Highly reducing polyketide synthase; part of the gene cluster that mediates the biosynthesis of the host-selective toxins (HSTs) ACR-toxins responsible for brown spot of rough lemon disease by the rough lemon pathotype (PubMed:22835272). ACR-toxins cause uncoupling of mitochondrial oxidative-phosphorylation similar to that of classic protonophore (PubMed:22846083). The structure of the major form of ACR-toxin (ACR-toxin I) consists of an alpha-dihydropyrone ring in a 19-carbon polyalcohol, a typical polyketide structure. Minor toxins were characterized as having a pyrone ring with polyalcohol side chains different in length and showing weaker toxicity (PubMed:22846083). The highly reducing polyketide synthase ACRTS2 has all necessary enzymatic domains for multiple cycles of condensation and beta-keto processing (PubMed:22779742). The cytochrome P450 monooxygenase ACRTS1 has also been shown to be essential for ACR-toxin biosynthesis, however its exact role in the pathway has not been elucidated yet (PubMed:22779742). Mycotoxin biosynthesis. Multidomain protein; including a ketosynthase (KS) that catalyzes repeated decarboxylative condensation to elongate the polyketide backbone; a malonyl-CoA:ACP transacylase (MAT) that selects and transfers the extender unit malonyl-CoA; a dehydratase (DH) domain that reduces hydroxyl groups to enoyl groups; a methyltransferase (CMeT) domain responsible for the incorporation of methyl groups; an enoylreductase (ER) domain that reduces enoyl groups to alkyl group; a ketoreductase (KR) domain that catalyzes beta-ketoreduction steps; and an acyl-carrier protein (ACP) that serves as the tether of the growing and completed polyketide via its phosphopantetheinyl arm. Abolishes the production of ACR-toxin and impairs the pathogenicity (PubMed:22835272). Does not affect growth rate of cultures, sporulation, and spore germination (PubMed:22835272). 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:22835272). The CDCs are not essential for saprophytic growth but controls host-selective pathogenicity (PubMed:22835272). Although conventional disruption of ACRTS2 could not be accomplished due to the high number of the copies identified in the genome, the high sequence identity among these copies of ACRTS2 is likely an advantage for RNA silencing, because it allows knockdown of all copies of this gene simultaneously (PubMed:22835272).