Ascospores act as the primary inoculum of Fusarium graminearum, which causes the destructive disease Fusarium head blight (FHB), or scab. MicroRNAs (miRNAs) have been reported in the F. graminearum vegetative stage, and Fgdcl2 is involved in microRNA-like RNA (milRNA) biogenesis but has no major impact on vegetative growth, abiotic stress or pathogenesis. In the present study, we found that ascospore discharge was decreased in the Fgdcl1 deletion mutant, and completely blocked in the double-deletion mutant of Fgdcl1 and Fgdcl2. Besides, more immature asci were observed in the double-deletion mutant. Interestingly, the up-regulated differentially expressed genes (DEGs) common to ΔFgdcl1 and ΔFgdcl1/2 were related to ion transmembrane transporter and membrane components. The combination of small RNA and transcriptome sequencing with bioinformatics analysis predicted 143 novel milRNAs in wild-type perithecia, and 138 of these milRNAs partly or absolutely depended on Fgdcl1, while only 5 novel milRNAs were still obtained in the Fgdcl1 and Fgdcl2 double-deletion mutant. Furthermore, 117 potential target genes were predicted. Overall, Fgdcl1 and Fgdcl2 genes were partly functionally redundant in ascospore discharge and perithecium-specific milRNA generation in F. graminearum, and these perithecium-specific milRNAs play potential roles in sexual development.

Background and aimMany studies have reported that genetic variants correlate with higher risk for coronary artery disease (CAD) or in-stent restenosis (ISR) after bare metal stent (BMS) implantation. However, there is limited data assessing the impact of these variants on ISR in patients treated with drug-eluting stent (DES). The purpose of this study was to investigate the effects of genetic risk factors on ISR in Chinese Han patients treated with DES.MethodsA total of 425 patients with a diagnosis of CAD who underwent successful revascularization in native coronary arteries with DES were included in this retrospective study. Genotyping was performed on six single nucleotide polymorphisms (SNPs) in the endothelial nitric oxide synthase gene (eNOS), the angiotensin converting enzyme gene (ACE), the angiotensin II type 1 receptor gene (AT1R), the transforming growth factor beta gene (TGF-β), and the vascular endothelial growth factor gene (VEGF). Quantitative coronary angiography (QCA) was performed during the follow-up period to detect ISR. Logistic regression models were used to test for association.ResultsFifty-four patients (12.7%) developed ISR during the follow-up period. Of the six analyzed SNPs, the frequency of the C allele of T786C polymorphism in eNOS was significantly higher in the ISR group (22.2%) compared to the non-ISR group (12.7%) (p<0.01). In the ISR group, the frequency of the TT, TC, and CC genotypes was 61.1%, 33.3%, and 5.6%, respectively, and in the non-ISR group, the frequencies were 76.8%, 21.0%, and 2.2%, respectively. The multivariable analysis adjusted for potential confounders and revealed that the T786C polymorphism increased the risk of ISR in both additive and dominant models with odds ratios of 1.870 (95% confidence interval [CI]: 1.079–3.240, p = 0.03) and 2.045 (95% CI: 1.056–3.958, p = 0.03), respectively.ConclusionThe eNOS T786C polymorphism was associated with ISR in Chinese Han patients treated with DES. Genotyping may be helpful to identify patients with higher risks of ISR after DES implantation.

Fusarium graminearum is an important worldwide pathogen that causes Fusarium head blight in wheat, barley, maize and other grains. LncRNAs play important roles in many biological processes, but little is known about their functions and mechanisms in filamentous fungi. Here, we report that a natural antisense RNA, GzmetE-AS, is transcribed from the opposite strand of GzmetE. GzmetE encodes a homoserine O-acetyltransferase, which is important for sexual development and plant infection. The expression of GzmetE-AS was increased significantly during the conidiation stage, while GzmetE was upregulated in the late stage of sexual reproduction. Overexpression of GzmetE-AS inhibited the transcription of GzmetE. In contrast, the expression of GzmetE was significantly increased in GzmetE-AS transcription termination strain GzmetE-AS-T. Furthermore, GzmetE-AS-T produced more perithecia and facilitated the ascospore discharge, resembling the phenotype of GzmetE overexpressing strains. However, overexpression of GzmetE-AS in Δdcl1/2 strain cannot inhibit the expression of GzmetE, and the GzmetE nat-siRNA is also significantly reduced in Δdcl1/2 mutant. Taken together, we have identified a novel antisense lncRNA GzmetE-AS, which is involved in asexual and sexual reproduction by regulating its antisense gene GzmetE through RNAi pathway. Our findings reveal that the lncRNA plays critical roles in the development of F. graminearum.

The regulatory roles of long noncoding RNAs (lncRNAs) have been well described in animals, plants, and fungi, where they serve as crucial regulators of transcription in a wide range of biological pro-

No abstract

No abstract

The transforming growth factor β-activated kinase-binding protein 3 (TAB3) plays a crucial role in modulating cell apoptosis and proliferation in many diseases, including hepatocellular carcinoma, lung cancer, and intracerebral hemorrhage. However, the functional role of TAB3 in the heart is not well reported. In our study, we first investigated the role of TAB3 in ischemia heart diseases. For in vitro studies, cardiomyocytes (CMs) were isolated from both TAB3 knockout (KO) and wild-type (WT) mice, and the apoptosis ratios were tested after a 48-h ischemic stimulation. A proliferation test and tubeformation assay were underwent at normoxia condition. For in vivo studies, the MI model was completed for both TAB3 KO and WT mice. Echocardiography was evaluated at 3 days and 28 days post-MI, whereas the hemodynamics test was performed 28 days post-MI. The histology results of the apoptosis, proliferation of myocardium, neovasculation of microvessels, and infarct zone assessments were determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining, Ki67 immunostaining, α-SMA/CD31 immunostaining, and the Masson-Trichrome method, respectively. Expression changes of the related proteins caused by TAB3 deficiency were confirmed using both quantitative real-time polymerase chain reaction and immunoblotting. Our results indicate that the absence of TAB3 induced more CMs apoptosis, decrease cardiomyocyte proliferation, and weaker angiogenesis in vitro and in vivo. Worse cardiac function and enlarged scar formation were detected in TAB3 KO mice, and increased expression of active-caspase-3 and decreased expression of NF-κB/p65, Akt, Bcl-2/Bax, and VEGF occurred. In summary, our findings indicate that the absence of TAB3 plays a harmful role in ischemic heart disease.