bluuebunny/crossref_metadata_2025 huggingface dataset:
The chemokine Bv8/prokineticin 2 is up-regulated in inflammatory granulocytes and modulates inflammatory pain
Authors: Giannini Elisa , Lattanzi Roberta , Nicotra Annalisa , Campese Antonio F. , Grazioli Paola , Screpanti Isabella , Balboni Gianfranco , Salvadori Severo , Sacerdote Paola , Negri Lucia
Published: August 2009

Neutrophil migration into injured tissues is invariably accompanied by pain. Bv8/prokineticin 2 (PK2), a chemokine characterized by a unique structural motif comprising five disulfide bonds, is highly expressed in inflamed tissues associated to infiltrating cells. Here, we demonstrate the fundamental role of granulocyte-derived PK2 (GrPK2) in initiating inflammatory pain and driving peripheral sensitization. In animal models of complete Freund's adjuvant-induced paw inflammation the development and duration of pain temporally correlated with the expression levels of PK2 in the inflamed sites. Such an increase in PK2 mRNA depends mainly on a marked up-regulation ofPK2gene transcription in granulocytes. A substantially lower up-regulation was also detected in macrophages. From a pool of peritoneal granulocytes, elicited in rats by oyster glycogen, we purified the GrPK2 protein, which displayed high affinity for the prokineticin receptors (PKRs) and, when injected into the rat paw, induced hypersensitivity to noxious stimuli as the amphibian prokineticin Bv8 did. Mice lacking PKR1 or PKR2 developed significantly less inflammation-induced hyperalgesia in comparison with WT mice, confirming the involvement of both PKRs in inflammatory pain. The inflammation-induced up-regulation of PK2 was significantly less inpkr1null mice than in WT andpkr2null mice, demonstrating a role of PKR1 in setting PK2 levels during inflammation. Pretreatment with a nonpeptide PKR antagonist, which preferentially binds PKR1, dose-dependently reduced and eventually abolished both prokineticin-induced hypernociception and inflammatory hyperalgesia. Inhibiting PK2 formation or antagonizing PKRs may represent another therapeutic approach for controlling inflammatory pain.
Genetic evidence for the role of Erk activation in a lymphoproliferative disease of mice
Authors: Miyaji Michihiko , Kortum Robert L. , Surana Rishi , Li Wenmei , Woolard Kevin D. , Simpson R. Mark , Samelson Lawrence E. , Sommers Connie L.
Published: August 2009

Germline mutation of the linker for activation of T cells (LAT) gene at the phospholipase C-γ1 (PLC-γ1)-binding site leads to a fatal lymphoproliferative disease in mice. The hyperactivated T cells that develop in these mice have defective T-cell antigen receptor (TCR)-induced calcium flux but enhanced mitogen-activated protein kinase (MAPK) activation. We used genetic analysis to investigate genes whose products might suppress MAPK activation and lymphoproliferative disease in LAT mutant mice. B-lymphocyte adaptor molecule of 32 kDa (Bam32) is a known mediator of MAPK activation in B cells. We recently reported that in CD4
+
T cells, Bam32 deficiency decreased MAPK activation and specifically extracellular-signal-regulated kinase (Erk) signaling, following TCR stimulation. By crossing the Bam32 null mutation onto the LAT knock-in background, we found that the Bam32 null mutation delayed the onset and decreased the severity of lymphoproliferative disease in LAT knock-in mice. The pulmonary lymphocyte infiltration seen in LAT knock-in mice was also markedly decreased in double-mutant mice. Additionally, Erk activation was diminished in LAT knock-in Bam32 knockout CD4
+
T cells. To more accurately determine the role of Erk in this delay of lymphoproliferative disease, we also bred a transgenic, hypersensitive Erk allele (the Erk2 sevenmaker mutant) onto the LAT knock-in Bam32 knockout double-mutant background. These triple transgenic mice demonstrated a role for Erk activation in lymphoproliferative disease caused by the LAT knock-in mutation.
Bioelectronic silicon nanowire devices using functional membrane proteins
Authors: Misra Nipun , Martinez Julio A. , Huang Shih-Chieh J. , Wang Yinmin , Stroeve Pieter , Grigoropoulos Costas P. , Noy Aleksandr
Published: August 2009

Modern means of communication rely on electric fields and currents to carry the flow of information. In contrast, biological systems follow a different paradigm that uses ion gradients and currents, flows of small molecules, and membrane electric potentials. Living organisms use a sophisticated arsenal of membrane receptors, channels, and pumps to control signal transduction to a degree that is unmatched by manmade devices. Electronic circuits that use such biological components could achieve drastically increased functionality; however, this approach requires nearly seamless integration of biological and manmade structures. We present a versatile hybrid platform for such integration that uses shielded nanowires (NWs) that are coated with a continuous lipid bilayer. We show that when shielded silicon NW transistors incorporate transmembrane peptide pores gramicidin A and alamethicin in the lipid bilayer they can achieve ionic to electronic signal transduction by using voltage-gated or chemically gated ion transport through the membrane pores.
Identification of plant cell wall mutants by means of a forward chemical genetic approach using hydrolases
Authors: Gille Sascha , Hänsel Ulrike , Ziemann Mark , Pauly Markus
Published: August 2009

