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Long intergenic non-coding RNAs (lincRNAs) are important regulators of cellular processes, including development and stress response. Many lincRNAs have been bioinformatically identified in plants, but their evolutionary dynamics and expression characteristics are still elusive. Here, we systematically identified thousands of lincRNAs in 26 plant species, including 6 non-flowering plants, investigated the conservation of the identified lincRNAs in different levels of plant lineages based on sequence and/or synteny homology and explored characteristics of the conserved lincRNAs during plant evolution and their co-expression relationship with protein-coding genes (PCGs). In addition to confirmation of the features well documented in literature for lincRNAs, such as species-specific, fewer exons, tissue-specific expression patterns and less abundantly expressed, we revealed that histone modification signals and/or binding sites of transcription factors were enriched in the conserved lincRNAs, implying their biological functionalities, as demonstrated by identifying conserved lincRNAs related to flower development in both the Brassicaceae and grass families and ancient lincRNAs potentially functioning in meristem development of non-flowering plants. Compared to PCGs, lincRNAs are more likely to be associated with transposable elements (TEs), but with different characteristics in different evolutionary lineages, for instance, the types of TEs and the variable level of association in lincRNAs with different conservativeness. Together, these results provide a comprehensive view on the evolutionary landscape of plant lincRNAs and shed new insights on the conservation and functionality of plant lincRNAs.

Verticillium wilt (VW) is an important and widespread disease of cotton and once established is long-lived and difficult to manage. In Australia, the non-defoliating pathotype of Verticillium dahliae is the most common, and extremely virulent. Breeding cotton varieties with increased VW resistance is the most economical and effective method of controlling this disease and is greatly aided by understanding the genetics of resistance. This study aimed to investigate VW resistance in 240 F7 recombinant inbred lines (RIL) derived from a cross between MCU-5, which has good resistance, and Siokra 1–4, which is susceptible. Using a controlled environment bioassay, we found that resistance based on plant survival or shoot biomass was complex but with major contributions from chromosomes D03 and D09, with genomic prediction analysis estimating a prediction accuracy of 0.73 based on survival scores compared to 0.36 for shoot biomass. Transcriptome analysis of MCU-5 and Siokra 1–4 roots uninfected or infected with V. dahliae revealed that the two cultivars displayed very different root transcriptomes and responded differently to V. dahliae infection. Ninety-nine differentially expressed genes were located in the two mapped resistance regions and so are potential candidates for further identifying the genes responsible for VW resistance.

Xishuangbanna (XIS) cucumber (Cucumis sativus L. var. xishuangbannanesis) is a semiwild variety originating from low latitude tropic areas, and therefore shows extreme cold sensitivity and heat tolerance. Here, we mapped the quantitative trait loci (QTLs) that control the cold sensitivity and heat tolerance of XIS cucumber seedlings. Using bulked segregant analysis (BSA), we identified three QTLs (HTT1.1, HTT3.1, and HTT3.2, with a total length of 11.98 Mb) for heat tolerance and two QTLs (LTT6.1 and LTT6.2, with a total length of 8.74 Mb) for cold sensitivity. The QTL LTT6.1 was then narrowed down to a length of 641 kb by using kompetitive allele-specific PCR (KASP) markers. Based on structural variants (SVs) and single-nucleotide polymorphisms (SNPs), we found the LTT6.1 is covered by a high divergent region including a 50 kb deletion in the XIS49 genome, which affects the gene structure of lipase abhydrolase domain containing 6 (ABHD6, Csa_6G032560). Accordingly, there is a very big difference in lipid composition, but not in other osmoprotectants like free amino acids and fatty acids, between XIS49 and cultivated cucumber CL. Moreover, we calculated the composite likelihood ratio (CLR) and identified selective sweeps from 115 resequencing data, and found that lipid- and fatty-acid-related processes are major aspects in the domestication of the XIS group cucumber. LTT6.1 is a particularly special region positioned nearby lipid-related selective sweeps. These studies above suggested that the lipid-related domestication of XIS cucumbers should account for their extreme cold sensitivity.

