The PERPETUAL FLOWERING locus: Necessary but insufficient for genomic prediction of runnerless and other asexual reproduction phenotypes in strawberry.

Strawberry (Fragaria ananassa) reproduces sexually through seeds and asexually through stolons. The ability to cost-effectively clonally propagate hybrid individuals on a large scale has shaped strawberry breeding and production practices. Despite the technical and economic importance of clonal propagation, little is known about the genetic regulation of runnering in strawberry, apart from the pleiotropic effects of PERPETUAL FLOWERING (PF), a dominant gene introgressed from a wild relative that abolishes temperature-dependent photoperiod sensitivity and incompletely and variably suppresses runnering.

Unraveling the f. sp. -Strawberry Interaction: Evolution, Infection, and Genetic Resistance.

Fusarium wilt of strawberry, caused by the soil-borne fungal pathogen f. sp. (), is one of the greatest threats to cultivated strawberry.

Loss-of-function mutations in the fruit softening gene doubled fruit firmness in strawberry.

Wildtype fruit of cultivated strawberry (  [Formula: see text]  ) are typically soft and highly perishable when fully ripe. The development of firm-fruited cultivars by phenotypic selection has greatly increased shelf-life, decreased postharvest perishability, and driven the expansion of strawberry production worldwide. Hypotheses for the firm-fruited phenotype include mutations affecting the expression of genes encoding polygalacturonases (PGs) that soften fruit by degrading cell wall pectins.

Cutin-derived oligomers induce hallmark plant immune responses.

The cuticle constitutes the outermost defensive barrier of most land plants. It comprises a polymeric matrix-cutin, surrounded by soluble waxes. Moreover, the cuticle constitutes the first line of defense against pathogen invasion, while also protecting the plant from many abiotic stresses.

Transgressive segregation, hopeful monsters, and phenotypic selection drove rapid genetic gains and breakthroughs in predictive breeding for quantitative resistance to in strawberry.

Two decades have passed since the strawberry () disease caused by , a necrotrophic soilborne fungal pathogen, began surfacing in California, Florida, and elsewhere. This disease has since become one of the most common causes of plant death and yield losses in strawberry. The problem emerged and expanded in the wake of the global phase-out of soil fumigation with methyl bromide and appears to have been aggravated by an increase in climate change-associated abiotic stresses.

COG-imposed Golgi functional integrity determines the onset of dark-induced senescence.

Plant survival depends on dynamic stress-response pathways in changing environments. To uncover pathway components, we screened an ethyl methanesulfonate-mutagenized transgenic line containing a stress-inducible luciferase construct and isolated a constitutive expression mutant. The mutant is the result of an amino acid substitution in the seventh subunit of the hetero-octameric conserved oligomeric Golgi (COG) complex of Arabidopsis thaliana.

Harnessing underutilized gene bank diversity and genomic prediction of cross usefulness to enhance resistance to Phytophthora cactorum in strawberry.

The development of strawberry (Fragaria × ananassa Duchesne ex Rozier) cultivars resistant to Phytophthora crown rot (PhCR), a devastating disease caused by the soil-borne pathogen Phytophthora cactorum (Lebert & Cohn) J. Schröt., has been challenging partly because the resistance phenotypes are quantitative and only moderately heritable.

Perception of a conserved family of plant signalling peptides by the receptor kinase HSL3.

Plant genomes encode hundreds of secreted peptides; however, relatively few have been characterised. We report here an uncharacterised, stress-induced family of plant signalling peptides, which we call CTNIPs. Based on the role of the common co-receptor BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED KINASE 1 (BAK1) in CTNIP-induced responses, we identified in the orphan receptor kinase HAESA-LIKE 3 (HSL3) as the CTNIP receptor via a proteomics approach.

Direct inhibition of phosphate transport by immune signaling in Arabidopsis.

