Genomic prediction of strawberry resistance to postharvest fruit decay caused by the fungal pathogen Botrytis cinerea.

Gray mold, a disease of strawberry (Fragaria × ananassa) caused by the ubiquitous necrotroph Botrytis cinerea, renders fruit unmarketable and causes economic losses in the postharvest supply chain. To explore the feasibility of selecting for increased resistance to gray mold, we undertook genetic and genomic prediction studies in strawberry populations segregating for fruit quality and shelf life traits hypothesized to pleiotropically affect susceptibility. As predicted, resistance to gray mold was heritable but quantitative and genetically complex. While every individual was susceptible, the speed of symptom progression and severity differed. Narrow-sense heritability ranged from 0.38 to 0.71 for lesion diameter (LD) and 0.39 to 0.44 for speed of emergence of external mycelium (EM). Even though significant additive genetic variation was observed for LD and EM, the phenotypic ranges were comparatively narrow and genome-wide analyses did not identify any large-effect loci. Genomic selection (GS) accuracy ranged from 0.28 to 0.59 for LD and 0.37 to 0.47 for EM. Additive genetic correlations between fruit quality and gray mold resistance traits were consistent with prevailing hypotheses: LD decreased as titratable acidity increased, whereas EM increased as soluble solid content decreased and firmness increased. We concluded that phenotypic and GS could be effective for reducing LD and increasing EM, especially in long shelf life populations, but that a significant fraction of the genetic variation for resistance to gray mold was caused by the pleiotropic effects of fruit quality traits that differ among market and shelf life classes.

Grey mould of strawberry, a devastating disease caused by the ubiquitous necrotrophic fungal pathogen Botrytis cinerea.

The fungal pathogen Botrytis cinerea causes grey mould, a commercially damaging disease of strawberry. This pathogen affects fruit in the field, storage, transport and market. The presence of grey mould is the most common reason for fruit rejection by growers, shippers and consumers, leading to significant economic losses. Here, we review the biology and epidemiology of the pathogen, mechanisms of infection and the genetics of host plant resistance. The development of grey mould is affected by environmental and genetic factors; however, little is known about how B. cinerea and strawberry interact at the molecular level. Despite intensive efforts, breeding strawberry for resistance to grey mould has not been successful, and the mechanisms underlying tolerance to B. cinerea are poorly understood and under-investigated. Current control strategies against grey mould include pre- and postharvest fungicides, yet they are generally ineffective and expensive. In this review, we examine available research on horticultural management, chemical and biological control of the pathogen in the field and postharvest storage, and discuss their relevance for integrative disease management. Additionally, we identify and propose approaches for increasing resistance to B. cinerea in strawberry by tapping into natural genetic variation and manipulating host factors via genetic engineering and genome editing.

What makes turnips: anatomy, physiology and transcriptome during early stages of its hypocotyl-tuber development.

Brassica species are characterized by their tremendous intraspecific diversity, exemplified by leafy vegetables, oilseeds, and crops with enlarged inflorescences or above ground storage organs. In contrast to potato tubers that are edible storage organs storing energy as starch and are the vegetative propagation modules, the storage organs of turnips, grown from true seed, are swollen hypocotyls with varying degrees of root and stem that mainly store glucose and fructose. To highlight their anatomical origin, we use the term "hypocotyl-tuber" for these turnip vegetative storage organs. We combined cytological, physiological, genetic and transcriptomic approaches, aiming to identify the initial stages, molecular pathways and regulatory genes for hypocotyl-tuber induction in turnips (B. rapa subsp. rapa). We first studied the development of the hypocotyl zone of turnip and Pak choi and found that 16 days after sowing (DAS) morphological changes occurred in the xylem which indicated the early tuberization stage. Tissue culture experiments showed a clear effect of auxin on hypocotyl-tuber growth. Differentially expressed genes between 1 and 6 weeks after sowing in turnip hypocotyls, located in genomic regions involved in tuber initiation and/or tuber growth defined by QTL and selective sweeps for tuber formation, were identified as candidate genes that were studied in more detail for their role in hypocotyl-tuber formation. This included a Bra-FLOR1 paralogue with increased expression 16 DAS, when the hypocotyl starts swelling, suggesting dual roles for duplicated flowering time genes in flowering and hypocotyl-tuber induction. Bra-CYP735A2 was identified for its possible role in tuber growth via trans-zeatin. Weigthed Co-expression Network Analysis (WGCNA) identified 59 modules of co-expressed genes. Bra-FLOR1 and Bra-CYP735A2 were grouped in a module that included several genes involved in carbohydrate transport and metabolism, cell-wall growth, auxin regulation and secondary metabolism that serve as starting points to illuminate the transcriptional regulation of hypocotyl-tuber formation and development.