Verticillum dahliae is a soil-borne phytopathogenic fungus causing destructive Verticillium wilt disease. We previously found a trehalase-encoding gene (VdPT1) in V. dahliae being significantly up-regulated after sensing root exudates from a susceptible cotton variety. In this study, we characterized the function of VdPT1 in the growth and virulence of V. dahliae using its deletion-mutant strains. The VdPT1 deletion mutants (ΔVdPT1) displayed slow colony expansion and mycelial growth, reduced conidial production and germination rate, and decreased mycelial penetration ability and virulence on cotton, but exhibited enhanced stress resistance, suggesting that VdPT1 is involved in the growth, pathogenesis, and stress resistance of V. dahliae. Host-induced silencing of VdPT1 in cotton reduced fungal biomass and enhanced cotton resistance against V. dahliae. Comparative transcriptome analysis between wild-type and mutant identified 1480 up-regulated and 1650 down-regulated genes in the ΔVdPT1 strain. Several down-regulated genes encode plant cell wall-degrading enzymes required for full virulence of V. dahliae to cotton, and down-regulated genes related to carbon metabolism, DNA replication, and amino acid biosynthesis seemed to be responsible for the decreased growth of the ΔVdPT1 strain. In contrast, up-regulation of several genes related to glycerophospholipid metabolism in the ΔVdPT1 strain enhanced the stress resistance of the mutated strain.

Objective : The triglyceride-glucose (TyG) index is a simple and reliable surrogate for insulin resistance. Recent studies have suggested that the TyG index is an independent predictor of cardiovascular disease. However, the prognostic value of the TyG index in patients with acute myocardial infarction (AMI) remains uncertain. Thus, this study aimed to evaluate the prognostic value of the TyG index in patients with AMI. Methods: AMI patients admitted to Zhongda Hospital from 2018 to 2020 were successively enrolled. After screening the inclusion criteria, 1144 patients were divided into three groups according to the tertiles of the TyG index distribution. Patients were followed up for 1 year as outpatients or contacted via telephone, and the occurrence and timing of all-cause deaths were recorded. Results: The TyG index was significantly correlated with heart failure (HF) in AMI patients. Patients with a high TyG index (group 3) (odds ratio: 9.070, 95% confidence interval [CI] 4.359-18.875, P ＜.001) had a significantly higher incidence of HF compared with patients with median TyG index (group 2). Similarly, the incidence of all-cause death in group 3 was significantly higher than that in group 2 during the 1-year follow-up (hazard ratio: 2.996, 95% CI 1.058-8.487, P = .039). Conclusion: The TyG index is closely related to HF and may be a valuable indicator to predict the long-term prognosis of patients with AMI.

The eukaryotic ribosome is essential for cancer cell survival. Perturbation of ribosome biogenesis induces nucleolar stress or ribosomal stress, which restrains cancer growth, as rapidly proliferating cancer cells need more active ribosome biogenesis. In this study, we found that UTP11 plays an important role in the biosynthesis of 18S ribosomal RNAs (rRNA) by binding to the pre-rRNA processing factor, MPP10. UTP11 is overexpressed in human cancers and associated with poor prognoses. Interestingly, depletion of UTP11 inhibits cancer cell growth in vitro and in vivo through p53-depedednt and -independent mechanisms, whereas UTP11 overexpression promotes cancer cell growth and progression. On the one hand, the ablation of UTP11 impedes 18S rRNA biosynthesis to trigger nucleolar stress, thereby preventing MDM2-mediated p53 ubiquitination and degradation through ribosomal proteins, RPL5 and RPL11. On the other hand, UTP11 deficiency represses the expression of SLC7A11 by promoting the decay of NRF2 mRNA, resulting in reduced levels of glutathione (GSH) and enhanced ferroptosis. Altogether, our study uncovers a critical role for UTP11 in maintaining cancer cell survival and growth, as depleting UTP11 leads to p53-dependent cancer cell growth arrest and p53-independent ferroptosis.

Parkinson's disease is characterized by loss of dopamine neurons in the substantia nigra1. Similar to other major neurodegenerative disorders, there are no disease-modifying treatments for Parkinson's disease. While most treatment strategies aim to prevent neuronal loss or protect vulnerable neuronal circuits, a potential alternative is to replace lost neurons to reconstruct disrupted circuits2. Here we report an efficient one-step conversion of isolated mouse and human astrocytes to functional neurons by depleting the RNA-binding protein PTB (also known as PTBP1). Applying this approach to the mouse brain, we demonstrate progressive conversion of astrocytes to new neurons that innervate into and repopulate endogenous neural circuits. Astrocytes from different brain regions are converted to different neuronal subtypes. Using a chemically induced model of Parkinson's disease in mouse, we show conversion of midbrain astrocytes to dopaminergic neurons, which provide axons to reconstruct the nigrostriatal circuit. Notably, re-innervation of striatum is accompanied by restoration of dopamine levels and rescue of motor deficits. A similar reversal of disease phenotype is also accomplished by converting astrocytes to neurons using antisense oligonucleotides to transiently suppress PTB. These findings identify a potentially powerful and clinically feasible approach to treating neurodegeneration by replacing lost neurons.

