Reactions of the bis(benzylamine)platinum(II) complex [Pt(COMe)2(NH2Bn)2] (2; Bn = benzyl) with (2-py)3COR (2-py = 2-pyridyl), (2-py)2PhCOR, and (2-py)2(m-Tol)COR (m-Tol = 3-methylphenyl) afforded the neutral diacetylplatinum(II) complexes [Pt(COMe)2{(2-py)3COR}] (R = H (3a), Me (3b), Et (3c), Bn (3d)), [Pt(COMe)2{(2-py)2PhCOR}] (R = H (4a), Me (4b)), and [Pt(COMe)2{(2-py)2(m-Tol)COR}] (R = H (5a) Me (5b)), respectively, having, due to a κ2 coordination of the ligands, a 2-pyridyl (3), a phenyl (4), or a m-tolyl (5) ring as the pendant group. The identities of all complexes were unambiguously proved by high-resolution mass spectrometric investigations and by NMR (1H, 13C, 195Pt) and IR spectroscopy as well as by single-crystal X-ray diffraction analyses (3a–d). In methanol solution, complexes 3b–d and 5b show a dynamic behavior. The thermodynamic parameters of these dynamics have been determined by variable-temperature 1H NMR measurements (Eyring plots). Furthermore, extensive DFT calculations will be presented, which indicate that the dynamics are caused by the interplay of hindered and respectively unhindered rotations of the substituent R and/or the pendant group.

Reactions of the dinuclear platina‐β‐diketone [Pt2{(COMe)2H}2(μ‐Cl)2] (1) with HC(pz)3 and HC(3,5‐Me2pz)3 (pz = pyrazol‐1‐yl; 3,5‐Me2pz = 3,5‐dimethylpyrazol‐1‐yl) afforded cationic, thermally labile diacetyl(hydrido)platinum(IV) complexes [Pt(COMe)2H{(pz)3CH}]Cl (3a) and [Pt(COMe)2H{(3,5‐Me2pz)3CH}]Cl (3b) with κ3‐coordinated tris(pyrazolyl)methane ligands, which were found to react with NaOH or NEt3 to yield neutral diacetylplatinum(II) complexes with κ2‐coordinated tris(pyrazolyl)methane ligands {[Pt(COMe)2{(pz)3CH}] (4a); [Pt(COMe)2{(3,5‐Me2pz)3CH}] (4b)}. In 4a/b, a molecular rearrangement (decoordination of a pyrazolyl ring and coordination of the originally pendant one) has been found that has been investigated by variable‐temperature 1H NMR spectroscopic measurements (coalescence method) as well as by DFT calculations. Diacetylplatinum(II) complexes 4 were found to react in oxidative addition reactions with ROTf (R = H, Me; OTf = trifluoromethanesulfonate) and methyl iodide to yield cationic diacetylplatinum(IV) complexes of the type [Pt(COMe)2R{(pz)3CH}]X (R/X = H/OTf, 5a; Me/OTf, 6a; Me/I, 7a) and [Pt(COMe)2R{(3,5‐Me2pz)3CH}]X [R/X = H/OTf (5b), Me/OTf (6b), Me/I (7b)] with κ3‐bonded tris(pyrazolyl)methane ligands. Treatment of 4b with alkynyliodine(III) reagents of the type [IPh(C≡CR)]X (R/X = SiMe3/OTf, Ph/OTf, tBu/OTos, iPr/OTos; OTos = p‐toluenesulfonate) led to the formation of cationic diacetyl(alkynyl)platinum(IV) complexes [Pt(COMe)2(C≡CR){(3,5‐Me2pz)3CH}]X [R/X = SiMe3/OTf (8a), Ph/OTf (8b), tBu/OTos (8c), iPr/OTos (8d)]. The identities of all platinum complexes were unambiguously proven by high‐resolution mass spectrometric investigations, by NMR (1H, 13C, 195Pt) and IR spectroscopy, as well as by single‐crystal X‐ray diffraction analyses (4a, 4b, 7a, 8a/d). The constitution of the thermally labile complexes 3a/b has been confirmed by low‐temperature (–80 °C) NMR (1H, 13C) spectroscopic measurements. The electronic and steric influence of the additional methyl groups in HC(3,5‐Me2pz)3 on reactivity, stability, and properties of the investigated compounds will be discussed.

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The leaf essential oil of Tarchonanthuscamphoratus(Asteraceae) was obtained by hydrodistillation and analyzed by GC-MS. Fifty-six components were characterized, representing 94.2% of the total oil with oxygenated monoterpenes (48.3%) and oxygenated sesquiterpenes (32.7%) as the major groups. The principal constituents were identified as endo-fenchol (21.2%), trans-pinene hydrate (8.8%), caryophyllene oxide (7.5%), α-terpineol (6.4%), τ-cadinol (6.4%), and α-cadinol (5.2%). The essential oil was evaluated for its antimicrobial activity using a disc diffusion assay resulting in the moderate inhibition of a number of common human pathogenic bacteria, including methicillin-resistant Staphylococcus aureus(MRSA) and the yeast Candida albicans. The inhibition zones varied from 10 to 14mm/disc. Furthermore, the antioxidant capacity of the essential oil was examined using an in vitroradical scavenging activity test. The T. camphoratus essential oil scavenged 1,1-diphenyl-2-picrylhydrazyl radical (DPPH), resulting in an IC50value of 5.6 mg/mL. At concentrations of 100 and 50μg/mL, the oil showed cytotoxic activity, with growth inhibition of 59.1% (±4.2), and 16.2% (±8.7) against HT29 tumor cells (human colonic adenocarcinoma cells), respectively(IC50 = 84.7 ± 7.5 μg/mL).

