele radius, but increased the ratio of total cross-sectional area of conduits to stele area in root tips across all species.

Conclusions

The observed anatomical changes of root tips contributed to the alternations of morphological root traits following N fertilization, with potentially important impacts on root physiological functions, like increased water and nutrient transport.

     

A review of the use of primates in studying human schistosomiasis

Rodents, useful models for studies of human schistosomiasis not ethically possible in man, are not satisfactory in every respect. Primates, in many ways better models than rodents, though too expensive for general use, remain invaluable for testing the relevance of rodent findings to man. Higher primates such as chimpanzees are ideal models but, as endangered species, should only be used for critical studies for which lower, nonhuman primates are unsuitable.     

Free radical pathology in chronic arterial disease

The generation of toxic oxygen metabolites is more usually associated with inflammation. However, pathological free radical reactions can cause tissue damage by adversely affecting prostacyclin (PGI2) synthesis allowing initiation of coagulation. We have assessed changes in the red cell defence to toxic oxygen metabolite generation, viz measurement of glutathione concentration (GSH) and superoxide dismutase activity (SOD). GSH and SOD were measured in 20 patients with peripheral arterial disease, 22 patients with vasculitis, and 11 patients with angina, and compared to 17 matched controls. The 53 subjects with arterial disease had significantly lower SOD levels: in contrast GSH levels were significantly higher. Extracellularly plasma thiol levels (PSH) were low and caeruloplasmin (Cp) levels were high. We suggest that free radical pathology exists not only in inflammatory vascular disease but also in atherosclerosis.     

Longitudinal studies on human schistosomiasis

A major difficulty in understanding the epidemiology of human schistosomiasis has been to distinguish between acquired immunity and reduced exposure as possible reasons for an observed decline, in older individuals, of levels of superinfection or of reinfection after chemotherapy. A series of studies of Schistosoma mansoni infections in Kenya has been undertaken to approach this problem, by investigation of intensities of reinfection after treatment of individuals whose levels of contact with contaminated water is subsequently observed. Intensities of reinfection are highest among younger children, thereafter declining sharply. This decline can be attributed only in part to age-related changes in the duration and nature of exposure; there is also evidence for the development of an acquired resistance to reinfection that is dependent both on age and on previous experience of infection, and that may be immunologically mediated. Evidence has been obtained that the slow development of this acquired immunity with age may be associated with the early development and subsequent slow decline of inappropriate immune responses that 'block' the effect of potentially protective responses. Implications of these findings for immunological intervention through vaccination are discussed.     

Soluble LDL-R are formed by cell surface cleavage in response to phorbol esters.

A 140-kDa soluble form of the low density lipoprotein (LDL) receptor has been isolated from the culture medium of HepG2 cells and a number of other cell types. It is produced from the 160-kDa mature LDL receptor by a proteolytic cleavage, which is stimulated in the presence of 4beta-phorbol 12-myristate 13-acetate (PMA), leading to the release of a soluble fragment that constitutes the bulk of the extracellular domain of the LDL receptor. By labeling HepG2 cells with [35S]methionine and chasing in the presence of PMA, we demonstrated that up to 20% of LDL-receptors were released into the medium in a 2-h period. Simultaneously, the level of labeled cellular receptors was reduced by 30% in those cells treated with PMA compared to untreated cells, as was the total number of cell surface LDL-receptors assayed by the binding of 125I-labeled antibody to whole cells. To determine if endocytosis was required for cleavage, internalization-defective LDL-receptors were created by mutagenesis or deletion of the NPXY internalization signal, transfected into Chinese hamster ovary cells, and assayed for cleavage in the presence and absence of PMA. Cleavage was significantly greater in the case of the mutant receptors than for wild-type receptors, both in the absence and presence of PMA. Similar results were seen in human skin fibroblasts homozygous for each of the internalization-defective LDL receptor phenotypes. LDL receptor cleavage was inhibited by the hydoxamate-based inhibitor TAPI, indicating the resemblance of the LDL receptor cleavage mechanism to that of other surface released membrane proteins.     

