The Plant Journal最新文献

Pennycress (Thlaspi arvense) is a winter oilseed domesticated recently to be incorporated as an intermediate crop between the existing cropping systems of the US Midwest. We show that a natural accession of pennycress, 2032, is more susceptible to the necrotrophic fungal pathogens Sclerotinia sclerotiorum and Alternaria japonica than the reference pennycress accession MN106. A previously identified marker associated with early flowering and maturity in pennycress was found to be present in a gene homologous to Arabidopsis Jumonji 14 (JMJ14). It has been reported that AtJMJ14 promotes disease resistance and represses flowering, and greenhouse studies of breeding populations suggested that this was also the case in pennycress. Plants with the 2032 TaJMJ14 allele were more susceptible to fungi and flowered early. CRISPR-Cas9 editing was used to generate additional TaJMJ14 alleles. A 9-base pair deletion in the sixth exon of TaJMJ14 showed trends of early flowering and S. sclerotiorum susceptibility, whereas a complete loss-of-function allele led to infertility. We further investigated the transcriptomes of MN106 and 2032 plants in the early stages of S. sclerotiorum and A. japonica infection to identify potential resistance and susceptibility genes. Differences in the expression of pathogen-associated molecular pattern-triggered immunity-associated genes led us to discover that 2032 plants have defects in elicitor-triggered oxidative bursts. The transcriptional responses unique to each accession lay a foundation for future gene editing and breeding approaches to keep the beneficial early flowering phenotype conferred by 2032 but uncouple it from disease susceptibility.

De novo centromeres refer to ectopic centromeres that acquire functionality in genomic regions lacking native centromeric repeat sequences. To investigate mechanisms underlying de novo centromere formation, we employed a multi-omics approach integrating genomic, transcriptomic, and epigenetic data from wheat–barley disomic addition line 7HS**. The barley 7HS chromosome arm forms a 4.7 Mbp de novo centromere without canonical repeats, revealed by specific CENH3 enrichment. The emergence of de novo centromere is characterized by reduced repetitive DNA content and earlier LTR retrotransposon insertions compared to native centromeres. Notably, we identified a GT-rich microsatellite, designated CentHv7, within this region—a sequence also conserved in the native centromeres of barley. We found that R-loops, three-stranded nucleic acid complexes, are preferentially enriched in the barley centromeric regions. In the de novo centromeric region of 7HS**, a de novo R-loop forms at exons 11 and 12 of the upregulated gene HORVU.MOREX.r3.7HG0694980, co-localizing with bivalent chromatin modifications H3K4me3 and H3K27me3. In conclusion, our findings emphasize that the sequence features of de novo centromeres, in combination with unique gene expression patterns, newly formed R-loop structures, and specialized poised chromatin states, may collectively create a unique epigenetic environment that correlates with the formation and stabilization of de novo centromeres in barley.

Tea (Camellia sinensis), a globally significant economic crop, is severely affected by anthracnose disease, impacting both yield and quality. Our previous research identified N-feruloylputrescine (Fer-Put) as enhancing tea's disease resistance, with CsHT9 potentially crucial for Fer-Put biosynthesis. In this investigation, we observed that invasion by the anthracnose pathogen activates the expression of CsMYB175/114 and CsHT9. Through in vivo and in vitro experiments, we discovered that CsHT9 is involved in Fer-Put synthesis and is directly regulated by CsMYB175 and CsMYB114. These MYB transcription factors activate CsHT9 expression, elevate Fer-Put levels, induce reactive oxygen species accumulation, and enhance tea plant resistance to anthracnose. Interestingly, within the optimal temperature range for anthracnose, increased temperature upregulates CsMYB175 expression, enhancing its ability to activate CsHT9 downstream. This study elucidates the CsMYBs-CsHT9-Fer-Put resistance pathway in tea plants, offering insights for environmentally friendly disease control and the development of disease-resistant woody plants such as tea.

Plants can specifically assemble beneficial rhizosphere microbiota through the ‘cry for help’ mechanism triggered by non-pathogenic elicitors, thereby promoting plant health. However, it remains unknown whether non-pathogenic strains can be used to induce plants to form a rhizomicrobiome capable of resisting herbivores. Here, we investigated how tomatoes enhance their defense capacity via the ‘cry for help’ response triggered by the entomopathogenic fungus Beauveria bassiana. Our findings show that B. bassiana induces the formation of beneficial soil legacy in tomatoes, which significantly impacts the performance of whitefly (Bemisia tabaci) on tomatoes. Amplicon sequencing revealed a specific enrichment of Pseudomonas in the soil legacy. Supplementing soils with Pseudomonas isolates reduced whitefly performance on tomatoes and increased the whitefly-induced levels of salicylic acid (SA) and jasmonic acid (JA) in the plants. Moreover, metabolomic and in vitro experiments demonstrated that the increased abundance of rhizosphere Pseudomonas, induced by enhanced root exudation of o-anisic acid, is responsible for the pest-suppressive effect of the soil legacy. This research uncovers a ‘cry for help’ mechanism whereby tomatoes, through interactions with a non-pathogenic strain, reshape their rhizosphere microbiome to bolster defense. It also deepens our understanding of microbiota-mediated plant defense and offers insights for biological control of herbivores.

At14a-Like 1 (AFL1) is highly induced during low water potential stress and remains at high levels during stress acclimation. AFL1, and the closely related At14a, are plant-specific proteins that have limited similarity to mammalian actin- and membrane-associated proteins. Previous research indicated that manipulation of AFL1 expression affects actin cytoskeleton dynamics and endocytic trafficking (as measured by uptake of membrane dye FM4-64). However, it has remained unclear whether this is a direct activity of AFL1 or an indirect effect. We found that AFL1 specifically bound actin filaments as well as the phosphoinositide phosphates (PIPs) phosphoinositide-3-monophosphate [PI(3)P], PI(5)P, and the diphosphate PI(3,5)P2 in co-sedimentation and PIP strip membrane assays, respectively. Interestingly, these binding activities were mediated by the same site within the C-terminal domain of AFL1. Mutation of a single amino acid in the AFL1 C-terminal domain was sufficient to disrupt both actin filament and PIP binding in vitro and to disrupt accumulation of the mutated protein in transgenic plants. We also found that the central hydrophobic region of AFL1 was required for AFL1 co-localization with actin filaments and plasma membrane. Mutation of AFL1 and At14a using genome editing confirmed that loss of these proteins reduced growth during low water potential stress and resulted in less extensive actin filament arrays and disrupted FM4-64 uptake. Together these observations indicate that AFL1 can directly participate in cytoskeleton organization and membrane dynamics via PIP and actin filament binding.