A previously undescribed forward chemical genetic screen using hydrolases affecting the extracellular matrix is introduced. The developed screen takes advantage of the power of chemical genetics and combines it with the known substrate specificity of glycosylhydrolases, resulting in the selection of conditional mutants that exhibit structural defects in their extracellular matrix. Identification of the responsible genetic locus in those mutants significantly extends our knowledge of genes involved in the biosynthesis, metabolism, signaling, and functionality of components of the extracellular matrix. The method is exemplified by a screen of mutagenized Arabidopsis plants subjected to growth in liquid culture in the presence of a xyloglucanase, an enzyme acting on the major cross-linking glycan found in the extracellular matrix of this plant. Using this hydrolase-based screen, dozens of plant cell wall mutants (
xeg
mutants) were identified, leading to the identification of 23 genetic loci that affect plant cell walls. One of the identified loci is
XEG113
, encoding a family 77 glycosyltransferase (GT77). Detailed analysis of the wall of this mutant indicated that its extensins, structural glyocoproteins present in walls, are underarabinosylated.
Xeg-113
plants exhibit more elongated hypocotyls than WT, providing genetic evidence that plant O-glycosylation—more specifically, extensin arabinosylation—is important for cell elongation.
Extracellular acidification exerts opposite actions on TREK1 and TREK2 potassium channels via a single conserved histidine residue
Authors: Sandoz Guillaume , Douguet Dominique , Chatelain Franck , Lazdunski Michel , Lesage Florian
Published: August 2009

Mechanosensitive K+channels TREK1 and TREK2 form a subclass of two P-domain K+channels. They are potently activated by polyunsaturated fatty acids and are involved in neuroprotection, anesthesia, and pain perception. Here, we show that acidification of the extracellular medium strongly inhibits TREK1 with an apparent pK near to 7.4 corresponding to the physiological pH. The all-or-none effect of pH variation is steep and is observed within one pH unit. TREK2 is not inhibited but activated by acidification within the same range of pH, despite its close homology with TREK1. A single conserved residue, H126 in TREK1 and H151 in TREK2, is involved in proton sensing. This histidine is located in the M1P1 extracellular loop preceding the first P domain. The differential effect of acidification, that is, activation for TREK2 and inhibition for TREK1, involves other residues located in the P2M4 loop, linking the second P domain and the fourth membrane-spanning segment. Structural modeling of TREK1 and TREK2 and site-directed mutagenesis strongly suggest that attraction or repulsion between the protonated side chain of histidine and closely located negatively or positively charged residues in P2M4 control outer gating of these channels. The differential sensitivity of TREK1 and TREK2 to external pH variations discriminates between these two K+channels that otherwise share the same regulations by physical and chemical stimuli, and by hormones and neurotransmitters.
Phosphatidylinositol 4,5-bisphosphate (PIP
2
) stimulates the electrogenic Na/HCO
3
cotransporter NBCe1-A expressed in
Xenopus
oocytes
Authors: Wu Jianping , McNicholas Carmel M. , Bevensee Mark O.
Published: August 2009

Bicarbonate transporters are regulated by signaling molecules/ions such as protein kinases, ATP, and Ca
2+
. While phospholipids such as PIP
2
can stimulate Na-H exchanger activity, little is known about phospholipid regulation of bicarbonate transporters. We used the patch-clamp technique to study the function and regulation of heterologously expressed rat NBCe1-A in excised macropatches from
Xenopus laevis
oocytes. Exposing the cytosolic side of inside-out macropatches to a 5% CO
2
/33 mM HCO
3
−
solution elicited a mean inward current of 14 pA in 74% of macropatches attached to pipettes (−V
p
= −60 mV) containing a low-Na
+
, nominally HCO
3
−
-free solution. The current was 80–90% smaller in the absence of Na
+
, approximately 75% smaller in the presence of 200 μM DIDS, and absent in macropatches from H
2
O-injected oocytes. NBCe1-A currents exhibited time-dependent rundown that was inhibited by removing Mg
2+
in the presence or absence of vanadate and F
−
to reduce general phosphatase activity. Applying 5 or 10 μM PIP
2
(diC8) in the presence of HCO
3
−
induced an inward current in 54% of macropatches from NBC-expressing, but not H
2
O-injected oocytes. PIP
2
-induced currents were HCO
3
−
-dependent and somewhat larger following more NBCe1-A rundown, 62% smaller in the absence of Na
+
, and 90% smaller in the presence of 200 μM DIDS. The polycation neomycin (250–500 μM) reduced the PIP
2
-induced inward current by 69%; spermine (100 μM) reduced the current by 97%. Spermine, poly-D-lysine, and neomycin all reduced the baseline HCO
3
−
-induced inward currents by as much as 85%. In summary, PIP
2
stimulates NBCe1-A activity, and phosphoinositides are regulators of bicarbonate transporters.
Mutations at the
BLK
locus linked to maturity onset diabetes of the young and β-cell dysfunction
Authors: Borowiec Maciej , Liew Chong W. , Thompson Ryan , Boonyasrisawat Watip , Hu Jiang , Mlynarski Wojciech M. , El Khattabi Ilham , Kim Sung-Hoon , Marselli Lorella , Rich Stephen S. , Krolewski Andrzej S. , Bonner-Weir Susan , Sharma Arun , Sale Michele , Mychaleckyj Josyf C. , Kulkarni Rohit N. , Doria Alessandro
Published: August 2009

