Star Formation Timescales and the Schmidt Law

We offer a simple parameterization of the rate of star formation in galaxies. In this new approach, we make explicit and decouple the timescales associated (a) with disruptive effects the star formation event itself, from (b) the timescales associated with the cloud assembly and collapse mechanisms leading up to star formation. The star formation law in near-by galaxies, as measured on sub-kiloparsec scales, has recently been shown by Bigiel et al. to be distinctly non-linear in its dependence on total gas density. Our parameterization of the spatially resolved Schmidt-Sanduleak relation naturally accommodates that dependence. The parameterized form of the relation is rho_* ~ epsilon x rho_g/(tau_s + rho_g ^{-n}), where rho_g is the gas density, epsilon is the efficiency of converting gas into stars, and rho_g^{-n} captures the physics of cloud collapse. Accordingly at high gas densities quiescent star formation is predicted to progress as rho_* ~ rho_g, while at low gas densities rho_* ~ rho_g^{1+n}, as is now generally observed. A variable efficiency in locally converting gas into stars as well as the unknown plane thickness variations from galaxy to galaxy, and radially within a given galaxy, can readily account for the empirical scatter in the observed (surface density rather than volume density) relations, and also plausibly account for the noted upturn in the relation at very high apparent projected column densities.Comment: Accepted to the Astrophysical Joirnal (Letters); 10 pages, 1 figure; Revised caption is now fully readable. One reference correcte

Deep proteogenomics; high throughput gene validation by multidimensional liquid chromatography and mass spectrometry of proteins from the fungal wheat pathogen Stagonospora nodorum

BACKGROUND: Stagonospora nodorum, a fungal ascomycete in the class dothideomycetes, is a damaging pathogen of wheat. It is a model for necrotrophic fungi that cause necrotic symptoms via the interaction of multiple effector proteins with cultivar-specific receptors. A draft genome sequence and annotation was published in 2007. A second-pass gene prediction using a training set of 795 fully EST-supported genes predicted a total of 10762 version 2 nuclear-encoded genes, with an additional 5354 less reliable version 1 genes also retained. RESULTS: In this study, we subjected soluble mycelial proteins to proteolysis followed by 2D LC MALDI-MS/MS. Comparison of the detected peptides with the gene models validated 2134 genes. 62% of these genes (1324) were not supported by prior EST evidence. Of the 2134 validated genes, all but 188 were version 2 annotations. Statistical analysis of the validated gene models revealed a preponderance of cytoplasmic and nuclear localised proteins, and proteins with intracellularassociated GO terms. These statistical associations are consistent with the source of the peptides used in the study. Comparison with a 6-frame translation of the S. nodorum genome assembly confirmed 905 existing gene annotations (including 119 not previously confirmed) and provided evidence supporting 144 genes with coding exon frameshift modifications, 604 genes with extensions of coding exons into annotated introns or untranslated regions (UTRs), 3 new gene annotations which were supported by tblastn to NR, and 44 potential new genes residing within un-assembled regions of the genome. CONCLUSION: We conclude that 2D LC MALDI-MS/MS is a powerful, rapid and economical tool to aid in the annotation of fungal genomic assemblies

Sensitivity to three Parastagonospora nodorum necrotrophic effectors in current Australian wheat cultivars and the presence of further fungal effectors