Soil availability of inorganic ortho-phosphate (PO, P) is a key determinant of plant growth and fitness. Plants regulate the capacity of their roots to take up inorganic phosphate by adapting the abundance of H-coupled phosphate transporters of the PHOSPHATE TRANSPORTER 1 (PHT1) family at the plasma membrane (PM) through transcriptional and post-translational changes driven by the genetic network of the phosphate starvation response (PSR). Increasing evidence also shows that plants integrate immune responses to alleviate phosphate starvation stress through the association with beneficial microbes.

Activation loop phosphorylation of a non-RD receptor kinase initiates plant innate immune signaling.

Receptor kinases (RKs) are fundamental for extracellular sensing and regulate development and stress responses across kingdoms. In plants, leucine-rich repeat receptor kinases (LRR-RKs) are primarily peptide receptors that regulate responses to myriad internal and external stimuli. Phosphorylation of LRR-RK cytoplasmic domains is among the earliest responses following ligand perception, and reciprocal transphosphorylation between a receptor and its coreceptor is thought to activate the receptor complex.

Plant immunity: Crosstalk between plant immune receptors.

Plant immunity has long been divided into two 'tiers', involving cell-surface versus intracellular immune receptors. Although both systems can induce similar diagnostic responses, they have been considered independent pathways. Recent work challenges this view, showing a striking requirement for both recognition layers to achieve maximum immune output.

The transcriptional landscape of Arabidopsis thaliana pattern-triggered immunity.

Plants tailor their metabolism to environmental conditions, in part through the recognition of a wide array of self and non-self molecules. In particular, the perception of microbial or plant-derived molecular patterns by cell-surface-localized pattern recognition receptors (PRRs) induces pattern-triggered immunity, which includes massive transcriptional reprogramming. An increasing number of plant PRRs and corresponding ligands are known, but whether plants tune their immune outputs to patterns of different biological origins or of different biochemical natures remains mostly unclear.

Low-cost and High-throughput RNA-seq Library Preparation for Illumina Sequencing from Plant Tissue.

Transcriptome analysis can provide clues to biological processes affected in different genetic backgrounds or/and under various conditions. The price of RNA sequencing (RNA-seq) has decreased enough so that medium- to large-scale transcriptome analyses in a range of conditions are feasible. However, the price and variety of options for library preparation of RNA-seq can still be daunting to those who would like to use RNA-seq for their first time or for a single experiment.

Initiation of ER Body Formation and Indole Glucosinolate Metabolism by the Plastidial Retrograde Signaling Metabolite, MEcPP.

Plants have evolved tightly regulated signaling networks to respond and adapt to environmental perturbations, but the nature of the signaling hub(s) involved have remained an enigma. We have previously established that methylerythritol cyclodiphosphate (MEcPP), a precursor of plastidial isoprenoids and a stress-specific retrograde signaling metabolite, enables cellular readjustments for high-order adaptive functions. Here, we specifically show that MEcPP promotes two Brassicaceae-specific traits, namely endoplasmic reticulum (ER) body formation and induction of indole glucosinolate (IGs) metabolism selectively, via transcriptional regulation of key regulators NAI1 for ER body formation and MYB51/122 for IGs biosynthesis).

Integrated omics analyses of retrograde signaling mutant delineate interrelated stress-response strata.

To maintain homeostasis in the face of intrinsic and extrinsic insults, cells have evolved elaborate quality control networks to resolve damage at multiple levels. Interorganellar communication is a key requirement for this maintenance, however the underlying mechanisms of this communication have remained an enigma. Here we integrate the outcome of transcriptomic, proteomic, and metabolomics analyses of genotypes including ceh1, a mutant with constitutively elevated levels of both the stress-specific plastidial retrograde signaling metabolite methyl-erythritol cyclodiphosphate (MEcPP) and the defense hormone salicylic acid (SA), as well as the high MEcPP but SA deficient genotype ceh1/eds16, along with corresponding controls.

Brassinosteroid's multi-modular interaction with the general stress network customizes stimulus-specific responses in Arabidopsis.