Infection Strategies Deployed by Botrytis cinerea, Fusarium acuminatum, and Rhizopus stolonifer as a Function of Tomato Fruit Ripening Stage.

Worldwide, 20-25% of all harvested fruit and vegetables are lost annually in the field and throughout the postharvest supply chain due to rotting by fungal pathogens. Most postharvest pathogens exhibit necrotrophic or saprotrophic lifestyles, resulting in decomposition of the host tissues and loss of marketable commodities. Necrotrophic fungi can readily infect ripe fruit leading to the rapid establishment of disease symptoms. However, these pathogens generally fail to infect unripe fruit or remain quiescent until host conditions stimulate a successful infection. Previous research on infections of fruit has mainly been focused on the host's genetic and physicochemical factors that inhibit or promote disease. Here, we investigated if fruit pathogens can modify their own infection strategies in response to the ripening stage of the host. To test this hypothesis, we profiled global gene expression of three fungal pathogens that display necrotrophic behavior-Botrytis cinerea, Fusarium acuminatum, and Rhizopus stolonifer-during interactions with unripe and ripe tomato fruit. We assembled and functionally annotated the transcriptomes of F. acuminatum and R. stolonifer as no genomic resources were available. Then, we conducted differential gene expression analysis to compare each pathogen during inoculations versus in vitro conditions. Through characterizing patterns of overrepresented pathogenicity and virulence functions (e.g., phytotoxin production, cell wall degradation, and proteolysis) among the differentially expressed genes, we were able to determine shared strategies among the three fungi during infections of compatible (ripe) and incompatible (unripe) fruit tissues. Though each pathogen's strategy differed in the details, interactions with unripe fruit were commonly characterized by an emphasis on the degradation of cell wall components, particularly pectin, while colonization of ripe fruit featured more heavily redox processes, proteolysis, metabolism of simple sugars, and chitin biosynthesis. Furthermore, we determined that the three fungi were unable to infect fruit from the non-ripening (nor) tomato mutant, confirming that to cause disease, these pathogens require the host tissues to undergo specific ripening processes. By enabling a better understanding of fungal necrotrophic infection strategies, we move closer to generating accurate models of fruit diseases and the development of early detection tools and effective management strategies.

Next-generation sequencing reveals differentially amplified tandem repeats as a major genome component of Northern Europe's oldest Camellia japonica.

Northern Europe's oldest and largest Camellia japonica growing at the Pillnitz Castle (Germany) for over 200 years is of botanical and cultural importance and is a reference for C. japonica molecular scale analysis. In order to provide a fundament for genome analysis of the genus Camellia, we characterize the C. japonica tandem repeat fraction, constituting 12.5 % of the Pillnitz camellia's genome. A genomic library of the Pillnitz C. japonica was produced and Illumina sequenced to generate 36 Gb of paired-end reads. We performed graph-based read clustering implemented in the RepeatExplorer pipeline to estimate the C. japonica repeat fraction of 73 %. This enabled us to identify and characterize the most prominent satellite DNAs, Camellia japonica satellite 1-4 (CajaSat1-CajaSat4), and the 5S ribosomal DNA (rDNA) by bioinformatics, fluorescent in situ and Southern hybridization. Within the Camellia genus, satellite spreading, array expansion and formation of higher-order structures highlight different modes of repeat evolution. The CajaSat satellites localize at prominent chromosomal sites, including (peri)centromeres and subtelomeres of all chromosomes, thus serving as chromosomal landmarks for their identification. This work provides an insight into the C. japonica chromosome organization and significantly expands the Camellia genomic knowledge, also with respect to the tea plant Camellia sinensis.