SIGNALING PATHWAYS OF CONIDIAL GERMINATION AND GROWTH OF BOTRYTIS CINEREA: HOST DETECTION, PATHOGENESIS ON VITIS VINIFERA AND PREFERENCE FOR WINE GRAPES

Abstract

Botrytis cinerea is a phytopathogenic filamentous fungus that infects and causes severe damages to numerous crops. However, the European grapevine (Vitis vinifera) remains the major host for the pathogen. Botrytis infects mainly ripe grapes (usually over 10 degrees Baumé) unless primary infections by other fungi, or infestations by viticultural insect pests, or mechanical damages have occurred. The disease is commonly known in viticulture as “Botrytis bunch rot” or “grey mold” and can spread rapidly causing devastating losses on the field and post-harvest. Regardless of its generalist action, B. cinerea must develop strategies to recognise and invade its host. The fungus responds to physical and chemical stimuli, emanated from the environment to activate spore germination and growth. Once a signal from the external environment meets a target molecule of the cell, the signaling process begins. The target molecule is a protein that acts as a receptor. The physical and chemical signals that stimulate conidial germination depend on factors such as surface hardness, surface hydrophobicity, carbon sources and nutrient-rich substrates. Among sugars, fructose is the best growth inducer of B. cinerea. Heterotrimeric guanine nucleotide binding proteins (G-proteins) are involved in the regulation of a range of functions including germination, growth and host detection. G-proteins consist of three subunits, α, β and γ. Two of these subunits attach to the cell membrane with small lipid tails. At rest, unit α is bound to Guanosine Diphosphate (GDP) and the G-protein is inactive. When an extracellular ligand binds to the receptor, the latter interacts with the G-protein and activates it, forcing the α subunit to excrete the bound GDP and replace it with Guanosine Triphosphate (GTP). In addition to signals that trigger spore germination, pathogenesis is also influenced by several biotic and abiotic factors. In general terms, interactions between pathogen, its potential host and the environment affect level, speed and nature of the infection and must be substantially considered in integrated control strategies.