The Genetic Architecture of Emerging Fungicide Resistance in Populations of a Global Wheat Pathogen

Abstract

Mammalian male meiosis requires homologous recombination between the X and Y chromosomes. In humans, such recombination occurs exclusively in the short arm pseudoautosomal region (PAR1) of 2.699 Mb in size. Although it is known that complete deletion of PAR1 causes spermatogenic arrest, no studies have addressed to what extent male meiosis tolerates PAR1 size reduction. Here, we report two families in which PAR1 partial deletions were transmitted from fathers to their offspring. Cytogenetic analyses revealed that a ∼400 kb segment at the centromeric end of PAR1, which accounts for only 14.8% of normal PAR1 and 0.26% and 0.68% of the X and Y chromosomes respectively, is sufficient to mediate sex chromosomal recombination during spermatogenesis. These results highlight the extreme recombinogenic activity of human PAR1. Our data, in conjunction with previous findings, indicate that the minimal size requirement of mammalian PARs to maintain male fertility is fairly small.

Population genomics of transposable element activation in the highly repressive genome of an agricultural pathogen

“…For this work, we significantly expanded previous population genomic analyses of P. nodorum for both geographical coverage and sample size [24, 43, 44]. Our results corroborate evidence for genetic admixture among North America, Europe (Switzerland) and the Middle East (Iran) consistent with earlier analyses based on microsatellite loci [51].…”

“…The gene annotation for the reference genome Sn2000 was previously established [ 43 ]. Briefly, predicted protein sequences of P. nodorum Sn15 strain were aligned and queries with a at least 95 % identity score were maintained.…”

“…In the wheat pathogen Parastagonospora nodorum , TEs have caused significant genetic alterations and likely facilitated the transfer of a key virulence gene. P. nodorum is a pathogen with high evolutionary potential to adapt to local conditions [24, 43, 44] and a worldwide distribution causing significant wheat-yield losses [45]. The pathogen harbours a repertoire of various effector genes (named Tox genes) that confer host adaptation by causing cell death in susceptible plants.…”

The complex genomic basis of rapid convergent adaptation to pesticides across continents in a fungal plant pathogen

“…Genome-wide mutations conferring small increases to resistance tend to impose small detrimental effects on pathogen growth and even virulence traits. Even though such trade-offs are not universal among pathogens (Pereira et al, 2020), exploiting evolutionary constraints in fungicide resistance could lead to durable control strategies.…”

New insights from short and long reads sequencing to explore cytochrome b variants of Plasmopara viticola populations collected in vineyard and related to resistance to complex III inhibitors

“…To go further and analyse cyt b polymorphism at a natural population scale, NGS technologies were first benchmarked to sequence the complete cyt b from single-sporangia strains and then applied to analyse field populations of P. viticola . Still relatively poorly present in studies associated to plant pathogen resistance to fungicide and targeting usually full pathogen genomes [23,24], both short-read (Ion Torrent and Illumina) and long-read (Oxford Nanopore Technologies, ONT) technologies were tested and compared in our study. They revealed to be efficient to identify and monitor cyt b variants in natural populations but also promising to become a robust tool for decision-support in management of fungicide resistance, potentially directly in the field, in near future.…”