Wound responses in plants have to be coordinated between organs so that locally reduced growth in a wounded tissue is balanced by appropriate growth elsewhere in the body. We used a JASMONATE ZIM DOMAIN 10 (JAZ10) reporter to screen for mutants affected in the organ-specific activation of jasmonate (JA) signaling in Arabidopsis thaliana seedlings. Wounding one cotyledon activated the reporter in both aerial and root tissues, and this was either disrupted or restricted to certain organs in mutant alleles of core components of the JA pathway including COI1, OPR3, and JAR1. In contrast, three other mutants showed constitutive activation of the reporter in the roots and hypocotyls of unwounded seedlings. All three lines harbored mutations in Novel Interactor of JAZ (NINJA), which encodes part of a repressor complex that negatively regulates JA signaling. These ninja mutants displayed shorter roots mimicking JA-mediated growth inhibition, and this was due to reduced cell elongation. Remarkably, this phenotype and the constitutive JAZ10 expression were still observed in backgrounds lacking the ability to synthesize JA or the key transcriptional activator MYC2. Therefore, JA-like responses can be recapitulated in specific tissues without changing a plant’s ability to make or perceive JA, and MYC2 either has no role or is not the only derepressed transcription factor in ninja mutants. Our results show that the role of NINJA in the root is to repress JA signaling and allow normal cell elongation. Furthermore, the regulation of the JA pathway differs between roots and aerial tissues at all levels, from JA biosynthesis to transcriptional activation.

Calcium (Ca2+) signaling modules are essential for adjusting plant growth and performance to environmental constraints. Differential interactions between sensors of Ca2+ dynamics and their molecular targets are at the center of the transduction process. Calmodulin (CaM) and CaM-like (CML) proteins are principal Ca2+-sensors in plants that govern the activities of numerous downstream proteins with regulatory properties. The families of IQ67-Domain (IQD) proteins are a large class of plant-specific CaM/CML-targets (e.g., 33 members in A. thaliana) which share a unique domain of multiple varied CaM retention motifs in tandem orientation. Genetic studies in Arabidopsis and tomato revealed first roles for IQD proteins related to basal defense response and plant development. Molecular, biochemical and histochemical analysis of Arabidopsis IQD1 demonstrated association with microtubules as well as targeting to the cell nucleus and nucleolus. In vivo binding to CaM and kinesin light chain-related protein-1 (KLCR1) suggests a Ca2+-regulated scaffolding function of IQD1 in kinesin motor-dependent transport of multiprotein complexes. Furthermore, because IQD1 interacts in vitro with single-stranded nucleic acids, the prospect arises that IQD1 and other IQD family members facilitate cellular RNA localization as one mechanism to control and fine-tune gene expression and protein sorting.

Liquid chromatography negative ion electrospray ionisation tandem mass spectrometry has been used for characterisation of naturally occurring prenylated fungal metabolites and synthetic derivatives. The fragmentation studies allow an elucidation of the decomposition pathways for these compounds. It could be shown, that the prenyl side chain is degraded by successive radical losses of C5 units. Both the benzoquinones and the phenolic derivatives display significant key ions comprising the aromatic ring. In some cases, the formation of significant oxygen-free key ions could be evidenced by high-resolution MS/MS measurements. Furthermore, the different types of basic skeletons, benzoquinones and phenol type as well as cyclic prenylated compounds, can be differentiated by their MS/MS behaviour.

In plant effector-triggered immunity (ETI), intracellular nucleotide binding-leucine rich repeat (NLR) receptors are activated by specific pathogen effectors. The ArabidopsisTIR (Toll-Interleukin-1 receptor domain)-NLR (denoted TNL) gene pair, RPS4 and RRS1, confers resistance to Pseudomonas syringae pv tomato (Pst) strain DC3000 expressing the Type III-secreted effector, AvrRps4. Nuclear accumulation of AvrRps4, RPS4, and the TNL resistance regulator EDS1 is necessary for ETI. RRS1 possesses a C-terminal “WRKY” transcription factor DNA binding domain suggesting that important RPS4/RRS1 recognition and/or resistance signaling events occur at the nuclear chromatin. In Arabidopsis accession Ws-0, the RPS4Ws/RRS1Ws allelic pair governs resistance to Pst/AvrRps4 accompanied by host programed cell death (pcd). In accession Col-0, RPS4Col/RRS1Col effectively limits Pst/AvrRps4 growth without pcd. Constitutive expression of HA-StrepII tagged RPS4Col (in a 35S:RPS4-HS line) confers temperature-conditioned EDS1-dependent auto-immunity. Here we show that a high (28°C, non-permissive) to moderate (19°C, permissive) temperature shift of 35S:RPS4-HS plants can be used to follow defense-related transcriptional dynamics without a pathogen effector trigger. By comparing responses of 35S:RPS4-HS with 35S:RPS4-HSrrs1-11 and 35S:RPS4-HSeds1-2 mutants, we establish that RPS4Col auto-immunity depends entirely on EDS1 and partially on RRS1Col. Examination of gene expression microarray data over 24 h after temperature shift reveals a mainly quantitative RRS1Col contribution to up- or down-regulation of a small subset of RPS4Col-reprogramed, EDS1-dependent genes. We find significant over-representation of WRKY transcription factor binding W-box cis-elements within the promoters of these genes. Our data show that RRS1Col contributes to temperature-conditioned RPS4Col auto-immunity and are consistent with activated RPS4Col engaging RRS1Col for resistance signaling.