Maturity-onset diabetes of the young (MODY) is a subtype of diabetes defined by an autosomal pattern of inheritance and a young age at onset, often before age 25. MODY is genetically heterogeneous, with 8 distinct MODY genes identified to date and more believed to exist. We resequenced 732 kb of genomic sequence at 8p23 in 6 MODY families unlinked to known MODY genes that showed evidence of linkage at that location. Of the 410 sequence differences that we identified, 5 had a frequency <1% in the general population and segregated with diabetes in 3 of the families, including the 2 showing the strongest support for linkage at this location. The 5 mutations were all placed within 100 kb corresponding to the
BLK
gene. One resulted in an Ala71Thr substitution; the other 4 were noncoding and determined decreased in vitro promoter activity in reporter gene experiments. We found that BLK—a nonreceptor tyrosine-kinase of the
src
family of proto-oncogenes—is expressed in β-cells where it enhances insulin synthesis and secretion in response to glucose by up-regulating transcription factors Pdx1 and Nkx6.1. These actions are greatly attenuated by the Ala71Thr mutation. These findings point to BLK as a previously unrecognized modulator of β-cell function, the deficit of which may lead to the development of diabetes.
Systematic haplotype analysis resolves a complex plasma plant sterol locus on the Micronesian Island of Kosrae
Authors: Kenny Eimear E. , Gusev Alexander , Riegel Kaitlin , Lütjohann Dieter , Lowe Jennifer K. , Salit Jacqueline , Maller Julian B. , Stoffel Markus , Daly Mark J. , Altshuler David M. , Friedman Jeffrey M. , Breslow Jan L. , Pe'er Itsik , Sehayek Ephraim
Published: August 2009

Pinpointing culprit causal variants along signal peaks of genome-wide association studies (GWAS) is challenging. To overcome confounding effects of multiple independent variants at such a locus and narrow the interval for causal allele capture, we developed an approach that maps local shared haplotypes harboring a putative causal variant. We demonstrate our method in an extreme isolate founder population, the pacific Island of Kosrae. We analyzed plasma plant sterol (PPS) levels, a surrogate measure of cholesterol absorption from the intestine, where previous studies have implicated 2p21 mutations in the ATP binding cassette subfamily G members 5 or 8 (ABCG5 or ABCG8) genes. We have previously reported that 11.1% of the islanders are carriers of a frameshift ABCG8 mutation increasing PPS levels in carriers by 50%. GWAS adjusted for this mutation revealed genomewide significant signals along 11 Mb around it. To fine-map this signal, we detected pairwise identity-by-descent haplotypes using our tool GERMLINE and implemented a clustering algorithm to identify haplotypes shared across multiple samples with their unique shared boundaries. A single 526-kb haplotype mapped strongly to PPS levels, dramatically refining the mapped interval. This haplotype spans the ABCG5/ABCG8 genes, is carried by 1.8% of the islanders, and results in a striking 100% increase of PPS in carriers. Resequencing of ABCG5 in these carriers found a D450H missense mutation along the associated haplotype. These findings exemplify the power of haplotype analysis for mapping mutations in isolated populations and specifically for dissecting effects of multiple variants of the same locus.
Ultraslow oligomerization equilibria of p53 and its implications
Authors: Natan Eviatar , Hirschberg Daniel , Morgner Nina , Robinson Carol V. , Fersht Alan R.
Published: August 2009

The tumor suppressor p53 is in equilibrium at cellular concentrations between dimers and tetramers. Oncogenic mutant p53 (mut) exerts a dominant-negative effect on co-expression of p53 wild-type (wt) and mut alleles in cancer cells. It is believed that wt and mut form hetero-tetramers of attenuated activity, via their tetramerization domains. Using electrospray mass spectrometry on isotopically labeled samples, we measured directly the composition and rates of formation of p53 complexes in the presence and absence of response element DNA. The dissociation of tetramers was unexpectedly very slow (
t
1/2
= 40 min) at 37 °C, matched by slow association of dimers, which is approximately four times longer than the half-life of spontaneous denaturation of wt p53. On mixing wt tetramers with the oncogenic contact mutant R273H of low DNA affinity, we observed the same slow formation of only wt
4
, wt
2
mut
2
, and mut
4
, in the ratio 1:2:1, on a cellular time scale. On mixing wt and mut with response element DNAs P21 and BAX, we observed only the complexes wt
4
.DNA, wt
2
mut
2
.DNA, and mut
4
.DNA, with relative dissociation constants 1:4:71 and 1:13:85, respectively, accounting for the dominant-negative effect by weakened affinity. p53 dimers assemble rapidly to tetramers on binding to response element DNA, initiated by the p53 DNA binding domains. The slow oligomerization of free p53, competing with spontaneous denaturation, has implications for the possible regulation of p53 by binding proteins and DNA that affect tetramerization kinetics as well as equilibria.
Parp1 facilitates alternative NHEJ, whereas Parp2 suppresses IgH/c-myc translocations during immunoglobulin class switch recombination
Authors: Robert Isabelle , Dantzer Françoise , Reina-San-Martin Bernardo
Published: August 2009

Immunoglobulin class switch recombination (CSR) is initiated by DNA breaks triggered by activation-induced cytidine deaminase (AID). These breaks activate DNA damage response proteins to promote appropriate repair and long-range recombination. Aberrant processing of these breaks, however, results in decreased CSR and/or increased frequency of illegitimate recombination between the immunoglobulin heavy chain locus and oncogenes like c-myc. Here, we have examined the contribution of the DNA damage sensors Parp1 and Parp2 in the resolution of AID-induced DNA breaks during CSR. We find that although Parp enzymatic activity is induced in an AID-dependent manner during CSR, neither Parp1 nor Parp2 are required for CSR. We find however, that Parp1 favors repair of switch regions through a microhomology-mediated pathway and that Parp2 actively suppresses IgH/c-myc translocations. Thus, we define Parp1 as facilitating alternative end-joining and Parp2 as a novel translocation suppressor during CSR.
Displaying Fel d1 on virus-like particles prevents reactogenicity despite greatly enhanced immunogenicity: a novel therapy for cat allergy
Authors: Schmitz Nicole , Dietmeier Klaus , Bauer Monika , Maudrich Melanie , Utzinger Stefan , Muntwiler Simone , Saudan Philippe , Bachmann Martin F.
Published: August 2009

