Host resistance and fungicide treatments are cornerstones of plant-disease control. Here, we show that these treatments allow sex and modulate parenthood in the fungal wheat pathogen Zymoseptoria tritici. We demonstrate that the Z. tritici-wheat interaction complies with the gene-for-gene model by identifying the effector AvrStb6, which is recognized by the wheat resistance protein Stb6. Recognition triggers host resistance, thus implying removal of avirulent strains from pathogen populations. However, Z. tritici crosses on wheat show that sex occurs even with an avirulent parent, and avirulence alleles are thereby retained in subsequent populations. Crossing fungicide-sensitive and fungicide-resistant isolates under fungicide pressure results in a rapid increase in resistance-allele frequency. Isolates under selection always act as male donors, and thus disease control modulates parenthood. Modeling these observations for agricultural and natural environments reveals extended durability of host resistance and rapid emergence of fungicide resistance. Therefore, fungal sex has major implications for disease control.

Microbial pathogens cause devastating diseases on economically and ecologically important plant species, threatening global food security, and causing billions of dollars of losses annually. During the infection process, pathogens secrete so-called effectors that support host colonization, often by deregulating host immune responses. Over the last decades, much of the research on molecular plant-microbe interactions has focused on the identification and functional characterization of such effectors. The increasing availability of sequenced plant pathogen genomes has enabled genomics-based discovery of effector candidates. Nevertheless, identification of full plant pathogen effector repertoires is often hampered by erroneous gene annotation and the localization effector genes in genomic regions that are notoriously difficult to assemble. Here, we argue that recent advances in genome sequencing technologies, genome assembly, gene annotation, as well as effector identification methods hold promise to disclose complete and correct effector repertoires. This allows to exploit complete effector repertoires, and knowledge of their diversity within pathogen populations, to develop durable and sustainable resistance breeding strategies, disease control, and management of plant pathogens.

20 42 strains that are able to infect the same host plant harbor highly divergent 43 LS effector repertoires. Furthermore, we observed differential V. dahliae 44 core effector gene expression between host plants. Our data suggest that 45 different V. dahliae lineages utilise divergent effector catalogs to colonize 46 the same host plant, suggesting considerable redundancy among the 47