Dataset Information

Interaction of CPR5 with cell cycle regulators UVI4 and OSD1 in Arabidopsis.

ABSTRACT: The impact of cell cycle on plant immunity was indicated by the enhancement of disease resistance with overexpressing OSD1 and UVI4 genes that are negative regulators of cell cycle controller APC (anaphase promoting complex). CPR5 is another gene that is implicated in cell cycle regulation and plant immunity, but its mode of action is not known. Here we report the analysis of genetic requirement for the function of UVI4 and OSD1 in cell cycle progression control and in particular the involvement of CPR5 in this regulation. We show that the APC activator CCS52A1 partially mediates the function of OSD1 and UVI4 in female gametophyte development. We found that the cpr5 mutation suppresses the endoreduplication defect in the uvi4 single mutant and partially rescued the gametophyte development defect in the osd1 uvi4 double mutant while the uvi4 mutation enhances the cpr5 defects in trichome branching and plant disease resistance. In addition, cyclin B1 genes CYCB1;1, CYCB1;2, and CYCB1;4 are upregulated in cpr5. Therefore, CPR5 has a large role in cell cycle regulation and this role has a complex interaction with that of UVI4 and OSD1. This study further indicates an intrinsic link between plant defense responses and cell cycle progression.

SUBMITTER: Bao Z

PROVIDER: S-EPMC4063785 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Interaction of CPR5 with cell cycle regulators UVI4 and OSD1 in Arabidopsis.

Bao Zhilong Z Hua Jian J

PloS one 20140619 6

The impact of cell cycle on plant immunity was indicated by the enhancement of disease resistance with overexpressing OSD1 and UVI4 genes that are negative regulators of cell cycle controller APC (anaphase promoting complex). CPR5 is another gene that is implicated in cell cycle regulation and plant immunity, but its mode of action is not known. Here we report the analysis of genetic requirement for the function of UVI4 and OSD1 in cell cycle progression control and in particular the involvement ...[more]

PMID: 24945150

Similar Datasets

Project description:UnlabelledIn latently infected marmoset T cells, Herpesvirus saimiri (HVS) expresses six microRNAs (known as miR-HSURs [H. saimiri U-rich RNAs]). The viral miR-HSURs are processed from chimeric primary transcripts, each containing a noncoding U-rich RNA (HSUR) and a pre-miRNA hairpin. To uncover the functions of miR-HSURs, we identified mRNA targets in infected cells using high-throughput sequencing of RNA isolated by cross-linking immunoprecipitation (HITS-CLIP). HITS-CLIP revealed hundreds of robust Argonaute (Ago) binding sites mediated by miR-HSURs that map to the host genome but few in the HVS genome. Gene ontology analysis showed that several pathways regulating the cell cycle are enriched among cellular targets of miR-HSURs. Interestingly, miR-HSUR4-3p represses expression of the p300 transcriptional coactivator by binding the open reading frame of its mRNA. miR-HSUR5-3p directly regulates BiP, an endoplasmic reticulum (ER)-localized chaperone facilitating maturation of major histocompatibility complex class I (MHC-I) and the antiviral response. miR-HSUR5-3p also robustly downregulates WEE1, a key negative regulator of cell cycle progression, leading to reduced phosphorylation of its substrate, cyclin-dependent kinase (Cdk1). Consistently, inhibition of miR-HSUR5-3p in HVS-infected cells decreases their proliferation. Together, our results shed light on the roles of viral miRNAs in cellular transformation and viral latency.ImportanceViruses express miRNAs during various stages of infection, suggesting that viral miRNAs play critical roles in the viral life cycle. Compared to protein-coding genes, the functions of viral miRNAs are not well understood. This is because it has been challenging to identify their mRNA targets. Here, we focused on the functions of the recently discovered HVS miRNAs, called miR-HSURs. HVS is an oncogenic gammaherpesvirus that causes acute T-cell lymphomas and leukemias in New World primates and transforms human T cells. A better understanding of HVS biology will help advance our knowledge of virus-induced oncogenesis. Because numerous cellular miRNAs play crucial roles in cancer, viral miRNAs from the highly oncogenic HVS might also be important for transformation. Here, we found that the miR-HSURs preferentially modulate expression of host cell cycle regulators, as well as antiviral response factors. Our work provides further insight into the functions of herpesviral miRNAs in virus-induced oncogenesis and latency.

Project description:Chondrosarcomas are malignant cartilage tumors that are relatively resistant towards conventional therapeutic approaches. Kinase inhibitors have been investigated and shown successful for several different cancer types. In this study we aimed at identifying kinase inhibitors that inhibit the survival of chondrosarcoma cells and thereby serve as new potential therapeutic strategies to treat chondrosarcoma patients. An siRNA screen targeting 779 different kinases was conducted in JJ012 chondrosarcoma cells in parallel with a compound screen consisting of 273 kinase inhibitors in JJ012, SW1353 and CH2879 chondrosarcoma cell lines. AURKA, CHK1 and PLK1 were identified as most promising targets and validated further in a more comprehensive panel of chondrosarcoma cell lines. Dose response curves were performed using tyrosine kinase inhibitors: MK-5108 (AURKA), LY2603618 (CHK1) and Volasertib (PLK1) using viability assays and cell cycle analysis. Apoptosis was measured at 24 h after treatment using a caspase 3/7 assay. Finally, chondrosarcoma patient samples (N = =34) were used to examine the correlation between AURKA, CHK1 and PLK1 RNA expression and documented patient survival. Dose dependent decreases in viability were observed in chondrosarcoma cell lines after treatment with MK-5108, LY2603618 and volasertib, with cell lines showing highest sensitivity to PLK1 inhibition. In addition increased sensitivity to conventional chemotherapy was observed after CHK1 inhibition in a subset of the cell lines. Interestingly, whereas AURKA and CHK1 were both expressed in chondrosarcoma patient samples, PLK1 expression was found to be low compared to normal cartilage. Analysis of patient samples revealed that high CHK1 RNA expression correlated with a worse overall survival. AURKA, CHK1 and PLK1 are identified as important survival genes in chondrosarcoma cell lines. Although further research is needed to validate these findings, inhibiting CHK1 seems to be the most promising potential therapeutic target for patients with chondrosarcoma.

Dataset Information

Interaction of CPR5 with cell cycle regulators UVI4 and OSD1 in Arabidopsis.

Publications

Interaction of CPR5 with cell cycle regulators UVI4 and OSD1 in Arabidopsis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets