Sphingosine N-acyltransferase-like protein; part of the gene cluster that mediates the biosynthesis of the host-selective toxins (HSTs) AAL-toxins, sphinganine-analog mycotoxins responsible for Alternaria stem canker on tomato by the tomato pathotype (PubMed:18435561, PubMed:19749175, PubMed:19449880). The biosynthesis starts with the polyketide synthase ALT1-catalyzed C-16 carbon chain assembly from one starter acetyl-CoA unit with malonyl-CoA extender units (PubMed:18435561, PubMed:19449880). ALT1 also selectively transfers methyl groups at the first and the third cycle of chain elongation for AAL toxin (PubMed:19449880). The C-16 polyketide chain is released from the enzyme by a nucleophilic attack of a carbanion, which is derived from R-carbon of glycin by decarboxylation, on the carbonyl carbon of polyketide acyl chain (Probable). This step is probably catalyzed by a pyridoxal 5'-phosphate-dependent aminoacyl transferase ALT4 (Probable). The respective functions of the other enzymes encoded by the cluster have still to be elucidated (Probable). The sphingosine N-acyltransferase-like protein ALT7 seems not to act as a resistance/self-tolerance factor against the toxin in the toxin biosynthetic gene cluster, contrary to what is expected (Ref.6). Mycotoxin biosynthesis. Does not cause any detectable defects in the vegetative and reproductive properties of the toxin-producing pathogen. The deletion of ALT7 has no deleterious effect on the toxin-producing pathogen, indicating that the gene does not act as a resistance/self-tolerance factor against the toxin in the toxin biosynthetic gene cluster. 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. The CDCs are not essential for saprophytic growth but controls host-selective pathogenicity. Belongs to the sphingosine N-acyltransferase family.