SUMMARY Fusarium graminearum is the causal agent of ear blight disease of cereals. Infection occurs at anthesis when ascospores and/or conidia directly penetrate exposed anther and ovary tissue. The hemibiotrophic hyphae colonize floral tissues and developing grains to cause premature ear senescence. During infection, Fusarium hyphae can also produce hazardous trichothecene mycotoxins, thereby posing a threat to human and animal health and safety. The Fusarium MAP1 gene was identified using a PCR approach by its homology to a known pathogenicity gene of Magnaporthe grisea, the mitogen-activated protein kinase gene PMK1. Gene replacement F. graminearum map1 mutants were non-pathogenic on wheat flowers and roots, and also could not infect wounded wheat floral tissue or tomato fruits. Unlike the wild-type strain, map1 mutant inoculations did not compromise grain yield. Map1 mutants lost their ability to form perithecia in vitro, but their rate of asexual conidiation was unaffected. DON mycotoxin production in planta was still detected. Collectively, the observed phenotypes suggest that the Map1 signalling protein controls multiple events in disease establishment and propagation. Novel approaches to control Fusarium ear blight disease by blocking perithecial development are discussed.

Recent experiments at JET combining reciprocating probe measurements upstream and infrared thermography at the plasma-facing components (PFC) on plasmas in limiter configurations show that the common approach to predicting the power load on the limiter underestimates the heat flux at the contact point by a factor 1.5–3. The current model and scaling laws used for predicting the power load onto the first wall during limiter current ramp-up/down in ITER are uncertain and a better understanding of the heat transport to the PFCs is required. The heat loads on PFCs are usually predicted by projecting the parallel heat flux associated with scrape-off layer (SOL) properties at the outer mid-plane (upstream) along the magnetic field lines to the limiter surface and deducing the surface heat flux through a cosine law, thus ignoring any local effect of the PFC on transport within the SOL. The underestimate of the heat flux is systematic in inner wall limiter configurations, independent of the plasma parameters, whereas in outer limiter configuration this is not observed, probably because of the much shorter SOL power decay length. Models that can explain this enhanced heat flux around the contact point are proposed and discussed although no definitive conclusion can be drawn.

The structure and motion of inter-ELM filaments on MAST