Onset Of Priming Research Articles

Immune priming in plants: from the onset to transgenerational maintenance.

Enhancing plant resistance against pests and diseases by priming plant immunity is an attractive concept for crop protection because it provides long-lasting broad-spectrum protection against pests and diseases. This review provides a selected overview of the latest advances in research on the molecular, biochemical and epigenetic drivers of plant immune priming. We review recent findings about the perception and signalling mechanisms controlling the onset of priming by the plant stress metabolite β-aminobutyric acid. In addition, we review the evidence for epigenetic regulation of long-term maintenance of priming and discuss how stress-induced reductions in DNA hypomethylation at transposable elements can prime defence genes. Finally, we examine how priming can be exploited in crop protection and articulate the opportunities and challenges of translating research results from the Arabidopsis model system to crops.

Arbuscular Mycorrhizal Symbiosis Leads to Differential Regulation of Genes and miRNAs Associated with the Cell Wall in Tomato Leaves.

Simple SummaryTomato can interact with arbuscular mycorrhizal fungi (AMF) to form a symbiotic association called arbuscular mycorrhiza. This symbiosis, in addition to providing nutritional benefits to plants, induces a plant defense response against biotic and abiotic stresses locally in the roots, and systemically throughout the entire plant. However, the mechanisms underlying these conferred systemic resistance-induced responses are largely unknown. This work aimed to identify which regulatory molecules could be involved in the response mechanisms elicited during priming. The findings presented here provide valuable information on the molecules that could participate in these responses, with the aim of elucidating the whole mechanism.Arbuscular mycorrhizal symbiosis is an association that provides nutritional benefits to plants. Importantly, it induces a physiological state allowing plants to respond to a subsequent pathogen attack in a more rapid and intense manner. Consequently, mycorrhiza-colonized plants become less susceptible to root and shoot pathogens. This study aimed to identify some of the molecular players and potential mechanisms related to the onset of defense priming by mycorrhiza colonization, as well as miRNAs that may act as regulators of priming genes. The upregulation of cellulose synthases, pectinesterase inhibitors, and xyloglucan endotransglucosylase/hydrolase, as well as the downregulation of a pectinesterase, suggest that the modification and reinforcement of the cell wall may prime the leaves of mycorrhizal plants to react faster and stronger to subsequent pathogen attack. This was confirmed by the findings of miR164a-3p, miR164a-5p, miR171e-5p, and miR397, which target genes and are also related to the biosynthesis or modification of cell wall components. Our findings support the hypothesis that the reinforcement or remodeling of the cell wall and cuticle could participate in the priming mechanism triggered by mycorrhiza colonization, by strengthening the first physical barriers upstream of the pathogen encounter.

Single Cell Transcriptome Mapping of Human Thymopoiesis Reveals a Continuum of Cell States during T-Lineage Specification and Commitment