Allergen-specific desensitization is the only disease-modifying therapy currently available for the treatment of allergies. These therapies require application of allergen over several years and some may induce life-threatening anaphylactic reactions. An ideal vaccine for desensitization should be highly immunogenic and should alleviate allergic symptoms upon few injections while being nonreactogenic. We describe such a vaccine for the treatment of cat allergy, consisting of the major cat allergen Fel d1 coupled to bacteriophage Qβ-derived virus-like particles (Qβ–Fel d1). Qβ–Fel d1 was highly immunogenic, and a single vaccination was sufficient to induce protection against type I allergic reactions. Allergen-specific immunoglobulin G antibodies were shown to be the critical effector molecules and alleviated symptoms by two distinct mechanisms. Although allergen-induced systemic basophil degranulation was inhibited in an FcγRIIb-dependent manner, inhibition of local mast cell degranulation in tissues occurred independently of FcγRIIb. In addition, treatment with Qβ–Fel d1 abolished IgE memory responses upon antigen recall. Despite high immunogenicity, the vaccine was essentially nonreactogenic and vaccination induced neither local nor systemic anaphylactic reactions in sensitized mice. Moreover, Qβ–Fel d1 did not induce degranulation of basophils derived from human volunteers with cat allergies. These data suggest that vaccination with Qβ–Fel d1 may be a safe and effective treatment for cat allergy.
Double error shrinkage method for identifying protein binding sites observed by tiling arrays with limited replication
Authors: Kim Youngchul , Bekiranov Stefan , Lee Jae K. , Park Taesung
Published: August 2009

Motivation: ChIP–chip has been widely used for various genome-wide biological investigations. Given the small number of replicates (typically two to three) per biological sample, methods of analysis that control the variance are desirable but in short supply. We propose a double error shrinkage (DES) method by using moving average statistics based on local-pooled error estimates which effectively control both heterogeneous error variances and correlation structures of an extremely large number of individual probes on tiling arrays.

Results: Applying DES to ChIP–chip tiling array study for discovering genome-wide protein-binding sites, we identified 8400 target regions that include highly likely TFIID binding sites. About 33% of these were well matched with the known transcription starting sites on the DBTSS library, while many other newly identified sites have a high chance to be real binding sites based on a high positive predictive value of DES. We also showed the superior performance of DES compared with other commonly used methods for detecting actual protein binding sites.

Contact:  tspark@snu.ac.kr; jaeklee@virginia.edu

Supplementary information:  Supplementary data are available at Bioinformatics online.
Efficient SCOP-fold classification and retrieval using index-based protein substructure alignments
Authors: Chi Pin-Hao , Pang Bin , Korkin Dmitry , Shyu Chi-Ren
Published: August 2009

Motivation: To investigate structure–function relationships, life sciences researchers usually retrieve and classify proteins with similar substructures into the same fold. A manually constructed database, SCOP, is believed to be highly accurate; however, it is labor intensive. Another known method, DALI, is also precise but computationally expensive. We have developed an efficient algorithm, namely, index-based protein substructure alignment (IPSA), for protein-fold classification. IPSA constructs a two-layer indexing tree to quickly retrieve similar substructures in proteins and suggests possible folds by aligning these substructures.

Results: Compared with known algorithms, such as DALI, CE, MultiProt and MAMMOTH, on a sample dataset of non-redundant proteins from SCOP v1.73, IPSA exhibits an efficiency improvement of 53.10, 16.87, 3.60 and 1.64 times speedup, respectively. Evaluated on three different datasets of non-redundant proteins from SCOP, average accuracy of IPSA is approximately equal to DALI and better than CE, MAMMOTH, MultiProt and SSM. With reliable accuracy and efficiency, this work will benefit the study of high-throughput protein structure–function relationships.

Availability: IPSA is publicly accessible at http://ProteinDBS.rnet.missouri.edu/IPSA.php

Contact:  ShyuC@missouri.edu

Supplementary information:  Supplementary data are available at Bioinformatics online.
PineSAP—sequence alignment and SNP identification pipeline
Authors: Wegrzyn Jill L. , Lee Jennifer M. , Liechty John , Neale David B.
Published: August 2009

Summary: The Pine Alignment and SNP Identification Pipeline (PineSAP) provides a high-throughput solution to single nucleotide polymorphism (SNP) prediction using multiple sequence alignments from re-sequencing data. This pipeline integrates a hybrid of customized scripting, existing utilities and machine learning in order to increase the speed and accuracy of SNP calls. The implementation of this pipeline results in significantly improved multiple sequence alignments and SNP identifications when compared with existing solutions. The use of machine learning in the SNP identifications extends the pipeline's application to any eukaryotic species where full genome sequence information is unavailable.

Availability: All code used for this pipeline is freely available at the Dendrome project website (http://dendrome.ucdavis.edu/adept2/resequencing.html)

Contact:  jlwegrzyn@ucdavis.edu
Knowledge-guided inference of domain–domain interactions from incomplete protein–protein interaction networks
Authors: Liu Mei , Chen Xue-wen , Jothi Raja
Published: August 2009

Motivation: Protein-protein interactions (PPIs), though extremely valuable towards a better understanding of protein functions and cellular processes, do not provide any direct information about the regions/domains within the proteins that mediate the interaction. Most often, it is only a fraction of a protein that directly interacts with its biological partners. Thus, understanding interaction at the domain level is a critical step towards (i) thorough understanding of PPI networks; (ii) precise identification of binding sites; (iii) acquisition of insights into the causes of deleterious mutations at interaction sites; and (iv) most importantly, development of drugs to inhibit pathological protein interactions. In addition, knowledge derived from known domain–domain interactions (DDIs) can be used to understand binding interfaces, which in turn can help discover unknown PPIs.

