A cytoplasmic Cu-Zn superoxide dismutase SOD1 contributes to hyphal growth and virulence of Fusarium graminearum

AbstractSuperoxide dismutases (SODs) are scavengers of superoxide radicals, one of the main reactive oxygen species (ROS) in the cell. SOD-based ROS scavenging system constitutes the frontline defense against intra- and extracellular ROS, but the roles of SODs in the important cereal pathogen Fusarium graminearum are not very clear. There are five SOD genes in F. graminearum genome, encoding cytoplasmic Cu-Zn SOD1 and MnSOD3, mitochondrial MnSOD2 and FeSOD4, and extracellular CuSOD5. Previous studies reported that the expression of SOD1 increased during infection of wheat coleoptiles and florets. In this work we showed that the recombinant SOD1 protein had the superoxide dismutase activity in vitro, and that the SOD1-mRFP fusion protein localized in the cytoplasm of F. graminearum. The Δsod1 mutants had slightly reduced hyphal growth and markedly increased sensitivity to the intracellular ROS generator menadione. The conidial germination under extracellular oxidative stress was significantly delayed in the mutants. Wheat floret infection assay showed that the Δsod1 mutants had a reduced pathogenicity. Furthermore, the Δsod1 mutants had a significant reduction in production of deoxynivalenol mycotoxin. Our results indicate that the cytoplasmic Cu-Zn SOD1 affects fungal growth probably depending on detoxification of intracellular superoxide radicals, and that SOD1-mediated deoxynivalenol production contributes to the virulence of F. graminearum in wheat head infection

A CROSS-SECTIONAL STUDY OF KNEE FLEXION SPEED IN CHINESE CHILDREN DURING GROWTH

INTRODUCTION: In recent years, some research has been done on the relationship between the revolving speed of the adults` knee angles and sports achievements (Sheng, 1992; 1989; 1995). However, there is little information concerning this issue in children. The purpose of this study was to explore the developing regularity of the flexion speed of children’s knee angles across age

Dimethyl 2,2-bis­(2-cyano­ethyl)malonate

The asymmetric unit of the title compound, C11H14N2O4, contains one half-mol­ecule; a twofold rotation axis passes through the central C atom. Inter­molecular C—H⋯N hydrogen bonds link the mol­ecules into a one-dimensional supra­molecular structure

2,2′-Hexamethyl­enedi-1,3-benzothia­zole

The title compound, C20H20N2S2, was prepared by the reaction of suberic acid and 2-amino­thio­phenol under microwave irradiation. The mol­ecule lies on an inversion center

Phenyl N-(1,3-thia­zol-2-yl)carbamate

In the title compound, C10H8N2O2S, the planes of the aromatic rings are oriented at a dihedral angle of 66.69 (3)°. In the crystal structure, inter­molecular N—H⋯N and C—H⋯O inter­actions link the mol­ecules into a two-dimensional network, forming R 2 2(8) ring motifs. π–π contacts between the thia­zole rings [centroid–centroid distance = 3.535 (1) Å] may further stabilize the structure. A weak C—H⋯π inter­action is also found

Regulation of the transcription factor NF-κB1 by microRNA-9 in human gastric adenocarcinoma

<p>Abstract</p> <p>Background</p> <p>MicroRNAs (miRNAs) are a new class of naturally occurring, small, non-coding RNAs that regulate protein-coding mRNAs by causing mRNA degradation or repressing translation. The roles of miRNAs in lineage determination and proliferation, as well as the localization of several miRNA genes at sites of translocation breakpoints or deletions, have led to speculation that miRNAs could be important factors in the development or maintenance of the neoplastic state.</p> <p>Results</p> <p>We showed that miR-9 was downregulated in human gastric adenocarcinoma. Overexpression of miR-9 suppressed the growth of human gastric adenocarcinoma cell line MGC803 cell as well as xenograft tumors derived from them in SCID mice. Bioinformatics analysis indicated a putative miR-9 binding site in the 3'-untranslated region (3'UTR) of the tumor-related gene NF-κB1 mRNA. In an EGFP reporter system, overexpression of miR-9 downregulated EGFP intensity, and mutation of the miR-9 binding site abolished the effect of miR-9 on EGFP intensity. Furthermore, both the NF-κB1 mRNA and protein levels were affected by miR-9. Finally, knockdown of NF-κB1 inhibited MGC803 cell growth in a time-dependent manner, while ectopic expression of NF-κB1 could rescue MGC803 cell from growth inhibition caused by miR-9.</p> <p>Conclusion</p> <p>These findings indicate that miR-9 targets NF-κB1 and regulates gastric cancer cell growth, suggesting that miR-9 shows tumor suppressive activity in human gastric cancer pathogenesis.</p

4,4-Diacetyl­hepta­nedinitrile

The asymmetric unit of the title compound, C11H14N2O2, contains one half-mol­ecule as the central C atom of the mol­ecule lies on a twofold rotation axis. In the crystal structure, weak inter­molecular C—H⋯N hydrogen bonds link the mol­ecules into zigzag chains along c