Secreted effector that acts as an elicitor of hypersensitive response (HR) specifically on plants carrying defense protein R1, through its interaction with this protein (PubMed:12000683, PubMed:25760731, PubMed:29910515). Acts also as a virulence factor that promotes colonization and suppresses cell death induced by CRN2 as well as callose deposition, a hallmark of basal defense (PubMed:26336092, PubMed:30329083). Interacts with host exocyst component Sec5 and thereby disturbs vesicle trafficking, a cellular process that is important for basal defense. By targeting and stabilizing Sec5 in the cytoplasm, the exocyst complex is thus out of balance and not able to mediate the focal secretion of PR-1 and callose (PubMed:26336092). Interacts with host exocyst component Sec5. Nuclear-localized Avr1 triggers the R1-mediated HR, whereas cytoplasmic localization is required for suppression of CRN2-induced cell death (PubMed:25760731). Also localized at Sec5-associated subcellular bodies (PubMed:30329083). Expression is induced during host plant infection. The RxLR-dEER motif acts to carry the protein into the host cell cytoplasm through binding to cell surface phosphatidylinositol-3-phosphate. The C-terminal domain of Avr1 comprises three motifs (W1, W2, and Y), two linker regions (ln1 and ln2), and at the very end the T-region. The T-region of AVR1 is important but not sufficient to trigger R1-mediated HR and W1, W2 and Y are equally important for recognition by R1. Belongs to the RxLR effector family.