Results: Here, we describe a novel method called K-GIDDI (knowledge-guided inference of DDIs) to narrow down the PPI sites to smaller regions/domains. K-GIDDI constructs an initial DDI network from cross-species PPI networks, and then expands the DDI network by inferring additional DDIs using a divide-and-conquer biclustering algorithm guided by Gene Ontology (GO) information, which identifies partial-complete bipartite sub-networks in the DDI network and makes them complete bipartite sub-networks by adding edges. Our results indicate that K-GIDDI can reliably predict DDIs. Most importantly, K-GIDDI's novel network expansion procedure allows prediction of DDIs that are otherwise not identifiable by methods that rely only on PPI data.

Contact:  xwchen@ku.edu

Availability:  http://www.ittc.ku.edu/∼xwchen/domainNetwork/ddinet.html

Supplementary information:  Supplementary data are available at Bioinformatics online.
Host Specialization and Phylogenetic Diversity of Corynespora cassiicola
Authors: Dixon L. J. , Schlub R. L. , Pernezny K. , Datnoff L. E.
Published: August 2009

The fungus Corynespora cassiicola is primarily found in the tropics and subtropics, and is widely diverse in substrate utilization and host association. Isolate characterization within C. cassiicola was undertaken to investigate how genetic diversity correlates with host specificity, growth rate, and geographic distribution. C. cassiicola isolates were collected from 68 different plant species in American Samoa, Brazil, Malaysia, and Micronesia, and Florida, Mississippi, and Tennessee within the United States. Phylogenetic analyses using four loci were performed with 143 Corynespora spp. isolates, including outgroup taxa obtained from culture collections: C. citricola, C. melongenae, C. olivacea, C. proliferata, C. sesamum, and C. smithii. Phylogenetic trees were congruent from the ribosomal DNA internal transcribed spacer region, two random hypervariable loci (caa5 and ga4), and the actin-encoding locus act1, indicating a lack of recombination within the species and asexual propagation. Fifty isolates were tested for pathogenicity on eight known C. cassiicola crop hosts: basil, bean, cowpea, cucumber, papaya, soybean, sweet potato, and tomato. Pathogenicity profiles ranged from one to four hosts, with cucumber appearing in 14 of the 16 profiles. Bootstrap analyses and Bayesian posterior probability values identified six statistically significant phylogenetic lineages. The six phylogenetic lineages correlated with host of origin, pathogenicity, and growth rate but not with geographic location. Common fungal genotypes were widely distributed geographically, indicating long-distance and global dispersal of clonal lineages. This research reveals an abundance of previously unrecognized genetic diversity within the species and provides evidence for host specialization on papaya.
Characterization of Hypersensitive Resistance to Bacterial Spot Race T3 (Xanthomonas perforans) from Tomato Accession PI 128216
Authors: Robbins Matthew D. , Darrigues Audrey , Sim Sung-Chur , Masud Mohammed Abu Taher , Francis David M.
Published: August 2009

Bacterial spot of tomato is caused by four species of Xanthomonas. The accession PI 128216 (Solanum pimpinellifolium) displays a hypersensitive reaction (HR) to race T3 strains (predominately Xanthomonas perforans). We developed an inbred backcross (IBC) population (BC2S5, 178 families) derived from PI 128216 and OH88119 (S. lycopersicum) as the susceptible recurrent parent for simultaneous introgression and genetic analysis of the HR response. These IBC families were evaluated in the greenhouse for HR to race T3 strain Xcv761. The IBC population was genotyped with molecular markers distributed throughout the genome in order to identify candidate loci conferring resistance. We treated the IBC population as a hypothesis forming generation to guide validation in subsequent crosses. Nonparametric analysis identified an association between HR and markers clustered on chromosome 11 (P < 0.05 to 0.0001) and chromosome 6 (0.04 > P > 0.002). Further analysis of the IBC population suggested that markers on chromosome 6 and 11 failed to assort independently, a phenomenon known as gametic phase disequilibrium. Therefore, to validate marker-trait linkages, resistant IBC plants were crossed with OH88119 and BC3F2progeny were evaluated for HR in the greenhouse. In these subsequent populations, the HR response was associated with the chromosome 11 markers (P < 0.0002) but not with the markers on chromosome 6 (P > 0.25). Independent F2families were developed by crossing resistant IBC lines to OH8245, OH88119, and OH7530. These populations were genotyped, organized into classes based on chromosome 11 markers, and evaluated for resistance in the field. The PI 128216 locus on chromosome 11 provided resistance that was dependent on gene dosage and genetic background. These results define a single locus, Rx-4, from PI 128216, which provides resistance to bacterial spot race T3, has additive gene action, and is located on chromosome 11.
Stolbur Phytoplasma Transmission to Maize by Reptalus panzeri and the Disease Cycle of Maize Redness in Serbia
Authors: Jović J. , Cvrković T. , Mitrović M. , Krnjajić S. , Petrović A. , Redinbaugh M. G. , Pratt R. C. , Hogenhout S. A. , Toševski I.
Published: August 2009

