The Arabidopsis (Arabidopsis thaliana) mutant stop1 (for sensitive to proton rhizotoxicity1) carries a missense mutation at an essential domain of the histidine-2-cysteine-2 zinc finger protein STOP1. Transcriptome analyses revealed that various genes were down-regulated in the mutant, indicating that STOP1 is involved in signal transduction pathways regulating aluminum (Al)- and H+-responsive gene expression. The Al hypersensitivity of the mutant could be caused by down-regulation of AtALMT1 (for Arabidopsis ALUMINUM-ACTIVATED MALATE TRANSPORTER1) and ALS3 (ALUMINUM-SENSITIVE3). This hypothesis was supported by comparison of Al tolerance among T-DNA insertion lines and a transgenic stop mutant carrying cauliflower mosaic virus 35S∷AtALMT1. All T-DNA insertion lines of STOP1, AtALMT1, and ALS3 were sensitive to Al, but introduction of cauliflower mosaic virus 35S∷AtALMT1 did not completely restore the Al tolerance of the stop1 mutant. Down-regulation of various genes involved in ion homeostasis and pH-regulating metabolism in the mutant was also identified by microarray analyses. CBL-INTERACTING PROTEIN KINASE23, regulating a major K+ transporter, and a sulfate transporter, SULT3;5, were down-regulated in the mutant. In addition, integral profiling of the metabolites and transcripts revealed that pH-regulating metabolic pathways, such as the γ-aminobutyric acid shunt and biochemical pH stat pathways, are down-regulated in the mutant. These changes could explain the H+ hypersensitivity of the mutant and would make the mutant more susceptible in acid soil stress than other Al-hypersensitive T-DNA insertion lines. Finally, we showed that STOP1 is localized to the nucleus, suggesting that the protein regulates the expression of multiple genes that protect Arabidopsis from Al and H+ toxicities, possibly as a transcription factor.

The rabies virus Ni-CE strain causes nonlethal infection in adult mice after intracerebral inoculation, whereas the parental Nishigahara (Ni) strain kills mice. We previously reported that the chimeric CE(NiN) strain with the N gene from the Ni strain in the genetic background of the Ni-CE strain kills adult mice, indicating that the N gene is related to the different pathogenicities of Ni and Ni-CE strains. In the present study, to obtain an insight into the mechanism by which the N gene determines viral pathogenicity, we compared the effects of Ni, Ni-CE, and CE(NiN) infections on host gene expressions using a human neuroblastoma cell line. Microarray analysis of these infected cells revealed that the expression levels of particular genes in Ni-and CE(NiN)-infected cells, including beta interferon (IFN-␤) and chemokine genes (i.e., CXCL10 and CCL5) were lower than those in Ni-CE-infected cells. We also demonstrated that Ni-CE infection activated the interferon regulatory factor 3 (IRF-3)-dependent IFN-␤ promoter and induced IRF-3 nuclear translocation more efficiently than did Ni or CE(NiN) infection. Furthermore, we showed that Ni-CE infection, but not Ni or CE(NiN) infection, strongly activates the IRF-3 pathway through activation of RIG-I, which is known as a cellular sensor of virus infection. These findings indicate that the N protein of rabies virus (Ni strain) has a function to evade the activation of RIG-I. To our knowledge, this is the first report that the Mononegavirales N protein functions to evade induction of host IFN and chemokines.Rabies virus, which belongs to Lyssavirus of the family Rhabdoviridae, which belongs to the order Mononegavirales, is known as a highly neurotropic virus and causes fatal encephalitis accompanied by severe neurological symptoms in almost all mammals, including humans. The genome is an unsegmented negative sense RNA and contains five genes (N, P, M, G, and L genes) encoding nucleoprotein (N protein), phosphoprotein (P protein), matrix (M) protein, glycoprotein (G protein), and large (L) protein, respectively (12). The N, P, and L proteins form helical ribonucleoprotein (RNP), together with the viral genomic RNA. The N protein participates in encapsidation of the genomic RNA. Only the encapsidated genomic RNA can be a template for replication of the viral genome and transcription of the viral mRNAs by the RNAdependent RNA polymerase, L protein. The P protein binds to both N and L proteins and functions as a cofactor of the viral RNA polymerase. During virus assembly, the RNP is wrapped into an envelope containing an inner layer of the M protein and the transmembrane spike protein, G protein.In response to viral infection (e.g., picornavirus, bunyavirus, and flavivirus infections), neurons in the brain produce type I interferon (IFN) comprised of the IFN-␣ family and IFN-␤, which induces an antiviral status of a cell and functions as a main player for the host innate immunity (8, 9). The brain neurons are also capable of responding to the produced type I

