Inversely, strongest responses to the infection were particularly activated in G stage through an over-accumulation of primary metabolism proteins, defense and stress-related proteins (e.g., oxygen evolving enhancer, S-adenosylmethionine synthetase, 2-cys peroxiredoxin, pathogenesis related protein 10) in correlation with a lower development of the necrosis. This evidence concerns the gene MAT1A and infection.