Adaptation to fluctuating environmental conditions is a universal feature of plant life, governed by fundamental mechanisms optimizing resource allocation. This balance is achieved in part through tightly regulated communication networks among growth and stress response signaling pathways. Understanding the communication modules between brassinosteroids (BRs), the ubiquitous hormones known to control growth and stress adaptation, and the general stress response (GSR), a rapid and transient transcriptional output in response to perturbations, provides an optimal platform to unravel new facet(s) of plant stress adaptation.

A Chemical Genetic Screening Procedure for Seedlings.

Unbiased screening approaches are powerful tools enabling identification of novel players in biological processes. Chemical genetic screening refers to the technique of using a reporter response, such as expression of luciferase driven by a promoter of interest, to discover small molecules that affect a given process when applied to plants. These chemicals then act as tools for identification of regulatory components that could not otherwise be detected by forward genetic screens due to gene family redundancy or mutant lethality.

Plastidial metabolite MEcPP induces a transcriptionally centered stress-response hub via the transcription factor CAMTA3.

The general stress response (GSR) is an evolutionarily conserved rapid and transient transcriptional reprograming of genes central for transducing environmental signals into cellular responses, leading to metabolic and physiological readjustments to cope with prevailing conditions. Defining the regulatory components of the GSR will provide crucial insight into the design principles of early stress-response modules and their role in orchestrating master regulators of adaptive responses. Overaccumulation of methylerythritol cyclodiphosphate (MEcPP), a bifunctional chemical entity serving as both a precursor of isoprenoids produced by the plastidial methylerythritol phosphate (MEP) pathway and a stress-specific retrograde signal, in ceh1 (constitutively expressing hydroperoxide lyase1)-mutant plants leads to large-scale transcriptional alterations.

The plastidial retrograde signal methyl erythritol cyclopyrophosphate is a regulator of salicylic acid and jasmonic acid crosstalk.

The exquisite harmony between hormones and their corresponding signaling pathways is central to prioritizing plant responses to simultaneous and/or successive environmental trepidations. The crosstalk between jasmonic acid (JA) and salicylic acid (SA) is an established effective mechanism that optimizes and tailors plant adaptive responses. However, the underlying regulatory modules of this crosstalk are largely unknown.

Determinants of timing and amplitude in the plant general stress response.

Plants have evolved intricate signaling cascades to rapidly and effectively respond to biotic and abiotic challenges. The precise timing of these responses enables optimal resource reallocation to maintain the balance between stress adaptation and growth. Thus, an in-depth understanding of the immediate and long-term mechanisms regulating resource allocation is critical in deciphering how plants withstand environmental challenges.

Distinct roles for mitogen-activated protein kinase signaling and CALMODULIN-BINDING TRANSCRIPTIONAL ACTIVATOR3 in regulating the peak time and amplitude of the plant general stress response.

To survive environmental challenges, plants have evolved tightly regulated response networks, including a rapid and transient general stress response (GSR), followed by well-studied stress-specific responses. The mechanisms underpinning the GSR have remained elusive, but a functional cis-element, the rapid stress response element (RSRE), is known to confer transcription of GSR genes rapidly (5 min) and transiently (peaking 90-120 min after stress) in vivo. To investigate signal transduction events in the GSR, we used a 4xRSRE:LUCIFERASE reporter in Arabidopsis (Arabidopsis thaliana), employing complementary approaches of forward and chemical genetic screens, and identified components regulating peak time versus amplitude of RSRE activity.

A viable Arabidopsis pex13 missense allele confers severe peroxisomal defects and decreases PEX5 association with peroxisomes.

Peroxisomes are organelles that catabolize fatty acids and compartmentalize other oxidative metabolic processes in eukaryotes. Using a forward-genetic screen designed to recover severe peroxisome-defective mutants, we isolated a viable allele of the peroxisome biogenesis gene PEX13 with striking peroxisomal defects. The pex13-4 mutant requires an exogenous source of fixed carbon for pre-photosynthetic development and is resistant to the protoauxin indole-3-butyric acid.