Maize redness (MR), induced by stolbur phytoplasma (‘Candidatus Phytoplasma solani’, subgroup 16SrXII-A), is characterized by midrib, leaf, and stalk reddening and abnormal ear development. MR has been reported from Serbia, Romania, and Bulgaria for 50 years, and recent epiphytotics reduced yields by 40 to 90% in South Banat District, Serbia. Potential vectors including leafhoppers and planthoppers in the order Hemiptera, suborder Auchenorrhyncha, were surveyed in MR-affected and low-MR-incidence fields, and 33 different species were identified. Only Reptalus panzeri populations displayed characteristics of a major MR vector. More R. panzeri individuals were present in MR-affected versus low-MR fields, higher populations were observed in maize plots than in field border areas, and peak population levels preceded the appearance of MR in late July. Stolbur phytoplasma was detected in 17% of R. panzeri adults using nested polymerase chain reaction but not in any other insects tested. Higher populations of R. panzeri nymphs were found on maize, Johnsongrass (Sorghum halepense), and wheat (Triticum aestivum) roots. Stolbur phytoplasma was detected in roots of these three plant species, as well as in R. panzeri L3 and L5 nymphs. When stolbur phytoplasma-infected R. panzeri L3 nymphs were introduced into insect-free mesh cages containing healthy maize and wheat plants, 89 and 7%, respectively, became infected. These results suggest that the MR disease cycle in South Banat involves mid-July transmission of stolbur phytoplasma to maize by infected adult R. panzeri. The adult R. panzeri lay eggs on infected maize roots, and nymphs living on these roots acquire the phytoplasma from infected maize. The nymphs overwinter on the roots of wheat planted into maize fields in the autumn, allowing emergence of phytoplasma-infected vectors the following July.
Mapping Quantitative Trait Loci Responsible for Resistance to Sheath Blight in Rice
Authors: Liu G. , Jia Y. , Correa-Victoria F. J. , Prado G. A. , Yeater K. M. , McClung A. , Correll J. C.
Published: August 2009

Rice sheath blight (ShB), caused by the soilborne pathogen Rhizoctonia solani, annually causes severe losses in yield and quality in many rice production areas worldwide. Jasmine 85 is an indica cultivar that has proven to have a high level of resistance to this pathogen. The objective of this study was to determine the ability of controlled environment inoculation assays to detect ShB resistance quantitative trait loci (QTLs) in a cross derived from the susceptible cv. Lemont and the resistant cv. Jasmine 85. The disease reactions of 250 F5 recombinant inbred lines (RILs) were measured on the seedlings inoculated using microchamber and mist-chamber assays under greenhouse conditions. In total, 10 ShB-QTLs were identified on chromosomes 1, 2, 3, 5, 6, and 9 using these two methods. The microchamber method identified four of five new ShB-QTLs, one on each of chromosomes 1, 3, 5, and 6. Both microchamber and mist-chamber methods identified two ShB-QTLs, qShB1 and qShB9-2. Four of the ShB-QTLs or ShB-QTL regions identified on chromosomes 2, 3, and 9 were previously reported in the literature. The major ShB-QTL qShB9-2, which cosegregated with simple sequence repeat (SSR) marker RM245 on chromosome 9, contributed to 24.3 and 27.2% of total phenotypic variation in ShB using microchamber and mistchamber assays, respectively. qShB9-2, a plant-stage-independent QTL, was also verified in nine haplotypes of 10 resistant Lemont/Jasmine 85 RILs using haplotype analysis. These results suggest that multiple ShB-QTLs are involved in ShB resistance and that microchamber and mist-chamber methods are effective for detecting plant-stage-independent QTLs. Furthermore, two SSR markers, RM215 and RM245, are robust markers and can be used in marker-assisted breeding programs to improve ShB resistance.
Ectopic 5′ Splice Sites Inhibit Gene Expression by Engaging RNA Surveillance and Silencing Pathways in Plants
Authors: Wypijewski Krzysztof , Hornyik Csaba , Shaw Jane A. , Stephens Jennifer , Goraczniak Rafal , Gunderson Samuel I. , Lacomme Christophe
Published: August 2009

The quality control of mRNA maturation is a highly regulated process that surveys pre-mRNA integrity and eliminates improperly matured pre-mRNAs. In nature, certain viruses regulate the expression of their genes by hijacking the endogenous RNA quality control machinery. We demonstrate that the inclusion of 5′ splice sites within the 3′-untranslated region of a reporter gene in plants alters the pre-mRNA cleavage and polyadenylation process, resulting in pre-mRNA degradation, exemplifying a regulatory mechanism conserved between kingdoms. Altered pre-mRNA processing was associated with an inhibition of homologous gene expression in trans and the preferential accumulation of 24-nucleotide (nt) short-interfering RNAs (siRNAs) as opposed to 21-nt siRNA subspecies, suggesting that degradation of the aberrant pre-mRNA involves the silencing machinery. However, gene expression was not restored by coexpression of a silencing suppressor or in an RNA-dependent RNA polymerase (RDR6)-deficient background despite reduced 24-nt siRNA accumulation. Our data highlight a complex cross talk between the quality control RNA machinery, 3′-end pre-mRNA maturation, and RNA-silencing pathways capable of discriminating among different types of aberrant RNAs.
Increased frequencies of T helper type 17 cells in the peripheral blood of patients with acute myeloid leukaemia
Authors: Wu C , Wang S , Wang F , Chen Q , Peng S , Zhang Y , Qian J , Jin J , Xu H
Published: August 2009

