By Hartshorne R., ed.
The ebook comprises survey papers in Algebraic Geometry.
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2 Current Knowledge of B. cinerea Infection Strategies Conidia, produced in large quantities in necrotized host tissue, are the main sources of infection by B. cinerea. In the presence of free water or high humidity ([93 % RH), germination is triggered by a combination of physical and chemical signals. While the mechanisms of signal perception are largely unknown yet, both a cAMP-dependent pathway and a MAP kinase cascade are involved in signal transduction leading to germination (Schumacher et al.
2012). Recent studies with S. sclerotiorum indicate that oxalic acid, on one hand promotes the apoptotic oxidative burst in the host plant that supports necrotrophic development, and on the other hand suppresses an early, defenseassociated oxidative burst during the initial stages of infection (Williams et al. 2011). B. cinerea can infect a variety of host tissues that greatly differ in their pH values, and the fungus itself modulates the pH during infection (Manteau et al. 2003; Billon-Grand et al.
5. How B. cinerea overcomes the strong defense reactions that accompany the HR, such as the release of reactive oxygen species (ROS), secretion of PR proteins and production of phytoalexins, is poorly understood. Surprisingly, a TF with a central role in ROS M. Hahn et al. detoxification, AP-1, was found to be not required for infection, which indicated that the fungus does not seem to suffer ROS stress during host invasion (Temme and Tudzynski, 2009). The situation is further complicated by the discovery that modulation of fungal apoptosis also plays a role in pathogenesis of B.