Parastagonospora nodorum is a major fungal pathogen of wheat in Australia causing septoria nodorum blotch (SNB). P. nodorum virulence is quantitative and depends to a large extent on multiple effector-host sensitivity gene interactions. The pathogen utilises a series of proteinaceous necrotrophic effectors to facilitate disease development on wheat cultivars that possess appropriate dominant sensitivity loci. Thus far, three necrotrophic effector genes have been cloned. Proteins derived from these genes were used to identify wheat cultivars that confer effector sensitivity. The goal of the study was to determine if effector sensitivity could be used to enhance breeding for SNB resistance. In this study, we have demonstrated that SnTox1 effector sensitivity is common in current commercial Western Australian wheat cultivars. Thirty-three of 46 cultivars showed evidence of sensitivity to SnTox1. Of these, 19 showed moderate or strong chlorotic/necrotic responses to SnTox1. Thirteen were completely insensitive to SnTox1. Disease susceptibility was most closely associated with SnTox3 sensitivity. In addition, we have identified biochemical evidence of a novel chlorosis-inducing protein or proteins in P. nodorum culture filtrates unmasked in strains that lack expression of ToxA, SnTox1 and SnTox3 activities

On the time variability of the star formation efficiency

A star formation efficiency per free fall time that evolves over the life time of giant molecular clouds (GMCs) may have important implications for models of supersonic turbulence in molecular clouds or for the relation between star formation rate and H2 surface density. We discuss observational data that could be interpreted as evidence of such a time variability. In particular, we investigate a recent claim based on measurements of H2 and stellar masses in individual GMCs. We show that this claim depends crucially on the assumption that H2 masses do not evolve over the life times of GMCs. We exemplify our findings with a simple toy model that uses a constant star formation efficiency and, yet, is able to explain the observational data.Comment: 5 pages, 2 figures, submitted to APJ

Proteomic identification of extracellular proteins regulated by the Gna1 Gα subunit in Stagonospora nodorum

The fungus Stagonospora nodorum is the causal agent of stagonospora nodorum blotch (syn.leaf and glume blotch) disease of wheat. The Gna1-encoded Ga protein is an important signaltransduction component in the fungus, which is required for full pathogenicity, sporulationand extracellular depolymerase production. In this study, we sought to gaina better understanding of defects associated with the gna1 mutant by using twodimensionalgel electrophoresis to analyse the extracellular proteome for differences tothe wildtype. Mass spectrometry analysis of altered abundant protein spots and peptidematching to the Stagonospora nodorum genome database have led to the identification ofgenes implicated in cell wall degradation, proteolysis, RNA hydrolysis and aromatic compoundmetabolism. In addition, quantitative RT-PCR has demonstrated that some of theencoding genes showed differential expression throughout host infection. Implicationsof these proteins and their corresponding genes in fungal virulence are discussed.The fungus Stagonospora nodorum is the causal agent of stagonospora nodorum blotch (syn. leaf and glume blotch) disease of wheat. The Gna1-encoded Gα protein is an important signal transduction component in the fungus, which is required for full pathogenicity, sporulation and extracellular depolymerase production. In this study, we sought to gain a better understanding of defects associated with the gna1 mutant by using two-dimensional gel electrophoresis to analyse the extracellular proteome for differences to the wildtype. Mass spectrometry analysis of altered abundant protein spots and peptide matching to the Stagonospora nodorum genome database have led to the identification of genes implicated in cell wall degradation, proteolysis, RNA hydrolysis and aromatic compound metabolism. In addition, quantitative RT-PCR has demonstrated that some of the encoding genes showed differential expression throughout host infection. Implications of these proteins and their corresponding genes in fungal virulence are discussed

SnTox3 Acts in Effector Triggered Susceptibility to Induce Disease on Wheat Carrying the Snn3 Gene

