Remodeling of Lipid A in pv. In Vitro.

species infect a variety of organisms, including mammals and plants. Mammalian pathogens of the Pseudomonas family modify their lipid A during host entry to evade immune responses and to create an effective barrier against different environments, for example by removal of primary acyl chains, addition of phosphoethanolamine (-EtN) to primary phosphates, and hydroxylation of secondary acyl chains. For pv.

Bacterial rhamnolipids and their 3-hydroxyalkanoate precursors activate innate immunity through two independent mechanisms.

Plant innate immunity is activated upon perception of invasion pattern molecules by plant cell-surface immune receptors. Several bacteria of the genera and produce rhamnolipids (RLs) from l-rhamnose and ()-3-hydroxyalkanoate precursors (HAAs). RL and HAA secretion is required to modulate bacterial surface motility, biofilm development, and thus successful colonization of hosts.

Bacterial medium-chain 3-hydroxy fatty acid metabolites trigger immunity in plants.

In plants, cell-surface immune receptors sense molecular non-self-signatures. Lipid A of Gram-negative bacterial lipopolysaccharide is considered such a non-self-signature. The receptor kinase LIPOOLIGOSACCHARIDE-SPECIFIC REDUCED ELICITATION (LORE) mediates plant immune responses to and but not enterobacterial lipid A or lipopolysaccharide preparations.