In most aerobic soils, nitrate (NO3(-)) is the main nitrogen source for plants and is often limiting for plant growth and development. To adapt to a changing environment, plants have developed complex regulatory mechanisms that involve short and long-range signalling pathways in response to both NO3(-) availability in the soil and other physiological processes like growth or nitrogen (N) and carbon (C) metabolisms. Over the past decade, transcriptomic approaches largely contributed to the identification of molecular elements involved in these regulatory mechanisms, especially at the level of root NO3(-)uptake. Most strikingly, the data obtained revealed the high level of interaction between N and both hormone and C signalling pathways, suggesting a strong dependence on growth, development, and C metabolism to adapt root NO3(-) uptake to both external NO3(-) availability and the N status of the plant. However, the signalling mechanisms involved in the cross-talk between N, C, and hormones for the regulation of root NO3(-) uptake remain largely obscure. The aim of this review is to discuss the recent advances concerning the regulatory pathways controlling NO3(-) uptake in response to N signalling, hormones, and C in the model plant Arabidopsis thaliana. Then, to further characterize the level of interaction between these signalling pathways we built on publicly available transcriptome data to determine how hormones and C treatments modify the gene network connecting root NO3(-) transporters and their regulators.
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http://dx.doi.org/10.1093/jxb/eru321 | DOI Listing |
This study evaluates the oncolytic potential of the Moscow strain of reovirus against human metastatic melanoma and glioblastoma cells. The Moscow strain effectively infects and replicates within human melanoma cell lines and primary glioblastoma cells, while sparing non-malignant human cells. Infection leads to the selective destruction of neoplastic cells, mediated by functional viral replication.
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December 2024
Departments of Surgery & Molecular Microbiology and Immunology, University of Missouri, Columbia, MO 65212, USA.
Pathogenic viruses trigger or disrupt multiple signaling networks to establish an environment optimized for their own replication and productive infection [...
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December 2024
Division of Virology, ICMR-National Institute of Translational Virology and AIDS Research, Pune 411026, MH, India.
Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), which are the only members of the gamma(γ) herpesviruses, are oncogenic viruses that significantly contribute to the development of various human cancers, such as Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's lymphoma, Kaposi's sarcoma, and primary effusion lymphoma. Oncogenesis triggered by γ-herpesviruses involves complex interactions between viral genetics, host cellular mechanisms, and immune evasion strategies. At the genetic level, crucial viral oncogenes participate in the disruption of cell signaling, leading to uncontrolled proliferation and inhibition of apoptosis.
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December 2024
Department of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, OH 43606, USA.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2'-5'-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis.
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December 2024
Department of Dermatology, School of Medicine, University of California Davis, Sacramento, CA 95817, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA gamma herpesvirus. Like other herpesviruses, KSHV establishes a latent infection with limited gene expression, while KSHV occasionally undergoes the lytic replication phase, which produces KSHV progenies and infects neighboring cells. KSHV genome encodes 80+ open reading frames.
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