Abhydrolase domain-containing protein; part of the gene clusters that mediate the biosynthesis of the host-selective toxins (HSTs) AK-toxins responsible for Japanese pear black spot disease by the Japanese pear pathotype (PubMed:10432635, PubMed:20348386). AK-toxins are esters of 9,10-epoxy 8-hydroxy 9-methyldecatrienoic acid (EDA) (PubMed:22846083). On cellular level, AK-toxins affect plasma membrane of susceptible cells and cause a sudden increase in loss of K(+) after a few minutes of toxin treatment (PubMed:22846083). The acyl-CoA ligase AKT1, the hydrolase AKT2 and enoyl-CoA hydratase AKT3 are all involved in the biosynthesis of the AK-, AF- and ACT-toxin common 9,10-epoxy-8-hydroxy-9-methyl-decatrienoic acid (EDA) structural moiety (PubMed:10432635, PubMed:10975654, PubMed:22846083). Part of the EDA biosynthesis occurs in the peroxisome since these 3 enzymes are localized in peroxisomes (PubMed:20348386). The exact roles of the 3 enzymes, as well as of additional AK-toxin clusters enzymes, including AKT4, AKT6 and AKTS1, have still to be elucidated (PubMed:10432635, PubMed:10975654, PubMed:22846083). The Cytochrome P450 monooxygenase AKT7 on the other side functions to limit production of EDA and AK-toxin, probably via the catalysis of a side reaction of EDA or its precursor (PubMed:24611558). Mycotoxin biosynthesis. The peroxisomal location requires the C-terminal tripeptide peroxisomal targeting signal. Abolishes the production of AK-toxin and impairs the pathogenicity. Gene clusters encoding host-selective toxins (HSTs) are localized on conditionally dispensable chromosomes (CDCs), also called supernumerary chromosomes, where they are present in multiple copies (PubMed:10975654). The CDCs are not essential for saprophytic growth but controls host-selective pathogenicity (PubMed:10975654). Belongs to the AB hydrolase superfamily. AKT2 hydrolase family.