Abstract Background Water deficit (WD) has serious effect on the productivity of crops. Formation of cuticular layer with increased content of wax and cutin on leaf surfaces is closely related to drought tolerance. Identification of drought tolerance associated wax components and cutin monomers and the genes responsible for their biosynthesis is essential for understanding the physiological and genetic mechanisms underlying drought tolerance and improving crop drought resistance. Result In this study, we conducted comparative phenotypic and transcriptomic analyses of two Gossypium hirsutum varieties that are tolerant (XL22) or sensitive (XL17) to drought stress. XL17 consumed more water than XL22, particularly under the WD conditions. WD significantly induced accumulation of most major wax components (C29 and C31 alkanes) and cutin monomers (palmitic acid and stearic acid) in leaves of both XL22 and XL17, although accumulation of the major cutin monomers, i.e., polyunsaturated linolenic acid (C18:3n-3) and linoleic acid (C18:2n-6), were significantly repressed by WD in both XL22 and XL17. According to the results of transcriptome analysis, although many genes and their related pathways were commonly induced or repressed by WD in both XL22 and XL17, WD-induced differentially expressed genes specific to XL22 or XL17 were also evident. Among the genes that were commonly induced by WD were the GhCER1 genes involved in biosynthesis of alkanes, consistent with the observation of enhanced accumulation of alkanes in cotton leaves under the WD conditions. Interestingly, under the WD conditions, several GhCYP86 genes, which encode enzymes catalyzing the omega-hydroxylation of fatty acids and were identified to be the hub genes of one of the co-expression gene modules, showed a different expression pattern between XL22 and XL17 that was in agreement with the WD-induced changes of the content of hydroxyacids or fatty alcohols in these two varieties. Conclusion The results contribute to our comprehending the physiological and genetic mechanisms underlying drought tolerance and provide possible solutions for the difference of drought resistance of different cotton varieties.

Abstract. Background:. The hepatitis B virus X (HBx) protein plays a critical role in the initiation and progression of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). In the early stage of the disease, HBx facilitates tumor onset by inactivating the tumor suppressor p53. The p53-encoding gene, however, is frequently mutated or deleted as the cancer progresses to the late stage and, under such circumstance, the p53 homolog TAp63 can harness HCC growth by transactivating several important p53-target genes. Methods:. To determine whether HBx regulates TAp63, we performed co-immunoprecipitation assay, real-time quantitative polymerase chain reaction, immunoblotting, and flow cytometry analysis in p53-null cancer cell lines, Hep3B and H1299. Results:. HBx interacts with the transactivation domain of TAp63, as HBx was co-immunoprecipitated with TAp63 but not with ΔNp63. The interaction between HBx and TAp63 abolished transcriptional activity of TAp63, as evidenced by the reduction of the levels of its target genes p21 and PUMA, consequently leading to restricted apoptosis and augmented proliferation of HCC cells. Conclusion:. HBV induces progression of HCC that harbors defective p53 by inhibiting the tumor suppressor TAp63.

At present, it is of great significance to develop an effective method of recycling cyclic olefin copolymers (rCOC) due to its increasing application. But, its poor toughness is still an important difficulty to limit its effective recycling. In this article, we introduced PA6 into the POE-g-MAH/rCOC composites. Because of the good compatibility of POE-g-MAH between PA6 and rCOC, it just led to an overall improvement in mechanical properties of PA6/POE-g-MAH/rCOC (45/15/40) composites. Its tensile strength reached 42.3 MPa, which was more than 41.9% compared with that of POE-g-MAH/rCOC composites. Its notched impact strength was 11.7 kJ/[m.sup.2], which was higher than 875.0% compared with rCOC. Furthermore, the component of PA6 was wrapped by nonpolar rCOC and POE-g-MAH, resulting in a low water absorption rate (1.0%). So, the strength of the composites only dropped a little after water adsorption. In summary, the addition of PA6 helped the composites effectively utilize the toughness of POE-g-MAH. Thus, we developed an easy method to recycle rCOC and prepare the responding composites with high strength and toughness. KEYWORDS compatibility, PA6, POE-g-MAH, recycled cycloolefin copolymer, toughening, 1 | INTRODUCTION Cyclic olefin copolymers (COCs) are amorphous transparent material prepared by metallocene polymerization with norbornene or its derivatives and ethylene. [1-5] Compared with traditional transparency plastics such as [...]

Habitual tea consumption can reduce the risk of ASCVD morbidity and mortality and all-cause mortality in China, and long-term adherence to this habit can provide greater protection. Pu-erh tea is one of the representatives of post-fermented teas, and the polymers in Pu-erh tea have anti-cancer and anti-hyperlipidemic activities, but their chemical composition is still unknown. In this study, the chemical composition of Pu-erh tea was investigated in detail and eight (1–8) known compounds were isolated. The polymers in Pu-erh tea were also degraded by thiol degradation, and the fragments of quercetin and (–)-epicatechin-3-O-gallate were found in the thiol degradation products of Pu-erh tea polymers by UPLC observation and separation and purification. This is the first time that this fragment was obtained in Pu-erh tea polymer.

The deltex family protein DTX3 is believed to possess E3 ubiquitin ligase activity, as it contains a classic RING finger domain. However, its biological role and the underlying mechanism in cancer remain largely elusive. Here, we identified DTX3 as a novel mutant p53-interacting protein in ovarian carcinoma. Mechanistically, DTX3 mediated mutant p53 ubiquitination and stabilization by perturbing the MDM2-mutant p53 interaction, consequently leading to activation of diverse mutant p53 target genes. Importantly, a positive correlation between the expression of DTX3 and mutant p53 target genes was further validated in ovarian carcinomas. Ectopic DTX3 promoted, while depletion of DTX3 suppressed, ovarian cancer cell proliferation and invasion. Remarkably, the pro-tumorigenic effect of DTX3 is dependent on mutant p53, because ablation of mutant p53 significantly impaired DTX3-induced gene expression and ovarian cancer cell growth and propagation. Furthermore, DTX3 elevated the expression of mutant p53 target genes and boosted ovarian tumor growth in vivo. Finally, DTX3 was amplified and overexpressed in ovarian carcinomas, which is significantly associated with unfavorable prognosis. Altogether, our findings unveil the oncogenic role of DTX3 in ovarian cancer development by bolstering mutant p53 activity.

Abstract Colorectal cancer (CRC) is the third most common malignant tumor. DNA damage plays a crucial role in tumorigenesis, and abnormal DNA repair pathways affect the occurrence and progression of CRC. In the current study, we aimed to construct a DNA repair-related gene (DRG) signature to predict the overall survival (OS) of patients with CRC patients. The differentially expressed DRGs (DE-DRGs) were analyzed using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The prognostic gene signature was identified by univariate Cox regression and least absolute shrinkage and selection operator (LASSO)-penalized Cox proportional hazards regression analysis. The predictive ability of the model was evaluated using the Kaplan–Meier curves and time-dependent receiver operating characteristic (ROC) curves. The gene set enrichment analysis (GSEA) was performed to explore the underlying biological processes and signaling pathways. ESTIMATE and CIBERSORT were implemented to estimate the tumor immune score and immune cell infiltration status between the different risk group. The half-maximal inhibitory concentration (IC50) was evaluated to representing the drug response of this signature. Nine DE-DRGs (ESCO2, AXIN2, PLK1, CDC25C, IGF1, TREX2, ALKBH2, ESR1 and MC1R) signatures was constructed to classify patients into high- and low-risk groups. The risk score was an independent prognostic indicator of OS (hazard ratio > 1, P

IntroductionVerticillium wilt (VW) caused by Verticillium dahliae is a soil-borne vascular fungal disease that severely affects cotton yield and fiber quality. Sugar metabolism plays an important role in the growth and pathogenicity of V. dahliae. However, limited information is known about the sugar transporter genes and their roles in the growth and pathogenicity of V. dahliae.MethodIn this study, genome-wide identification of sugar transporter genes in V. dahliae was conducted and the expression profiles of these genes in response to root exudates from cotton varieties susceptible or resistant to V. dahliae were investigated based on RNA-seq data. Tobacco Rattle Virus-based host-induced gene silencing (TRV-based HIGS) and artificial small interfering RNAs (asiRNAs) were applied to investigate the function of candidate genes involved in the growth and pathogenic process of V. dahliae.ResultsA total of 65 putative sugar transporter genes were identified and clustered into 8 Clades. Of the 65 sugar transporter genes, 9 were found to be induced only by root exudates from the susceptible variety, including VdST3 and VdST12 that were selected for further functional study. Silencing of VdST3 or VdST12 in host plants by TRV-based HIGS reduced fungal biomass and enhanced cotton resistance against V. dahliae. Additionally, silencing of VdST12 and VdST3 by feeding asiRNAs targeting VdST12 (asiR815 or asiR1436) and VdST3 (asiR201 or asiR1238) inhibited fungal growth, exhibiting significant reduction in hyphae and colony diameter, with a more significant effect observed for the asiRNAs targeting VdST12. The inhibitory effect of asiRNAs on the growth of V. dahliae was enhanced with the increasing concentration of asiRNAs. Silencing of VdST12 by feeding asiR815+asiR1436 significantly decreased the pathogenicity of V. dahliae.DiscussionThe results suggest that VdST3 and VdST12 are sugar transporter genes required for growth and pathogenicity of V. dahliae and that asiRNA is a valuable tool for functional characterization of V. dahliae genes.