Genomics and domestication of wheat: Modern wheat, which underlies the diet of many across the globe, has a long history of selection and crosses among different species. Avni et al. used the Hi-C method of genome confirmation capture to assemble and annotate the wild allotetraploid wheat ( Triticum turgidum ). They then identified the putative causal mutations in genes controlling shattering (a key domestication trait among cereal crops). They also performed an exome capture–based analysis of domestication among wild and domesticated genotypes of emmer wheat. The findings present a compelling overview of the emmer wheat genome and its usefulness in an agricultural context for understanding traits in modern bread wheat. Science , this issue p. 93

Botrytis cinerea, a widespread plant pathogen with a necrotrophic lifestyle, causes gray mold disease in many crops. Massive secretion of enzymes and toxins was long considered to be the main driver of infection, but recent studies have uncovered a rich toolbox for B. cinerea pathogenicity. The emerging picture is of a multilayered infection process governed by the exchange of factors that collectively contribute to disease development. No plant shows complete resistance against B. cinerea, but pattern-triggered plant immune responses have the potential to significantly reduce disease progression, opening new possibilities for producing B. cinerea-tolerant plants. We examine current B. cinerea infection models, highlight knowledge gaps, and suggest directions for future studies.

Aegilops tauschii, the diploid wild progenitor of the D subgenome of bread wheat, is a reservoir of genetic diversity for improving bread wheat performance and environmental resilience. Here we sequenced 242 Ae. tauschii accessions and compared them to the wheat D subgenome to characterize genomic diversity. We found that a rare lineage of Ae. tauschii geographically restricted to present-day Georgia contributed to the wheat D subgenome in the independent hybridizations that gave rise to modern bread wheat. Through k-mer-based association mapping, we identified discrete genomic regions with candidate genes for disease and pest resistance and demonstrated their functional transfer into wheat by transgenesis and wide crossing, including the generation of a library of hexaploids incorporating diverse Ae. tauschii genomes. Exploiting the genomic diversity of the Ae. tauschii ancestral diploid genome permits rapid trait discovery and functional genetic validation in a hexaploid background amenable to breeding.

Cells of all living organisms are programmed to self-destruct under certain conditions. The most well known form of programmed cell death is apoptosi

Necrotrophic fungi are unable to occupy living plant cells. How such pathogens survive first contact with living host tissue and initiate infection is therefore unclear. Here, we show that the necrotrophic grey mold fungus Botrytis cinerea undergoes massive apoptotic-like programmed cell death (PCD) following germination on the host plant. Manipulation of an anti-apoptotic gene BcBIR1 modified fungal response to PCD-inducing conditions. As a consequence, strains with reduced sensitivity to PCD were hyper virulent, while strains in which PCD was over-stimulated showed reduced pathogenicity. Similarly, reduced levels of PCD in the fungus were recorded following infection of Arabidopsis mutants that show enhanced susceptibility to B. cinerea. When considered together, these results suggest that Botrytis PCD machinery is targeted by plant defense molecules, and that the fungal anti-apoptotic machinery is essential for overcoming this host-induced PCD and hence, for establishment of infection. As such, fungal PCD machinery represents a novel target for fungicides and antifungal drugs. Our work provides a fundamental new insight into the biology and infection strategy of Botrytis cinerea, an economically important plant pathogen, which is used as a model for studying pathogenicity of necrotrophic plant pathogens. A fundamental question that we sought to address in this study is how B. cinerea, and possibly other necrotrophic pathogens, overcome the plant defenses in living host cells. For the first time we show evidence that help explain the basic events behind early stages of necrotrophic interaction. Our results show that plant defense molecules target the fungal PCD machinery and trigger massive cell death in the pathogen. Conversely, the fungal anti-apoptotic machinery, mediated by the IAP-like protein BcBir1, protects the fungus from host-induced PCD, thereby allowing establishment of small infection zones, from which spreading lesions will be produced at the second infection stage. Weakening or strengthening of B. cinerea anti-apoptotic machinery results in reduced or enhanced disease symptoms, respectively, whereas weakening of the plant defense system is associated with reduced fungal PCD and enhanced disease. While the current results are restricted to B. cinerea, we believe that our findings have important implications for understanding of fungal-host interactions, including the interplay between pathogenic fungi and animal hosts, particularly human pathogens.

The infection of maize by Fusarium verticillioides can result in highly variable disease symptoms ranging from asymptomatic plants to severe rotting and wilting. We produced F. verticillioides green fluorescent protein-expressing transgenic isolates and used them to characterize early events in the F. verticillioides- maize interaction that may affect later symptom appearance. Plants grown in F. verticillioides- infested soil were smaller and chlorotic. The fungus colonized all of the underground parts of a plant but was found primarily in lateral roots and mesocotyl tissue. In some mesocotyl cells, conidia were produced within 14 to 21 days after infection. Intercellular mycelium was detected, but additional cells were not infected until 21 days after planting. At 25 to 30 days after planting, the mesocotyl and main roots were heavily infected, and rotting developed in these tissues. Other tissues, including the adventitious roots and the stem, appeared to be healthy and contained only a small number of hyphae. These results imply that asymptomatic systemic infection is characterized by a mode of fungal development that includes infection of certain tissues, intercellular growth of a limited number of fungal hyphae, and reproduction of the fungus in a few cells without invasion of other cells. Development of visibly rotted tissue is associated with massive production of fungal mycelium and much less organized growth.