The initial stages of thymopoiesis are characterized by the induction of T-lineage genes (specification) and the repression of alternative lineage genes (commitment). Multilineage (Thy1 and Thy2) and committed (Thy3) populations representing successive differentiation stages have been defined within CD34+ progenitor cells in the human thymus by the expression of CD7 and CD1a. However, due to intra-population heterogeneity and unstudied transitional states between populations, our understanding of the transcriptional programs that launch human thymopoiesis remains incomplete. Also, the interpretation of species specific gene expression profiles seen in these populations is confounded by species related differences in progenitor immunophenotypes. To our knowledge, whole transcriptome profiles of human thymic CD34+ progenitors at single cell resolution have not been reported. To resolve the transcriptional landscape of the initial stages of thymopoiesis, we performed single cell RNA-Seq (sRNA-Seq) of FACS sorted unfractionated human thymic CD34+CD4-CD8- cells from 3 donors using 10X (1 thymus, 5000 cells), Indrop (1 thymus, 2000 cells), or BD genomics (1 thymus, 192 index sorted cells) sequencing Averaged sRNA-Seq expression profiles recapitulated previous bulk RNASeq data validating our sRNA-Seq pipeline. Transcriptomes of index sorted cells mapped appropriately to those predicted to be Thy1,Thy2, or Thy3 cells from CD34, CD7, and CD1a RNA levels in the 10x and indrops data indicating the validity of identifying Thy1-3 cells by RNA levels. Seurat clustering showed that CD34+ thymocytes consist of a continuum of cell states rather than discrete populations. Nine cell states marked by gradual changes in CD2, CD44, CD7, CD1A, and CD34 RNA levels were seen: state 1 (Thy1), states 2-6 (Thy2), and states 7-9 (Thy3). Thy2 and Thy3 cells spanned several previously undescribed states with distinct expression profiles. Single cells co-expressing stem and T-lineage genes were seen in state 1 indicating an early onset of T-lineage priming that occurs prior to downregulation of stem cell genes. Within Thy2 cells, high expression of stem and alternative lineage genes was mostly restricted to states 2 and 3, which represent novel Thy2 subpopulations. State 2 cells co-expressed T-cell and high levels of innate immune genes, particularly IRF8. State 3 cells showed low CD2 expression and co-expressed T-cell and stem, myeloid, B-cell, and/ or NK genes. These results indicate concomitant priming of multiple lineage transcriptional programs rather than just the presence of unilineage gene program expressing subpopulations in the earliest thymic progenitor cells. In preliminary experiments, FACS sorted CD2 low Thy2 cells generated T-cells as well as a higher output of alternative lineage cells than CD2 high Thy2 cells. States 7-9 showed committed profiles with upregulated T-cell genes and silenced stem and alternative lineage genes. While state 9 (late Thy3) showed high RAG1 expression and cell cycle arrest, most Thy3 cells (states 7 and 8) were cycling indicating that commitment, which precedes T-cell receptor rearrangement, is not associated with proliferation arrest. Monocle pseudotime analysis finely resolved expression profiles along the differentiation trajectory within Thy1-3 populations: e.g. genes repressed earlier (e.g. MEIS1) vs later (e.g. DTX1). BCL11B, a key T-cell commitment gene was one of the earliest transcription factors (TF) to be induced during human thymopoiesis, and upregulation of TCF7 and BCL11B occurred concurrently. In contrast, in mice induction of Bcl11b occurs later after Tcf7 is fully upregulated. Thus, the initial stages of thymopoiesis are characterized by a continuum of multilineage transcriptional priming followed by a gradual transition to a T-lineage restricted gene program, a process similar to that recently described for lineage commitment of bone marrow hematopoietic progenitors but not previously reported in the thymus. SRNA-Seq yielded expression profiles along numerous data-points on the differentiation trajectory within heterogenous populations, providing high transcriptional resolution not possible with bulk data. We found differences in key TF expression profiles that could imply species specific regulatory mechanisms. Our data are a resource for elucidating transcriptional networks in T-cell development and T-cell leukemias. Disclosures No relevant conflicts of interest to declare.

The onset and time course of semantic priming during rapid recognition of visual words.

In 2 experiments, we assessed the effects of response latency and task-induced goals on the onset and time course of semantic priming during rapid processing of visual words as revealed by ocular response tasks. In Experiment 1 (ocular lexical decision task), participants performed a lexical decision task using eye movement responses on a sequence of 4 words. In Experiment 2, the same words were encoded for an episodic recognition memory task that did not require a metalinguistic judgment. For both tasks, survival analyses showed that the earliest observable effect (divergence point [DP]) of semantic priming on target-word reading times occurred at approximately 260 ms, and ex-Gaussian distribution fits revealed that the magnitude of the priming effect increased as a function of response time. Together, these distributional effects of semantic priming suggest that the influence of the prime increases when target processing is more effortful. This effect does not require that the task include a metalinguistic judgment; manipulation of the task goals across experiments affected the overall response speed but not the location of the DP or the overall distributional pattern of the priming effect. These results are more readily explained as the result of a retrospective, rather than a prospective, priming mechanism and are consistent with compound-cue models of semantic priming. (PsycINFO Database Record

The onset and time course of semantic priming during rapid recognition of visual words.

The onset and time course of semantic priming during rapid recognition of visual words.

