Search

Stem canker and black scurf of potatoes, caused by Rhizoctonia solani, are economically important diseases. Although the field application of sodium silicate has been shown to improve potato's resistance against R. solani, the underlying mechanism remains unclear. In this study, we examined this resistance using transcriptomic analysis. Potato stems inoculated with R. solani were treated with sodium silicate, while a control group received no sodium silicate treatment. The plants were grown under natural environmental conditions at the farm of Inner Mongolia Agricultural University. Potato stems were sampled 4, 8, and 12 days after treatment. Total RNA was extracted using the TRIzol reagent and transformed into cDNA. The cDNA was sequenced, the reads were aligned, and the expression levels of genes were quantified and compared between the treated and control groups. A total of 1491 genes were identified as differentially expressed genes (DEGs). Furthermore, these DEGs were found to be involved in hydrolase activity, plant–pathogen interactions, hormone signal transduction, and the phenylpropanoid biosynthesis pathway. To confirm the up- and down-regulation of DEGs, quantitative real-time polymerase chain reaction (qRT-PCR) was performed on randomly selected genes. The results showed that the application of sodium silicate induces a complex defense network in potato plants involving physical barriers, innate immunity, phytohormone signaling, and various phenylpropanoid compounds to combat R. solani infection. This study provides valuable insights into the molecular mechanisms underlying sodium-silicate-induced resistance and its potential for reducing stem canker and black scurf in potato crops. [ABSTRACT FROM AUTHOR]

Introduction: Transposable element (TE) dysregulation is associated with neuroinflammation in Alzheimer's disease (AD) brains. Yet, TE quantitative trait loci (teQTL) have not been well characterized in human aged brains with AD., Methods: We leveraged large-scale bulk and single-cell RNA sequencing, whole-genome sequencing (WGS), and xQTL from three human AD brain biobanks to characterize TE expression dysregulation and experimentally validate AD-associated TEs using CRISPR interference (CRISPRi) assays in human induced pluripotent stem cell (iPSC)-derived neurons., Results: We identified 26,188 genome-wide significant TE expression QTLs (teQTLs) in human aged brains. Subsequent colocalization analysis of teQTLs with AD genetic loci identified AD-associated teQTLs and linked locus TEs. Using CRISPRi assays, we pinpointed a neuron-specific suppressive role of the activated short interspersed nuclear element (SINE; chr11:47608036-47608220) on expression of C1QTNF4 via reducing neuroinflammation in human iPSC-derived neurons., Discussion: We identified widespread TE dysregulation in human AD brains and teQTLs offer a complementary analytic approach to identify likely AD risk genes., Highlights: Widespread transposable element (TE) dysregulations are observed in human aging brains with degrees of neuropathology, apolipoprotein E (APOE) genotypes, and neuroinflammation in Alzheimer's disease (AD). A catalog of TE quantitative trait loci (teQTLs) in human aging brains was created using matched RNA sequencing and whole-genome sequencing data. CRISPR interference assays reveal that an upregulated intergenic TE from the MIR family (chr11: 47608036-47608220) suppresses expression of its nearest anti-inflammatory gene C1QTNF4 in human induced pluripotent stem cell-derived neurons., (© 2024 The Author(s). Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)

The regulation of leaf senescence and disease resistance plays a crucial role in determining rice grain yield and quality, which are important to meet the ever-increasing food demands of the world. Here, we identified an atypical Dof transcriptional factor OsDes1 that contributes to the stay-green phenotype, grain yield, and disease resistance in rice. The expression level of OsDes1 is positively associated with stay-green in natural variations of japonica rice, suggesting that OsDes1 would be alternatively used in breeding programs. Mechanistically, OsDes1 targets the promoter of the Rieske FeS protein gene OsPetC to activate its expression and interacts with OsPetC to protect against its degradation, thus promoting stay-green and ultimately improving the grain yield. OsDes1 also binds to the promoter region of defense-related genes, such as OsPR1b , and activates their expression, leading to enhanced disease resistance. These findings offer a potential strategy for breeding rice to enhance grain yield and disease resistance.

Although human cerebellum is known to be neuropathologically impaired in Alzheimer's disease (AD) and AD-related dementias (ADRD), the cell type-specific transcriptional and epigenomic changes that contribute to this pathology are not well understood. Here, we report single-nucleus multiome (snRNA-seq and snATAC-seq) analysis of 103,861 nuclei isolated from cerebellum from 9 human cases of AD/ADRD and 8 controls, and with frontal cortex of 6 AD donors for additional comparison. Using peak-to-gene linkage analysis, we identified 431,834 significant linkages between gene expression and cell subtype-specific chromatin accessibility regions enriched for candidate cis-regulatory elements (cCREs). These cCREs were associated with AD/ADRD-specific transcriptomic changes and disease-related gene regulatory networks, especially for RAR Related Orphan Receptor A (RORA) and E74 Like ETS Transcription Factor 1 (ELF1) in cerebellar Purkinje cells and granule cells, respectively. Trajectory analysis of granule cell populations further identified disease-relevant transcription factors, such as RORA, and their regulatory targets. Finally, we prioritized two likely causal genes, including Seizure Related 6 Homolog Like 2 (SEZ6L2) in Purkinje cells and KAT8 Regulatory NSL Complex Subunit 1 (KANSL1) in granule cells, through integrative analysis of cCREs derived from snATAC-seq, genome-wide AD/ADRD loci, and Hi-C looping data. This first cell subtype-specific regulatory landscape in the human cerebellum identified here offer novel genomic and epigenomic insights into the neuropathology and pathobiology of AD/ADRD and other neurological disorders if broadly applied.