PUF-8, a C. elegans ortholog of the RNA-binding proteins PUM1 and PUM2, is required for robustness of the cell death fate.

During C. elegans development, 1090 somatic cells are generated, of which 959 survive and 131 die, many through apoptosis. We present evidence that PUF-8, a C. elegans ortholog of the mammalian RNA-binding proteins PUM1 and PUM2, is required for the robustness of this 'survival and death' pattern. We found that PUF-8 prevents the inappropriate death of cells that normally survive, and we present evidence that this anti-apoptotic activity of PUF-8 is dependent on the ability of PUF-8 to interact with ced-3 (a C. elegans ortholog of caspase) mRNA, thereby repressing the activity of the pro-apoptotic ced-3 gene. PUF-8 also promotes the death of cells that are programmed to die, and we propose that this pro-apoptotic activity of PUF-8 may depend on the ability of PUF-8 to repress the expression of the anti-apoptotic ced-9 gene (a C. elegans ortholog of Bcl2). Our results suggest that stochastic differences in the expression of genes within the apoptosis pathway can disrupt the highly reproducible and robust survival and death pattern during C. elegans development, and that PUF-8 acts at the post-transcriptional level to level out these differences, thereby ensuring proper cell number homeostasis.

Ectopic expression of the Arabidopsis florigen gene FLOWERING LOCUS T in seeds enhances seed dormancy via the GA and DOG1 pathways.

Ectopic expression of specific genes in seeds could be a tool for molecular design of crops to alter seed dormancy and germination, thereby improving production. Here, a seed-specific vector, 12S-pLEELA, was applied to study the roles of genes in Arabidopsis seeds. Transgenic lines containing FLOWERING LOCUS T (FT) driven by the 12S promoter exhibited significantly increased seed dormancy and earlier flowering. Mutated FT(Y85H) and TERMINAL FLOWER1 (TFL1) transgenic lines also showed increased seed dormancy but without altered flowering time. FT(Y85H) and TFL1 caused weaker seed dormancy enhancement compared to FT. The FT and TFL1 transgenic lines showed hypersensitivity to paclobutrazol, but not to abscisic acid in seed germination. The levels of bioactive gibberellin 3 (GA3 ) and GA4 were significantly reduced, consistent with decreased expression of COPALYL DIPHOSPHATE SYNTHASE (CPS), KAURENE OXIDASE (KO), GIBBERELLIN 3-OXIDASE2 (GA3ox2), and GA20ox1 in p12S::FT lines. Exogenous GA4+7 could recover the germination ability of FT transgenic lines. These results revealed that FT regulates GA biosynthesis. A genetic analysis indicated that the GA signaling regulator SPINDLY (SPY) is epistatic to FT in GA-mediated seed germination. Furthermore, DELAY OF GERMINATION1 (DOG1) showed significantly higher transcript levels in p12S::FT lines. Seed dormancy analysis of dog1-2 spy-3 p12S::FT-2 indicated that the combination of SPY and DOG1 is epistatic to FT in the regulation of dormancy. Overall, we showed that ectopic expression of FT and TFL1 in seeds enhances dormancy through affecting GA and DOG1 pathways.

Role of naringin in the treatment of atherosclerosis.

Atherosclerosis (AS) is a major pathological basis of coronary heart disease. However, the currently available medications are unable to effectively reduce the incidence of cardiovascular events in the majority of patients with AS. Therefore, naringin has been attracting considerable attention owing to its anti-AS effects. Naringin can inhibit the growth, proliferation, invasion, and migration of vascular smooth muscle cells, ameliorate endothelial cell inflammation and apoptosis, lower blood pressure, halt the cell cycle at the G1 phase, and impede growth via its antioxidant and free radical scavenging effects. These activities suggest the potential anti-AS effects of naringin. In this review article, we comprehensively summarized the latest findings on the anti-AS effects of naringin and their underlying mechanisms, providing a crucial reference for future research on the anti-AS potential of this agent.

The Monocyte-to-Lymphocyte Ratio Was Associated With Intraplaque Neovascularization of the Carotid Artery on AngioPLUS.

