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P orcine reproductive and respiratory syndrome virus (PRRSV) is one of the most economically important viruses affecting the swine industry worldwide, resulting in significant economic losses each year (1-3). PRRSV is a small, enveloped, linear, single positive-stranded RNA virus and a member of the order Nidovirales, family Arteriviridae (4). Current vaccination strategies cannot effectively control PRRSV infection because of the high antigenic heterogeneity (5, 6), the replication in and destruction of lung alveolar macrophages (7-9), and the observed antibody-dependent enhancement of PRRSV (10, 11). Therefore, it is imperative to study PRRSV pathogenesis mechanisms so that more effective control measures can be developed.Heme oxygenase-1 (HO-1) is the rate-limiting enzyme of heme degradation, and it functions to catabolize free heme into biliverdin, carbon monoxide, and iron. HO-1 and its end products have antioxidant, anti-inflammatory, and antiviral properties, and it is known to be a pivotal cytoprotective enzyme (12). Upregulation of HO-1 expression suppresses replication of a number of viruses, including hepatitis C virus (HCV), HIV-1, hepatitis B virus (HBV), and influenza virus (13-17). Our previous work showed that PRRSV significantly downregulates HO-1

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Multilocular trait has recently attracted considerable attention for its potential to increase yield. Our previous studies indicated that two genes (Bjln1 and Bjln2) are responsible for multilocular siliques in Brassica juncea and the Bjln1 gene has been delimited to a 208-kb region. In present study, the Bjln1 gene was successfully isolated using the map-based cloning method. Complementation test indicated that the BjuA07.CLV1 (equivalent to BjLn1) could rescue the multilocular phenotype and generate bilocular siliques. Two amino acids changes at positions 28 and 63 in BjuA07.clv1 as well as a 702-bp deletion in its promoter have been proved to affect the carpel numbers. Microscopic analyses suggested that BjuA07.CLV1 is involved in the maintenance of shoot and floral meristem size. The expression level of BjuA07.clv1 was significantly reduced in the SAM. Furthermore, WUS, CLV2, CLV3, RPK2 and POL, key genes in the CLV/WUS signal pathway, showed lower expression level in the multilocular plants. These data suggest that the mutations in the CDS and promoter of BjuA07.clv1 reduced its function and expression level, which disturbed CLV/WUS signal pathway, thereby leading to the enlargement of the shoot and floral meristem and resulting in the multilocular siliques.

Osteosarcoma is the most frequent malignant bone tumor, affecting the extremities of adolescents and young adults. Ubiquitin-specific protease 1 (USP1) plays a critical role in many cellular processes including proteasome degradation, chromatin remodeling and cell cycle regulation. In the present study, we discovered that USP1 was overexpressed in 26 out of 30 osteosarcoma tissues compared to cartilage tumor tissues and normal bone tissues. We then constructed a lentiviral vector mediating RNA interference (RNAi) targeting USP1 and demonstrated that it significantly suppressed the mRNA and protein expression of the USP1 gene in U2OS cells. Knockdown of USP1 inhibited the growth and colony-forming, as well as significantly reduced the invasiveness of U2OS cells. Western blot analysis indicated that suppression of USP1 downregulated the expression of many proteins including SIK2, MMP-2, GSK-3β, Bcl-2, Stat3, cyclin E1, Notch1, Wnt-1 and cyclin A1. Most of these proteins are associated with tumor genesis and development. RNAi of SIK2 significantly decreased SIK2 protein expression and inhibited the ability of forming colonies, as well as induced apoptosis and reduced the invasiveness of U2OS cells. Collectively, our results suggest that silencing USP1 inhibits cell proliferation and invasion in U2OS cells. Therefore, USP1 may provide a novel therapeutic target for the treatment of osteosarcoma.