Signaling Pathway
Biosynthesis Pathway
P. graminicola
De Vleesschauwer et al., 2012 showed that Phythium graminicola, P. graminicola, indirectly initiates stabilization and accumulation of DELLA proteins to reduce GA signaling, resulting in a decrease of host resistance.
XopDxcc8004
Tan et al., 2014 showed that XopDxcc8004 is an effector protein from Xanthomonas campestris that inhibits GA-degradation of DELLA proteins. If GA-degradation of DELLA proteins is affected, this results in DELLA-mediated repression of GA-signaling and defense responses.
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RDV P2
Zhu et al., 2005 showed that a protein from the RICE DWARF VIRUS, RDV P2, can interact with the GA biosynthetic enzyme, ent-KAURENE OXIDASE. This results in lower levels of bioactive GA1 synthesis and increased susceptibility to RDV.
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GA signaling pathway: Binding of GA to its nuclear receptor GID1 leading to conformation changes to GID1 favoring recruitment of DELLA proteins. DELLA proteins act as negative regulators of GA responses. Formation of the GID1-GA-DELLA complex initiates ubiquitylation and degradation of DELLA proteins through a 26S proteasome. Degradation of DELLA proteins is done by E3-ligase SCF complex with F-box proteins SLY1 (Arabidopsis) and GID2 (rice). The degradation of the negative regulator DELLA proteins, relieves the negative regulation of the GA pathway and allows for activation of GA-dependent responses.Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).
GA biosynthesis pathway: GA is synthesized in the plastids from the precursor GGDP, geranylgeranyl diphosphate. GGDP is converted to ent-CDP, ent-copalyl diphosphate, by CPS, then converted to ent-kaurene by KS. ent-kaurene is then converted into G12 by cytochrome P450 monooxygenases, KO and KAO. G12 can be converted into G53 by the 13-hydroxylation pathway, which results in bioactive forms of GA through oxidation steps by GA20ox and GA3ox to activate GA-dependent genes and responses.Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).