Rapid priming, accumulation, and recharge of magma driving recent eruptions at a hyperactive caldera volcano

A major challenge in volcanology is determining the factors that control the frequency and magnitude of eruptions at hazardous caldera volcanoes. Understanding the critical sequence of events that may lead to future eruptions is vital for volcanic monitoring and risk assessment. Here we use magma chemistry and mineral diffusion modeling to interpret the magmatic processes and time scales involved in the youngest three eruptions (2.15–1.7 ka) from Taupo volcano (New Zealand), which peaked with the voluminous A.D. 232 eruption. Of the rhyolites erupted since ca. 12 ka, the 2.75 ka) rhyolites that were tapped from the same magma reservoir. Orthopyroxene Fe-Mg diffusion time scales indicate that the onset of rapid heating and priming of the host silicic mush occurred <120 yr prior to the <2.15 ka eruptions, with subsequent melt accumulation occurring in only decades. Elevated mafic magma supply to the silicic mush pile, rapid melt accumulation, and high differential tectonic stress built up and culminated in the ∼105 km3 A.D. 232 eruption, one of the largest and most violent Holocene eruptions globally. These youngest eruptions demonstrate how Taupo’s magmatic system can rapidly change behavior to generate large eruptible melt bodies on time scales of direct relevance to humans and monitoring initiatives.

Accounting for the delay in the transition from acute to chronic pain: axonal and nuclear mechanisms.

Acute insults produce hyperalgesic priming, a neuroplastic change in nociceptors that markedly prolongs inflammatory mediator-induced hyperalgesia. After an acute initiating insult, there is a 72 h delay to the onset of priming, for which the underlying mechanism is unknown. We hypothesized that the delay is due to the time required for a signal to travel from the peripheral terminal to the cell body followed by a return signal to the peripheral terminal. We report that when an inducer of hyperalgesic priming (monocyte chemotactic protein 1) is administered at the spinal cord of Sprague Dawley rats, priming is detected at the peripheral terminal with a delay significantly shorter than when applied peripherally. Spinally induced priming is detected not only when prostaglandin E2 (PGE2) is presented to the peripheral nociceptor terminals, but also when it is presented intrathecally to the central terminals in the spinal cord. Furthermore, when an inducer of priming is administered in the paw, priming can be detected in spinal cord (as prolonged hyperalgesia induced by intrathecal PGE2), but only when the mechanical stimulus is presented to the paw on the side where the priming inducer was administered. Both spinally and peripherally induced priming is prevented by intrathecal oligodeoxynucleotide antisense to the nuclear transcription factor CREB mRNA. Finally, the inhibitor of protein translation reversed hyperalgesic priming only when injected at the site where PGE2 was administered, suggesting that the signal transmitted from the cell body to the peripheral terminal is not a newly translated protein, but possibly a newly expressed mRNA.

Granzyme B Is Dispensable in the Development of Diabetes in Non-Obese Diabetic Mice

Pancreatic beta cell destruction in type 1 diabetes is mediated by cytotoxic CD8+ T lymphoctyes (CTL). Granzyme B is an effector molecule used by CTL to kill target cells. We previously showed that granzyme B-deficient allogeneic CTL inefficiently killed pancreatic islets in vitro. We generated granzyme B-deficient non-obese diabetic (NOD) mice to test whether granzyme B is an important effector molecule in spontaneous type 1 diabetes. Granzyme B-deficient islet antigen-specific CD8+ T cells had impaired homing into islets of young mice. Insulitis was reduced in granzyme B-deficient mice at 70 days of age (insulitis score 0.043±0.019 in granzyme B-deficient versus 0.139±0.034 in wild-type NOD mice p<0.05), but was similar to wild-type at 100 and 150 days of age. We observed a reduced frequency of CD3+CD8+ T cells in the islets and peripheral lymphoid tissues of granzyme B-deficient mice (p<0.005 and p<0.0001 respectively), but there was no difference in cell proportions in the thymus. Antigen-specific CTL developed normally in granzyme B-deficient mice, and were able to kill NOD islet target cells as efficiently as wild-type CTL in vitro. The incidence of spontaneous diabetes in granzyme B-deficient mice was the same as wild-type NOD mice. We observed a delayed onset of diabetes in granzyme B-deficient CD8-dependent NOD8.3 mice (median onset 102.5 days in granzyme B-deficient versus 57.50 days in wild-type NOD8.3 mice), which may be due to the delayed onset of insulitis or inefficient priming at an earlier age in this accelerated model of diabetes. Our data indicate that granzyme B is dispensable for beta cell destruction in type 1 diabetes, but is required for efficient early activation of CTL.

