Comparative Genomics of Smut Pathogens: Insights From Orphans and Positively Selected Genes Into Host Specialization

Pang

et al. 2018

Sci Rep

Tilletia horrida is a soil-borne, mononucleate basidiomycete fungus with a biotrophic lifestyle that causes rice kernel smut, a disease that is distributed throughout hybrid rice growing areas worldwide. Here we report on the high-quality genome sequence of T. horrida; it is composed of 23.2 Mb that encode 7,729 predicted genes and 6,973 genes supported by RNA-seq. The genome contains few repetitive elements that account for 8.45% of the total. Evolutionarily, T. horrida lies close to the Ustilago fungi, suggesting grass species as potential hosts, but co-linearity was not observed between T. horrida and the barley smut Ustilago hordei. Genes and functions relevant to pathogenicity were presumed. T. horrida possesses a smaller set of carbohydrate-active enzymes and secondary metabolites, which probably reflect the specific characteristics of its infection and biotrophic lifestyle. Genes that encode secreted proteins and enzymes of secondary metabolism, and genes that are represented in the pathogen-host interaction gene database genes, are highly expressed during early infection; this is consistent with their potential roles in pathogenicity. Furthermore, among the 131 candidate pathogen effectors identified according to their expression patterns and functionality, we validated two that trigger leaf cell death in Nicotiana benthamiana. In summary, we have revealed new molecular mechanisms involved in the evolution, biotrophy, and pathogenesis of T. horrida.

Section: Discussionmentioning

confidence: 99%

The pathogenic mechanisms of Tilletia horrida as revealed by comparative and functional genomics

Pang

et al. 2018

Sci Rep

“…Once the effector targets have been identified, some of these could be exploited for resistance breeding (Gawehns et al, 2013). Also in this respect functional genomics can be deployed because effectors usually contain common regulatory cis-elements in their promoters or secretion signals in their peptides, which can be searched in pathogen genomes to identify candidate genes for further analysis (Zwiesler-Vollick et al, 2002;Benevenuto et al, 2018;Ai et al, 2020). Altering the host targets to prevent manipulation by pathogen effectors will impair compatibility and render the plant more resistant.…”

Section: Pipeline For Target Gene Identification In Resistance Breedingmentioning

confidence: 99%

Applications of CRISPR/Cas to Improve Crop Disease Resistance: Beyond Inactivation of Susceptibility Factors

Schenke

Cai

2020

iScience

Current crop production systems are prone to increasing pathogen pressure. Fundamental understanding of molecular plant-pathogen interactions, the availability of crop and pathogen genomic information, as well as emerging genome editing permits a novel approach for breeding of crop disease resistance. We describe here strategies to identify new targets for resistance breeding with focus on interruption of the compatible plant-pathogen interaction by CRISPR/ Cas-mediated genome editing. Basically, crop genome editing can be applied in several ways to achieve this goal. The most common approach focuses on the ''simple'' knockout by non-homologous end joining repair of plant susceptibility factors required for efficient host colonization. However, genome rewriting via homology-directed repair or base editing can also prevent host manipulation by changing the targets of pathogen-derived effectors or molecules beyond recognition, which also decreases plant susceptibility. We conclude that genome editing by CRISPR/Cas will become increasingly indispensable to generate in relatively short time beneficial resistance traits in crops to meet upcoming challenges.

“…However, prominent intron loss has also occurred in Ustilaginomycotina (Kämper et al 2006;Stajich et al 2007) . Many of these smuts and allies have evolved into plant pathogens and evolved a yeast state as part of their life cycle (Rush and Aime 2013;Wang et al 2015;Benevenuto et al 2018;Kijpornyongpan et al 2018) .…”

Section: Widespread Intron Loss In the Fungal Kingdommentioning

confidence: 99%

Analysis of fungal genomes reveals commonalities of intron loss/gain and functions in intron-poor species

Lim

Weinstein

Roy

et al. 2020

Preprint

Current evolutionary reconstructions predict that early eukaryotic ancestors including both the last common ancestor of eukaryotes and of all fungi had intron-rich genomes. However, some extant eukaryotes have few introns, raising the question as to why these few introns are retained. Here we have used recently available fungal genomes to address this question. Evolutionary reconstruction of intron presence and absence using 263 diverse fungal species support the idea that massive intron loss has occurred in multiple clades. The intron densities estimated in the fungal ancestral states differ from zero to 8.28 introns per one kbp of protein-coding gene. Massive intron loss has occurred not only in microsporidian parasites and saccharomycetous yeasts (0.01 and 0.05 introns/kbp on average, respectively), but also in diverse smuts and allies (e.g. Ustilago maydis, Meira miltonrushii and Malassezia globosa have 0.06, 0.10 and 0.20 introns/kbp, respectively). To investigate the roles of introns, we searched for their special characteristics using 1302 orthologous genes from eight intron-poor fungi. Notably, most of these introns are found close to the translation initiation codons. Our transcriptome and translatome data analyses showed that these introns are from genes with both higher mRNA expression and translation efficiency. Furthermore, these introns are common in specific classes of genes (e.g. genes involved in translation and Golgi vesicle transport), and rare in others (e.g. base-excision repair genes). Our study shows that fungal introns have a complex evolutionary history and underappreciated roles in gene expression.