The necrotrophic fungus Stagonospora nodorum produces multiple proteinaceous host-selective toxins (HSTs) which act in effector triggered susceptibility. Here, we report the molecular cloning and functional characterization of the SnTox3-encoding gene, designated SnTox3, as well as the initial characterization of the SnTox3 protein. SnTox3 is a 693 bp intron-free gene with little obvious homology to other known genes. The predicted immature SnTox3 protein is 25.8 kDa in size. A 20 amino acid signal sequence as well as a possible pro sequence are predicted. Six cysteine residues are predicted to form disulfide bonds and are shown to be important for SnTox3 activity. Using heterologous expression in Pichia pastoris and transformation into an avirulent S. nodorum isolate, we show that SnTox3 encodes the SnTox3 protein and that SnTox3 interacts with the wheat susceptibility gene Snn3. In addition, the avirulent S. nodorum isolate transformed with SnTox3 was virulent on host lines expressing the Snn3 gene. SnTox3-disrupted mutants were deficient in the production of SnTox3 and avirulent on the Snn3 differential wheat line BG220. An analysis of genetic diversity revealed that SnTox3 is present in 60.1% of a worldwide collection of 923 isolates and occurs as eleven nucleotide haplotypes resulting in four amino acid haplotypes. The cloning of SnTox3 provides a fundamental tool for the investigation of the S. nodorum-wheat interaction, as well as vital information for the general characterization of necrotroph-plant interactions.This work was supported by USDA-ARS CRIS projects 5442-22000-043-00D and 5442-22000-030-00D

Differential effector gene expression underpins epistasis in a plant fungal disease.

Fungal effector-host sensitivity gene interactions play a key role in determining the outcome of septoria nodorum blotch disease (SNB) caused by Parastagonospora nodorum on wheat. The pathosystem is complex and mediated by interaction of multiple fungal necrotrophic effector-host sensitivity gene systems. Three effector-sensitivity gene systems are well characterised in this pathosystem; SnToxA-Tsn1, SnTox1-Snn1 and SnTox3-Snn3. We tested a wheat mapping population that segregated for Snn1 and Snn3 with SN15, an aggressive P. nodorum isolate that produces SnToxA, SnTox1 and SnTox3, to study the inheritance of sensitivity to SnTox1 and SnTox3 and disease susceptibility. Interval quantitative trait locus (QTL) mapping showed that the SnTox1-Snn1 interaction was paramount in SNB development on both seedlings and adult plants. No effect of the SnTox3-Snn3 interaction was observed under SN15 infection. The SnTox3-Snn3 interaction was however, detected in a strain of SN15 in which SnTox1 had been deleted (tox1-6). Gene expression analysis indicates increased SnTox3 expression in tox1-6 compared to SN15. This indicates that the failure to detect the SnTox3-Snn3 interaction in SN15 is due - at last in part - to suppressed expression of SnTox3 mediated by SnTox1 Furthermore, infection of the mapping population with a strain deleted in SnToxA, SnTox1 and SnTox3 (toxa13) unmasked a significant SNB QTL on 2DS where the SnTox2 effector sensitivity gene, Snn2, is located.This QTL was not observed in SN15 and tox1–6 infections and thus suggesting that SnToxA and/or SnTox3 were epistatic. Additional QTLs responding to SNB and effectors sensitivity were detected on 2AS1 and 3AL

Essential role for ALCAM gene silencing in megakaryocytic differentiation of K562 cells

<p>Abstract</p> <p>Background</p> <p>Activated leukocyte cell adhesion molecule (ALCAM/CD166) is expressed by hematopoietic stem cells. However, its role in hematopoietic differentiation has not previously been defined.</p> <p>Results</p> <p>In this study, we show that ALCAM expression is silenced in erythromegakaryocytic progenitor cell lines. In agreement with this finding, the ALCAM promoter is occupied by GATA-1 <it>in vivo</it>, and a cognate motif at -850 inhibited promoter activity in K562 and MEG-01 cells. Gain-of-function studies showed that ALCAM clusters K562 cells in a process that requires PKC. Induction of megakaryocytic differentiation in K562 clones expressing ALCAM activated PKC-δ and triggered apoptosis.</p> <p>Conclusions</p> <p>There is a lineage-specific silencing of ALCAM in bi-potential erythromegakaryocytic progenitor cell lines. Marked apoptosis of ALCAM-expressing K562 clones treated with PMA suggests that aberrant ALCAM expression in erythromegakaryocytic progenitors may contribute to megakaryocytopenia.</p