Functions as both a virulence and an avirulence gene in Arabidopsis (PubMed:17951377, PubMed:23736288). Causes disease on the Kashmir (Kas) ecotype, but not on Columbia (Col-0) ecotype (PubMed:17951377). Acts by directly uridylylating the conserved phosphorylation sites in the activation loop of a number of host receptor-like cytoplasmic protein kinases (RLCK), including BIK1, RIPK, PBL1 and PBL2, preventing the activation of these kinases and subsequent signal transduction (PubMed:22504181, PubMed:26355215). In susceptible Arabidopsis plants, uridylylation of BIK1 inhibits the PAMP-triggered immunity (PTI) signaling cascade and thereby promotes bacterial virulence (PubMed:22504181). It also inhibits RPM1-dependent effector-triggered immunity (ETI) in mesophyll tissues by targeting RIPK (PubMed:22504181). In contrast, in the resistant ecotype Col-0, xopAC is a major avirulence gene (PubMed:23951354, PubMed:26355215). Uridylylation of PBL2 triggers the PBL2-RKS1 interaction and thus the assembly of the PBL2-RKS1-ZAR1 complex, which, in turn, activates effector-triggered immunity (ETI) against X.campestris (PubMed:26355215). L-seryl-[protein] + UTP = diphosphate + uridylyl-L-seryl-[protein] L-threonyl-[protein] + UTP = diphosphate + uridylyl-L-threonyl-[protein] Interacts with several members of the Arabidopsis RLCK VIIa subfamily. Secreted via the type III secretion system (TTSS) (Probable). Localization to the host plasma membrane requires the LRR domain (PubMed:23951354). Transcriptionally regulated by HrpG and HrpX. The LRR domain, the Fic/Fido domain and the uridylylation activity are required for avirulence function on Col-0. Mutant becomes virulent on Col-0 plants (PubMed:17951377, PubMed:23736288, PubMed:23951354). Mutant still induces disease on the Kashmir ecotype (PubMed:17951377, PubMed:23951354). In the C-terminal section; belongs to the fic family.