背景回顾-病原菌+寄主：In the absence of these typical pathogenicity factors, P. ananatis induces necrotic symptoms and extensive cell death in onion tissue dependent on the HiVir proposed secondary metabolite synthesis gene cluster.

背景回顾-寄主特性：Onion (Allium. cepa L), garlic (A. sativumL.), and other members of the Allium genus produce volatile antimicrobial thiosulfinates upon cellular damage.

提出问题：However, the roles of endogenous thiosulfinate production in host-bacterial pathogen interactions have not been described.

主要发现：We found a strong correlation between the genetic requirements for P. ananatis to colonize necrotized onion tissue and its capacity for tolerance to the thiosulfinate“allicin” based on the presence of an eleven-gene, plasmid-borne, virulence cluster of sulfur redox genes.

研究结果：We have designated them “alt” genes for allicin tolerance. We show that allicin and onion thiosulfinates restrict bacterial growth with similar kinetics. The alt gene cluster is sufficient to confer allicin tolerance and protects the glutathione pool during allicin treatment. Independent alt genes make partial phenotypic contributions indicating that they function as a collective cohort to manage thiol stress. 

结论：Our work implicates endogenous onion thiosulfinates produced during cellular damage as major mediators of interactions with bacteria.

展望：The P. ananatis-onion pathosystem can be modeled as a chemical arms race of pathogen attack, host chemical counterattack, and pathogen defense.