Anti-MOAP1 (center region) polyclonal antibody

We have shown previously that the transcription factor MoAP1 governs the oxidative response and is important for pathogenicity in the rice blast fungus Magnaporthe oryzae. To explore the underlying mechanism, we have identified thioredoxin MoTrx2 as a target of MoAP1 in M. oryzae. Thioredoxins are highly conserved 12-kDa oxidoreductase enzymes containing a dithiol-disulfide active site, and function as antioxidants against free radicals, such as reactive oxygen species (ROS). In yeast and fungi, thioredoxins are important for oxidative stress tolerance and growth. To study the functions of MoTrx2, we generated Delta Motrx2 mutants that exhibit various defects, including sulfite assimilation, asexual and sexual differentiation, infectious hyphal growth and pathogenicity. We found that Delta Motrx2 mutants possess a defect in the scavenging of ROS during host cell invasion and in the active suppression of the rice defence response. We also found that Delta Motrx2 mutants display higher intracellular ROS levels during conidial germination, but lower peroxidase and laccase activities, which contribute to the attenuation in virulence. Given that the function of MoTrx2 overlaps that of MoAP1 in the stress response and pathogenicity, our findings further indicate that MoTrx2 is a key thioredoxin protein whose function is subjected to transcriptional regulation by MoAP1 in M. oryzae.

Objective. To characterize the gene expression profile and determine potential diagnostic markers and therapeutic targets in pigmented villonodular synovitis (PVNS). Methods. Gene expression patterns in 11 patients with PVNS, 18 patients with rheumatoid arthritis (RA), and 19 patients with osteoarthritis (OA) were investigated using genome-wide complementary DNA microarrays. Validation of differentially expressed genes was performed by real-time quantitative polymerase chain reaction and immunohistochemical analysis on tissue arrays (80 patients with PVNS, 51 patients with RA, and 20 patients with OA). Results. The gene expression profile in PVNS was clearly distinct from those in RA and OA. One hundred forty-one up-regulated genes and 47 down-regulated genes were found in PVNS compared with RA, and 153 up-regulated genes and 89 down-regulated genes were found in PVNS compared with OA (fold change >= 1.5; Q <= 0.001). Genes differentially expressed in PVNS were involved in apoptosis regulation, matrix degradation, and inflammation (ALOX5AP, ATP6V1B2, CD53, CHBL1, CTSL, CXCR4, HSPA8, HSPCA, LAPTM5, MHP9, MOAP1, and SPP1). Conclusion. The gene expression signature in PVNS is similar to that of activated macrophages and is consistent with the local destructive course of the disease. The gene and protein expression patterns suggest that the ongoing proliferation in PVNS is sustained by apoptosis resistance. This result suggests the possibility of a potential novel therapeutic intervention against PVNS.