Machado, M. A. | bioRxiv Science

bioRxiv2020

Mating-type locus rearrangement leads to shift from homothallism to heterothallism in Citrus-associated Phyllosticta species

Currently, eight Phyllosticta species are known to be associated with Citrus hosts, incorporating endophytic and pathogenic lifestyles. As sexual reproduction is a key factor involved in host-interaction, it could be related to the differences in lifestyle. To evaluate this hypothesis, we characterized the mating-type loci of six Citrus-associated Phyllosticta species from whole genome assemblies. Mating-type genes are highly variable in their sequence content, but the genomic locations and organization of the mating-type loci are conserved. Phyllosticta citriasiana, P. citribraziliensis and P. paracitricarpa are heterothallic, and P. citrichinaensis was confirmed to be homothallic. In addition, the P. citrichinaensis MAT1-2 idiomorph occurs in a separate location from the mating-type locus. Ancestral state reconstruction suggests that homothallism is the ancestral thallism state in Phyllosticta, with a shift to heterothallism in Phyllosticta species that are pathogenic to Citrus. Moreover, the homothallic strategies of P. capitalensis and P. citrichinaensis result from independent evolutionary events. As the pathogenic species P. citriasiana, P. citricarpa and P. paracitricarpa are heterothallic and incapable of selfing, disease management practices focused in preventing the occurrence of sexual reproduction could assist in the control of Citrus Black Spot and Citrus Tan Spot diseases. This study emphasizes the importance of studying Citrus-Phyllosticta interactions under evolutionary and genomic perspectives, as these approaches can provide valuable information about the association between Phyllosticta species and their hosts, and also serve as guidance for the improvement of disease management practices.

evolutionary biology↗

bioRxiv2018

The ecnA antitoxin is not only important for human pathogens: Evidences of its role in the plant pathogen Xathomonas citri subsp. citri

Xanthomonas citri subsp. citri causes citrus canker disease worldwide in most commercial varieties of citrus. Its transmission occurs mainly through wind-driven rain. Once on the leaf X. citri can epiphytically survive forming biofilm, which enhances persistence of the bacteria to different environmental stresses and play an important role in the early stages of host infection. Therefore, the study of genes involved in biofilm formation has been an important step towards the understanding of the bacterial strategy to survive and infect the plant host. In this work we show that ecnAB a Toxin-Antitoxin (TA) system, previously identified only in human bacterial pathogen, is conserved in many Xanthomonas spp. In general TA systems consist of a pair of genes in operon that encodes a stable toxin and an unstable antitoxin that, under normal conditions, binds to the toxin and blocks its activity. On the other hand, under stress the antitoxin is degraded, allowing the toxin to act decreasing cell growth and metabolism. When normal growth conditions are re-established, the antitoxin is produced, blocking the toxin and allowing the cells to grow. Thus, this mechanism represents an important bacterial strategy of survival under stress conditions. In this work, we show that in X. citri ecnAB is regulated by quorum sensing and it is involved in important processes such as biofilm formation, EPS production, and motility. In addition, we show that ecnAB plays a role in X. citri survival and virulence in plant host.\n\nIMPORTANCEVery little is known about TA systems in phytopathogenic bacteria. The ecnAB in special has been only studied in bacterial human pathogens. Here we showed that it is present in a wide range of the phytopathogen Xanthomonas spp., and moreover this is the first work that investigated the functional role of this TA system in Xanthomonas citri biology suggesting an important new role in adaptation and survival with implications in the bacterial pathogenicity.

microbiology↗