T helper type 17 (Th17) cells, which represent a novel subset of CD4+ T cells, play an active role in inflammatory and autoimmune diseases. Recent studies have also suggested that they have an impact on solid tumours. However, the nature of Th17 cells in haematological malignancies remains unknown. In this study, we investigated Th17 cell frequency and secretion of related cytokines in patients with acute myeloid leukaemia (AML). First, we found that Th17 cell frequencies were increased significantly in peripheral blood samples from untreated patients with AML, compared with those from healthy volunteers. Moreover, increased interleukin (IL)-17 concentrations accompanied the increased Th17 cell frequencies in these patients. These results suggest that Th17 cells may play a role in the pathogenesis of AML. Secondly, we found that the increased Th17 cell frequencies were reduced when patients achieved complete remission after chemotherapy, suggesting that measurement of Th17 cell frequencies may have clinical value in the evaluation of therapeutic effect. In addition, we found that IL-6 and transforming growth factor (TGF)-β1 concentrations increased in the untreated patients and that IL-6 concentrations showed a positive correlation with the frequencies of Th17 cells, suggesting that IL-6 may play an important role in Th17 cell differentiation in patients with AML.
Contribution of fungal biomass to the growth of the shredder, Pycnopsyche gentilis (Trichoptera: Limnephilidae)
Authors: CHUNG NAMIL , SUBERKROPP KELLER
Published: August 2009

1. 1. It has been accepted that aquatic hyphomycetes colonising submerged leaves increase the nutritional value of leaf detritus and suggested that fungal biomass plays a greater role in the growth of shredders than leaf tissue itself. However, it is not clear what proportion of the nutritional needs of shredders is met by fungal biomass.

2. We fed Pycnopsyche gentilis larvae with tulip poplar (Liriodendron tulipifera) leaf discs colonised by the aquatic hyphomycete, Anguillospora filiformis, which had been radiolabelled to quantify the contribution of fungal carbon to the growth of the shredder at different larval developmental stages. Instantaneous growth rates of larvae on this diet were also estimated.

3. When provided with fungal‐colonised leaves (14–16% fungal biomass), the third and the fifth instar larvae of P. gentilis grew at the rates of 0.061 and 0.034 day−1, respectively, but on a diet of sterile leaves, both larval instars lost weight. The incorporation rates of fungal carbon were 31.6 μg C mg−1 AFDM day−1, accounting for 100% of the daily growth rate of the third instar larvae and 8.6 μg C mg−1 AFDM day−1, accounting for 50% of the daily growth rate of the fifth instar larvae.

4. These results suggest that leaf material colonised by A. filiformis is a high quality food resource for P. gentilis larvae, and that fungal biomass can contribute significantly to the growth of these larvae. Differences in feeding behaviour and digestive physiology may explain the significantly greater assimilation of fungal biomass by the earlier instar than the final instar. To satisfy their nutritional needs the fifth instar larvae would have to assimilate detrital mass that may have been modified by fungal exoenzymes.
Effect of non‐random dispersal strategies on spatial coexistence mechanisms
Authors: Amarasekare Priyanga
Published: August 2009

1.  Random dispersal leads to spatial coexistence via two mechanisms (emigration‐mediated and source–sink), both of which involve the movement of organisms from areas of higher to lower fitness. What is not known is whether such coexistence would occur if organisms dispersed non‐randomly, using cues such as density and habitat quality to gauge fitness differences between habitats. Here, I conduct a comparative analysis of random and non‐random dispersal strategies in a foodweb with a basal resource, top predator, and two intermediate consumers that exhibit a trade‐off between competitive ability and predator susceptibility.

2.  I find a striking contrast between density‐ and habitat‐dependent dispersal in their effects on spatial coexistence. Dispersal in response to competitor and predator density facilitates coexistence while dispersal in response to habitat quality (resource productivity and predator pressure) inhibits it. Moreover, density‐dependent dispersal changes species’ distribution patterns from interspecific segregation to interspecific aggregation, while habitat‐dependent dispersal preserves the interspecific segregation observed in the absence of dispersal. Under density‐dependent dispersal, widespread spatial coexistence results in an overall decline in the abundance of the inferior competitor that is less susceptible to predation and an overall increase in the abundance of the superior competitor that is more susceptible to predation. Under habitat‐dependent dispersal, restricted spatial coexistence results in species’ abundances being essentially unchanged from those observed in the absence of dispersal.

3.  A key outcome is that when the superior competitor moves in the direction of increasing fitness but the inferior competitor does not, spatial coexistence is possible in both resource‐poor and resource‐rich habitats. However, when the inferior competitor moves in the direction of increasing fitness but the superior competitor does not, spatial coexistence is precluded in resource‐poor habitats and greatly reduced in resource‐rich habitats. This suggests that species‐specific differences may play an important role in driving spatial coexistence patterns.

4.  The comparative framework yields predictions that can be tested with experiments that manipulate the relative mobilities of interacting species, or observational data on relative abundances and distribution patterns.
The changing global carbon cycle: linking plant–soil carbon dynamics to global consequences
Authors: Stuart Chapin III F. , McFarland Jack , David McGuire A. , Euskirchen Eugenie S. , Ruess Roger W. , Kielland Knut
Published: August 2009

1.
 Most current climate–carbon cycle models that include the terrestrial carbon (C) cycle are based on a model developed 40 years ago by Woodwell & Whittaker (1968) and omit advances in biogeochemical understanding since that time. Their model treats net C emissions from ecosystems as the balance between net primary production (NPP) and heterotrophic respiration (HR, i.e. primarily decomposition).

2.  Under conditions near steady state, geographic patterns of decomposition closely match those of NPP, and net C emissions are adequately described as a simple balance of NPP and HR (the Woodwell‐Whittaker model). This close coupling between NPP and HR occurs largely because of tight coupling between C and N (nitrogen) cycles and because NPP constrains the food available to heterotrophs.

