“…Indirect physiological alterations induced in cell wall-defective mutants or after transgenic or pharmacological interference with cell wall biosynthesis or structure [, induction of; Y, suppression of; as, antisense suppression; ASR, abiotic stress resistance; AXS, UDP-apiose/UDP-xylose synthase; CalS, callose synthase; CD, cell death, both programmed and necrotic; CE, cellulose; CesA, cellulose synthase catalytic subunit; CH, carbohydrates; DCB, 2,6-dichlorobenzonitrile; DR, disease resistance and reduced pathogen susceptibility; ET, ethylene; EXT, extensin; GM, glucomannan; GMD, GDP-Dmannose 4,6-dehydratase; HSR, hypersensitive to sugar; JA, jasmonic acid; PE, pectin; PME, pectin methyl esterase; SA, salicylic acid. (Aziz et al, 2007) acting as potent elicitors of innate immunity. This class of elicitors has been termed host-associated molecular patterns (Galletti et al, 2009) or damage-associated molecular patterns (Zipfel, 2009), in analogy to pathogen-associated molecular patterns (PAMPs; for review, see Zipfel, 2009).…”