Accelerated dendritic-cell migration and T-cell priming in SPARC-deficient mice

On their path to draining lymph nodes, epidermal Langerhans cells traverse collagen-dense connective tissue before reaching lymphatic vessels. The matricellular protein SPARC (secreted protein, acidic and rich in cysteine), which is induced during inflammation and tissue repair, organizes collagen deposition in tissue stroma. We analyzed Langerhans cell and dendritic-cell migration and its impact on T-cell priming in SPARC-null (SPARC(-/-)) and SPARC-sufficient (SPARC(+/+)) mice. Although the same number of Langerhans cells populate the ear skin of SPARC(-/-) and SPARC(+/+) mice, more Langerhans cells were found in the lymph nodes draining antigen-sensitized ears of SPARC(-/-) mice and significantly more Langerhans cells migrated from null-mice-derived ear skin explants. Such favored Langerhans cell migration is due to the host environment, as demonstrated by SPARC(+/+)>SPARC(-/-) and reciprocal chimeras, and have a profound influence on T-cell priming. Contact-, delayed type-hypersensitivity and naive T-cell receptor-transgenic T-cell priming, together indicate that the lack of SPARC in the environment accelerates the onset of T-cell priming by hastening Langerhans cell/dendritic-cell migration.

Priming of strong semantic relations in the left and right visual fields: a time-course investigation

Prior time-course investigations of cerebral asymmetries in word processing have sometimes reported hemisphere differences in the onset and duration of semantic priming. In the current study, very strongly related word pairs (categorical associates such as arm– leg) were employed in a low relatedness proportion lexical decision priming paradigm. A range of prime–target stimulus onset asynchronies (SOAs: 150–800 ms) was included. Only very weak evidence was obtained for a LVF priming lag at the briefest SOA, while priming was bilateral at moderately long SOAs. We consider these data in the context of previous time-course studies and suggest that, when highly semantically similar word pairs are used, a right hemisphere priming lag is, at best, a very small effect.

Rapid Activation of the Lexicon: A Further Investigation with Behavioral and Computational Results

Priming effects were observed in a categorization task for both prime–target synonym pairs (e.g., boat–ship) and first-associate pairs (e.g., boat–sea). However, the amount and onset of priming were different for synonyms and associated pairs. The effect appeared sooner for synonyms (at prime duration of 43 ms) than for associated words (57 ms onset) but was present for both these relationships at 71 ms of prime presentation. A prime visibility pretest was conducted with the same participants in order to determine the rate of recognition of our prime words. Last, a French matrix of the HAL model was built, which showed that synonyms pairs were semantically closer than associated pairs. These results are in accordance with our previous study (Frenck-Mestre & Bueno, 1999) and are discussed in relation with semantic models, such as Plaut's (1995) distributed model.

Aging and the time course of semantic activation.

Fifty-four young (M age = 20.2 years) and 54 elderly participants (M age = 68.4 years) completed a task in which a prime was followed by a target. People were to respond "yes" if the target was a word and "no" otherwise. On word-target trials, three kinds of prime were presented: associated (e.g., the prime-target pair DOG-CAT), unassociated (e.g., SEW-CAT), and neutral (e.g., BLANK-CAT). The stimulus onset asynchrony (SOA) between onset of the prime and target was varied, with SOAs of 150, 450, and 1,000 ms. The most important finding was an age difference in the minimum SOA at which priming (i.e., faster response time on associated than on unassociated trials) was observed. It is argued that the age difference in onset of priming reflects a slowing with age in one or more aspects of semantic activation. Contrary to the Hasher and Zacks (1979) hypothesis, there is evidence of an age difference in the speed of automatic activation.