HyLiTE: accurate and flexible analysis of gene expression in hybrid and allopolyploid species

Background

Forming a new species through the merger of two or more divergent parent species is increasingly seen as a key phenomenon in the evolution of many biological systems. However, little is known about how expression of parental gene copies (homeologs) responds following genome merger. High throughput RNA sequencing now makes this analysis technically feasible, but tools to determine homeolog expression are still in their infancy.

Results

Here we present HyLiTE – a single-step analysis to obtain tables of homeolog expression in a hybrid or allopolyploid and its parent species directly from raw mRNA sequence files. By implementing on-the-fly detection of diagnostic parental polymorphisms, HyLiTE can perform SNP calling and read classification simultaneously, thus allowing HyLiTE to be run as parallelized code. HyLiTE accommodates any number of parent species, multiple data sources (including genomic DNA reads to improve SNP detection), and implements a statistical framework optimized for genes with low to moderate expression.

Conclusions

HyLiTE is a flexible and easy-to-use program designed for bench biologists to explore patterns of gene expression following genome merger. HyLiTE offers practical advantages over manual methods and existing programs, has been designed to accommodate a wide range of genome merger systems, can identify SNPs that arose following genome merger, and offers accurate performance on non-model organisms.

Electronic supplementary material

The online version of this article (doi:10.1186/s12859-014-0433-8) contains supplementary material, which is available to authorized users.     

High-Resolution Crystal Structures of Drosophila melanogaster Angiotensin-Converting Enzyme in Complex with Novel Inhibitors and Antihypertensive Drugs

Angiotensin I-converting enzyme (ACE), one of the central components of the renin-angiotensin system, is a key therapeutic target for the treatment of hypertension and cardiovascular disorders. Human somatic ACE (sACE) has two homologous domains (N and C). The N- and C-domain catalytic sites have different activities toward various substrates. Moreover, some of the undesirable side effects of the currently available and widely used ACE inhibitors may arise from their targeting both domains leading to defects in other pathways. In addition, structural studies have shown that although both these domains have much in common at the inhibitor binding site, there are significant differences and these are greater at the peptide binding sites than regions distal to the active site. As a model system, we have used an ACE homologue from Drosophila melanogaster (AnCE, a single domain protein with ACE activity) to study ACE inhibitor binding. In an extensive study, we present high-resolution structures for native AnCE and in complex with six known antihypertensive drugs, a novel C-domain sACE specific inhibitor, lisW-S, and two sACE domain-specific phosphinic peptidyl inhibitors, RXPA380 and RXP407 (i.e., nine structures). These structures show detailed binding features of the inhibitors and highlight subtle changes in the orientation of side chains at different binding pockets in the active site in comparison with the active site of N- and C-domains of sACE. This study provides information about the structure-activity relationships that could be utilized for designing new inhibitors with improved domain selectivity for sACE.     

Identification and characterization of the intracellular poly-3-hydroxybutyrate depolymerase enzyme PhaZ of Sinorhizobium meliloti

Background  

S. meliloti forms indeterminate nodules on the roots of its host plant alfalfa (Medicago sativa). Bacteroids of indeterminate nodules are terminally differentiated and, unlike their non-terminally differentiated counterparts in determinate nodules, do not accumulate large quantities of Poly-3-hydroxybutyrate (PHB) during symbiosis. PhaZ is in intracellular PHB depolymerase; it represents the first enzyme in the degradative arm of the PHB cycle in S. meliloti and is the only enzyme in this half of the PHB cycle that remains uncharacterized.     

Novel ketomethylene inhibitors of angiotensin I-converting enzyme (ACE): inhibition and molecular modelling

Inhibition of angiotensin I-converting enzyme (ACE) has become an effective strategy in the treatment of hypertension and cardiovascular disease. Keto-ACE, a previously described C-domain selective ACE inhibitor, was used as the basis for the design, synthesis and molecular modelling of a series of novel ketomethylene derivatives for which ACE inhibition profiles and structural characterisation are reported. Ki determinations indicated that the introduction of a bulky aromatic tryptophan at the P2' position of keto-ACE significantly increased selectivity for the C-domain, while an aliphatic P2 Boc group conferred N-domain selectivity. These data were supported by the potential energies of the compounds docked with the C- and N-domains of ACE.