Disease relevance of BON1

• In wild-type plants, CPN1 transcript accumulation was rapidly, locally, and transiently induced by both avirulent and virulent strains of Pseudomonas syringae pv tomato bacteria [1].

High impact information on BON1

• Plant growth homeostasis is controlled by the Arabidopsis BON1 and BAP1 genes [2].
• BON1 contains a Ca(2+)-dependent phospholipid-binding domain and is associated with the plasma membrane [2].
• Plants with even moderately reduced ACL activity have a complex, bonsai phenotype, with miniaturized organs, smaller cells, aberrant plastid morphology, reduced cuticular wax deposition, and hyperaccumulation of starch, anthocyanin, and stress-related mRNAs in vegetative tissue [3].
• BON1 is a negative regulator of a haplotype-specific Resistance (R) gene SNC1 [4].
• A humidity-sensitive Arabidopsis copine mutant exhibits precocious cell death and increased disease resistance [5].

Biological context of BON1

• Furthermore, the BAP1 protein probably functions together with an evolutionarily conserved C2 domain protein BON1/CPN1 to negatively regulate defense responses in plants [6].
• Thus BON1 and BAP1 may have a direct role in regulating cell expansion and cell division at lower temperatures [2].
• The loss of function of BON1 combined with that of BON2 or BON3 leads to extensive cell death phenotypes resembling the hypersensitive response (HR) in defense responses [7].
• The phenotype of mutants in BON1/CPN1 is both humidity- and temperature-sensitive [8].
• Alternatively, the primary function of CPN1 may be the regulation of plant responses to low humidity, and the effect of the cpn1-1 mutation on disease resistance may be indirect [5].

Associations of BON1 with chemical compounds

• When latrunculin B was added during germination, morphologically normal Arabidopsis and rye seedlings developed but, as a result of the absence of cell elongation, these were stunted, resembling either genetic dwarfs or environmental bonsai plants [9].
• CPN1 transcript accumulation was induced by salicylic acid treatment but was not observed during lesion formation in the lesion mimic mutants lsd1 and lsd5 [1].

References