Comparative genomics and transcriptomics reveal differences in effector complement and expression between races of f.sp. .

This study presents the first genome and transcriptome analyses for f. sp. (Fola) which causes Fusarium wilt disease of lettuce. Long-read genome sequencing of three race 1 (Fola1) and three race 4 (Fola4) isolates revealed key differences in putative effector complement between races and with other ff. spp. following -based bioinformatic analyses. Notably, homologues of () genes, also present in many other ff. spp, were identified in Fola, with both and (multiple copies with sequence variants) present in both Fola1 and Fola4. All Fola4 isolates also contained an additional single copy of . RNAseq of lettuce following infection with Fola1 and Fola4 isolates identified highly expressed effectors, some of which were homologues of those reported in other ff. spp. including several in f. sp. . Although , and were all highly expressed in Fola4, of the two genes present in Fola1, only was expressed as further analysis revealed that gene copies were disrupted by insertion of a transposable element. Two variants of Fola4 were also identified based on different genome and effector-based analyses. This included two different sequence variants which were divergently transcribed from a shared promoter with either or respectively. In addition, there was evidence of two independent instances of HCT in the different Fola4 variants. The involvement of helitrons in Fola genome rearrangement and gene expression is discussed.