Background: Rhizotoxic ions in problem soils inhibit nutrient and water acquisition by roots, which in turn leads to reduced crop yields. Previous studies on the effects of rhizotoxic ions on root growth and physiological functions suggested that some mechanisms were common to all rhizotoxins, while others were more specific. To understand this complex system, we performed comparative transcriptomic analysis with various rhizotoxic ions, followed by bioinformatics analysis, in the model plant Arabidopsis thaliana.

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Many plant species excrete organic acids into the rhizosphere in response to aluminum stress to protect sensitive cells from aluminum rhizotoxicity. When the roots of Eucalyptus camaldulensis, a major source of pulp production, were incubated in aluminum-toxic medium, citrate released into the solution increased as a function of time. Citrate excretion was inducible by aluminum, but not by copper or sodium chloride stresses. This indicated that citrate is the major responsive organic acid released from the roots of this plant species to protect the root tips from aluminum damage. Four genes highly homologs to known citrate-transporting multidrugs and toxic compounds exclusion proteins, named EcMATE1-4, were isolated using polymerase chain reaction-based cloning techniques. Their predicted proteins included 12 membrane spanning domains, a common structural feature of citrate-transporting MATE proteins, and consisted of 502-579 amino acids with >60 % homology to orthologous genes in other plant species. One of the homologs, designated EcMATE1, was expressed in the roots more abundantly than in the shoots and in response to both Al and low pH stresses. Ectopic expression of EcMATE1 and 3 in tobacco hairy roots enhanced Al-responsive citrate excretion. Pharmacological characterization indicated that Al-responsive citrate excretion involved a protein phosphorylation/dephosphorylation process. These results indicate that citrate excretion through citrate-transporting multidrugs and toxic compounds exclusion proteins is one of the important aluminum-tolerance mechanisms in Eucalyptus camaldulensis.

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Alteration of metabolic processes is a common adaptive response of plants to various stress conditions and is likely to be under complex regulatory control. To understand the metabolic responses to rhizotoxic treatments in Arabidopsis thaliana, transcriptome profiles of major carbon and amino acid metabolic pathways were compared among aluminum (Al), copper (Cu) and cadmium (Cd) ion and NaCl treatments with a similar level of severity. All stress treatments induced genes encoding enzymes for synthesizing trehalose and polyamine, as well as tryptophan‐synthesizing enzymes previously identified as critical for resistance to various stresses. Genes encoding enzymes critical for ascorbic acid and spermine synthesis had higher specificity to Cd and NaCl among the genes upregulated by each stress. Major isoforms of malic enzymes and glutamate decarboxylases were more specifically upregulated by the Al treatment than were other genes; these enzymes belong to cellular pH‐regulating pathways, namely the biochemical pH stat pathway and the γ‐amino butyric acid shunt. Characterization of the grouped genes with higher Cu specificity indicated that amino acid degradation and sugar starvation‐like symptoms were enhanced by Cu treatment. Pathway analysis in the trehalose synthesis pathway accounted for the activation of the pathway and for the accumulation of trehalose by all stressors. These metabolic alterations might form part of the tolerance mechanisms of Arabidopsis roots against rhizotoxic ions.