BACKGROUND: The monocyte-lymphocyte ratio (MLR) is a hematological test parameter that reflects the status of both monocytes and lymphocytes as inflammatory cells. This study aims to investigate the relationship between MLR and carotid intraplaque neovascularization (IPN) in patients with asymptomatic carotid stenosis. METHODS: We performed the Angio Planewave Ultrasensitive (AngioPLUS) screening for patients with carotid plaques. The carotid plaque stability was evaluated by semiquantitative visual grading of carotid IPN. Binary logistic regression models were performed to determine the associations between different clinical and laboratory indicators and the presence of high IPN. RESULTS: A total of 160 patients were eventually enrolled with 99 in the low IPN group (Scores 0-1) and 61 in the high IPN group (Score 2). Univariate logistic regression showed that age, monocytes, lymphocytes, glycated hemoglobin (HbA1c), fibrinogen, d-dimmer, and MLR were significantly associated with the presence of high IPN (all p < 0.05). Multivariate logistic regression models showed that MLR was significantly associated with the presence of high IPN after adjusting for other covariates. An MLR value of 32.9 was the optimal cutoff value to differentiate high and low IPN. High MLR was also significantly correlated with the presence of high IPN (odds ratio [OR] = 4.08, 95% confidence interval [CI]: 1.69-9.88, p = 0.002) when included in the above multivariate logistic regression model. CONCLUSION: Elevated MLR is closely associated with the presence of high IPN and may serve as a surrogate biomarker for carotid IPN.

Genome-Wide Linkage Mapping Reveals QTLs for Seed Vigor-Related Traits Under Artificial Aging in Common Wheat (Triticum aestivum).

Long-term storage of seeds leads to lose seed vigor with slow and non-uniform germination. Time, rate, homogeneity, and synchrony are important aspects during the dynamic germination process to assess seed viability after storage. The aim of this study is to identify quantitative trait loci (QTLs) using a high-density genetic linkage map of common wheat (Triticum aestivum) for seed vigor-related traits under artificial aging. Two hundred and forty-six recombinant inbred lines derived from the cross between Zhou 8425B and Chinese Spring were evaluated for seed storability. Ninety-six QTLs were detected on all wheat chromosomes except 2B, 4D, 6D, and 7D, explaining 2.9-19.4% of the phenotypic variance. These QTLs were clustered into 17 QTL-rich regions on chromosomes 1AL, 2DS, 3AS (3), 3BS, 3BL (2), 3DL, 4AS, 4AL (3), 5AS, 5DS, 6BL, and 7AL, exhibiting pleiotropic effects. Moreover, 10 stable QTLs were identified on chromosomes 2D, 3D, 4A, and 6B (QaMGT.cas-2DS.2, QaMGR.cas-2DS.2, QaFCGR.cas-2DS.2, QaGI.cas-3DL, QaGR.cas-3DL, QaFCGR.cas-3DL, QaMGT.cas-4AS, QaMGR.cas-4AS, QaZ.cas-4AS, and QaGR.cas-6BL.2). Our results indicate that one of the stable QTL-rich regions on chromosome 2D flanked by IWB21991 and IWB11197 in the position from 46 to 51 cM, presenting as a pleiotropic locus strongly impacting seed vigor-related traits under artificial aging. These new QTLs and tightly linked SNP markers may provide new valuable information and could serve as targets for fine mapping or markers assisted breeding.

Arabidopsis seed germination speed is controlled by SNL histone deacetylase-binding factor-mediated regulation of AUX1.

Histone acetylation is known to affect the speed of seed germination, but the molecular regulatory basis of this remains ambiguous. Here we report that loss of function of two histone deacetylase-binding factors, SWI-INDEPENDENT3 (SIN3)-LIKE1 (SNL1) and SNL2, results in accelerated radicle protrusion and growth during seed germination. AUXIN RESISTANT 1 (AUX1) is identified as a key factor in this process, enhancing germination speed downstream of SNL1 and SNL2. AUX1 expression and histone H3 acetylation at lysines 9 and 18 is regulated by SNL1 and SNL2. The D-type cyclins encoding genes CYCD1;1 and CYCD4;1 display increased expression in AUX1 over-expression lines and the snl1snl2 double mutant. Accordingly, knockout of CYCD4;1 reduces seed germination speed of AUX1 over-expression lines and snl1snl2 suggesting the importance of cell cycling for radicle protrusion during seed germination. Together, our work identifies AUX1 as a link between histone acetylation mediated by SNL1 and SNL2, and radicle growth promoted by CYCD1;1 and CYCD4;1 during seed germination.