3.
 Processes in addition to NPP and HR become important to understanding net C emissions from ecosystems under conditions of rapid changes in climate, hydrology, atmospheric CO2, land cover, species composition and/or N deposition. Inclusion of these processes in climate–C cycle models would improve their capacity to simulate recent and future climatic change.

4.  Processes that appear critical to soil C dynamics but warrant further research before incorporation into ecosystem models include below‐ground C flux and its partitioning among roots, mycorrhizas and exudates; microbial community effects on C sequestration; and the effects of temperature and labile C on decomposition. The controls over and consequences of these processes are still unclear at the ecosystem scale.

5.  Carbon fluxes in addition to NPP and HR exert strong influences over the climate system under conditions of rapid change. These fluxes include methane release, wildfire, and lateral transfers of food and fibre among ecosystems.

6.  Water and energy exchanges are important complements to C cycle feedbacks to the climate system, particularly under non‐steady‐state conditions. An integrated understanding of multiple ecosystem–climate feedbacks provides a strong foundation for policies to mitigate climate change.

7.
 Synthesis. Current climate systems models that include only NPP and HR are inadequate under conditions of rapid change. Many of the recent advances in biogeochemical understanding are sufficiently mature to substantially improve representation of ecosystem C dynamics in these models.
Vegetation composition promotes carbon and nitrogen storage in model grassland communities of contrasting soil fertility
Authors: De Deyn Gerlinde B. , Quirk Helen , Yi Zou , Oakley Simon , Ostle Nick J. , Bardgett Richard D.
Published: August 2009

1. The benefits of plant functional group and plant species diversity for sustaining primary productivity have been extensively studied. However, few studies have simultaneously explored potential benefits of plant species and functional group richness and composition for the delivery of other ecosystem services and their dependency on resource availability.

2. Here, we investigated in soils of different fertility the effects of plant species and functional group richness and composition on carbon (C) and nitrogen (N) stocks in vegetation, soil and soil microbes and on CO2 exchange and the loss of C and N from soil through leaching. We established plant communities from a pool of six mesotrophic grassland species belonging to one of three functional groups (C3 grasses, forbs and legumes) in two soils of contrasting fertility. We varied species richness using one, two, three or six species and one, two or three functional groups.

3. After 2 years, vegetation C and N and soil microbial biomass were greater in the more fertile soil and increased significantly with greater numbers of plant species and functional group richness. The positive effect of plant diversity on vegetation C and N coincided with reduced loss of water and N through leaching, which was especially governed by forbs, and increased rates of net ecosystem CO2 exchange.

4. Soil C and N pools were not affected by the number of plant species or functional group richness per se after 2 years, but were enhanced by the presence and biomass of the legumes Lotus corniculatus and Trifolium repens.

5. 
Synthesis. Collectively, our findings indicate that changes in plant species and functional group richness influence the storage and loss of both C and N in model grassland communities but that these responses are related to the presence and biomass of certain plant species, notably N fixers and forbs. Our results therefore suggest that the co‐occurrence of species from specific functional groups is crucial for the maintenance of multifunctionality with respect to C and N storage in grasslands.
An experimental comparison of chemical traits and litter decomposition rates in a diverse range of subarctic bryophyte, lichen and vascular plant species
Authors: Lang Simone I. , Cornelissen Johannes H. C. , Klahn Thorsten , Van Logtestijn Richard S. P. , Broekman Rob , Schweikert Wenka , Aerts Rien
Published: August 2009

1. Climate change in the subarctic is expected to influence vegetation composition, specifically bryophyte and lichen communities, thereby modifying litter decomposition rates and carbon (C) dynamics of these systems with possible feedbacks to climate.

2. In a 2‐year experiment, we investigated decomposition rates and chemical traits of 27 bryophytes, 17 lichens and 5 vascular plants in litter beds in subarctic Sweden. The majority of the sampled cryptogam species are widespread at higher northern latitudes.

3. Average 2‐year litter decomposition rates (exponential mass loss constantk) of lichen (0.44 ± 0.01) and vascular plant (0.56 ± 0.03) species were higher than that of bryophytes (0.11 ± 0.01), while within main cryptogam taxa, species identity was an important determinant of mass loss rates. At cryptogam group level, 2‐year litter mass loss ofSphagnumwas significantly lower than for non‐Sphagnummosses and liverworts. Within lichens, N2‐fixing versus non‐N2‐fixing lichens showed no variation in decomposability.

4. In a subset of the large species set, mass loss differed both among incubation environments (reflecting nutrient‐rich and poor birch forest andSphagnumpeatlands, respectively) and species. The pattern of mass loss across incubation environments was not consistent among cryptogam species. N2‐fixing, in contrast to non‐N2‐fixing lichens with lower nitrogen (N) levels displayed similar decomposition rates across incubation environments. Mass loss of non‐Sphagnummosses was correlated with initial N irrespective of incubation environment.

5. Litter mass loss of cryptogam taxa could be predicted very well from infrared spectra of the initial chemical composition of the species, by application of Fourier transform infrared using an attenuated total reflectance probe. The initial macronutrient concentrations (N, phosphorus, C and cations) and initial litter pH correlated less well.

6. Synthesis. We showed comprehensively that decomposition rates of bryophytes are generally lower than those of lichens and vascular plants. Among bryophyte or lichen species there is also great variation in litter decomposability which depends strongly on species‐specific chemistry. Our data will help predict changing land surface feedback to C cycles and climate in cold biomes by understanding long‐term climate effects on litter decomposability through shifting vegetation composition.