123 research outputs found

    Nuclei in motion: movement and positioning of plant nuclei in development, signaling, symbiosis, and disease

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    While textbook figures imply nuclei as resting spheres at the center of idealized cells, this picture fits few real situations. Plant nuclei come in many shapes and sizes, and can be actively transported within the cell. In several contexts, this nuclear movement is tightly coupled to a developmental program, the response to an abiotic signal, or a cellular reprogramming during either mutualistic or parasitic plant-microbe interactions. While many such phenomena have been observed and carefully described, the underlying molecular mechanism and the functional significance of the nuclear movement are typically unknown. Here, we survey recent as well as older literature to provide a concise starting point for applying contemporary molecular, genetic and biochemical approaches to this fascinating, yet poorly understood phenomenon

    A nuclear localization signal targets tail-anchored membrane proteins to the inner nuclear envelope in plants

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    Protein targeting to the inner nuclear membrane (INM) is one of the least understood protein targeting pathways. INM proteins are important for chromatin organization, nuclear morphology and movement, and meiosis, and have been implicated in human diseases. In opisthokonts, one mechanism for INM targeting is transport factor-mediated trafficking, in which nuclear localization signals (NLSs) function in nuclear import of transmembrane proteins. To explore whether this pathway exists in plants, we fused the SV40 NLS to a plant ER tail-anchored protein and showed that the GFP-tagged fusion protein was significantly enriched at the nuclear envelope (NE) of leaf epidermal cells. Airyscan subdiffraction limited confocal microscopy showed that this protein displays a localization consistent with an INM protein. Nine different monopartite and bipartite NLSs from plants and opisthokonts, fused to a chimeric tail-anchored membrane protein, were all sufficient for NE enrichment, and both monopartite and bipartite NLSs were sufficient for trafficking to the INM. Tolerance for different linker lengths and protein conformations suggests that INM trafficking rules might differ from those in opisthokonts. The INM proteins developed here can be used to target new functionalities to the plant nuclear periphery

    A cyclic nucleotide-gated channel (CNGC16) in pollen is critical for stress tolerance in pollen reproductive development

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    Cyclic nucleotide-gated channels (CNGCs) have been implicated in diverse aspects of plant growth and development, including responses to biotic and abiotic stress, as well as pollen tube growth and fertility. Here, genetic evidence identifies CNGC16 in Arabidopsis (Arabidopsis thaliana) as critical for pollen fertility under conditions of heat stress and drought. Two independent transfer DNA disruptions of cngc16 resulted in a greater than 10-fold stress-dependent reduction in pollen fitness and seed set. This phenotype was fully rescued through pollen expression of a CNGC16 transgene, indicating that cngc16-1 and 16-2 were both loss-of-function null alleles. The most stress-sensitive period for cngc16 pollen was during germination and the initiation of pollen tube tip growth. Pollen viability assays indicate that mutant pollen are also hypersensitive to external calcium chloride, a phenomenon analogous to calcium chloride hypersensitivities observed in other cngc mutants. A heat stress was found to increase concentrations of 3′,5′-cyclic guanyl monophosphate in both pollen and leaves, as detected using an antibody-binding assay. A quantitative PCR analysis indicates that cngc16 mutant pollen have attenuated expression of several heat-stress response genes, including two heat shock transcription factor genes, HsfA2 and HsfB1. Together, these results provide evidence for a heat stress response pathway in pollen that connects a cyclic nucleotide signal, a Ca(2+)-permeable ion channel, and a signaling network that activates a downstream transcriptional heat shock response

    Mapping far-IR emission from the central kiloparsec of NGC 1097

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    Using photometry of NGC 1097 from the Herschel PACS (Photodetector Array Camera and Spectrometer) instrument, we study the resolved properties of thermal dust continuum emission from a circumnuclear starburst ring with a radius ~ 900 pc. These observations are the first to resolve the structure of a circumnuclear ring at wavelengths that probe the peak (i.e. lambda ~ 100 micron) of the dust spectral energy distribution. The ring dominates the far-infrared (far-IR) emission from the galaxy - the high angular resolution of PACS allows us to isolate the ring's contribution and we find it is responsible for 75, 60 and 55% of the total flux of NGC 1097 at 70, 100 and 160 micron, respectively. We compare the far-IR structure of the ring to what is seen at other wavelengths and identify a sequence of far-IR bright knots that correspond to those seen in radio and mid-IR images. The mid- and far-IR band ratios in the ring vary by less than +/- 20% azimuthally, indicating modest variation in the radiation field heating the dust on ~ 600 pc scales. We explore various explanations for the azimuthal uniformity in the far-IR colors of the ring including a lack of well-defined age gradients in the young stellar cluster population, a dominant contribution to the far-IR emission from dust heated by older (> 10 Myr) stars and/or a quick smoothing of local enhancements in dust temperature due to the short orbital period of the ring. Finally, we improve previous limits on the far-IR flux from the inner ~ 600 pc of NGC 1097 by an order of magnitude, providing a better estimate of the total bolometric emission arising from the active galactic nucleus and its associated central starburst.Comment: Accepted for publication in the A&A Herschel Special Editio

    Obscured and powerful AGN and starburst activities at z~3.5

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    We report the discovery of two sources at z=3.867 and z=3.427 that exhibit powerful starburst and AGN activities. They benefit from data from radio to X rays from the CFHTLS-D1/SWIRE/XMDS surveys. Follow-up optical and near-infrared spectroscopy, and millimeter IRAM/MAMBO observations are also available. We performed an analysis of their spectral energy distributions to understand the origin of their emission and constrain their luminosities. A comparison with other composite systems at similar redshifts from the literature is also presented. The AGN and starburst bolometric luminosities are ~10^13 Lsun. The AGN emission dominates at X ray, optical, mid-infrared wavelengths, and probably in the radio. The starburst emission dominates in the far-infrared. The estimated star formation rates range from 500 to 3000Msun/yr. The AGN near-infrared and X ray emissions are heavily obscured in both sources with an estimated dust extinction Av>4, and Compton-thick gas column densities. The two sources are the most obscured and most luminous AGNs detected at millimeter wavelengths currently known. The sources presented in this work are heavily obscured QSOs, but their properties are not fully explained by the standard AGN unification model. In one source, the ultraviolet and optical spectra suggest the presence of outflowing gas and shocks, and both sources show emission from hot dust, most likely in the vicinity of the nucleus. Evidence of moderate AGN-driven radio activity is found in both sources. The two sources lie on the local M_BH-M_bulge relation. To remain on this relation, their star formation rate has to decrease. Our results support evolutionary models that invoke radio feedback as star formation quenching mechanism, and suggest that such a mechanism might play a major role also in powerful AGNs.Comment: Accepted for publication in Astronomy & Astrophysics (12 pages; 6 figures); replaced version includes minor language editing and revised reference

    Mechanistic implications of the active species involved in the oxidation of hydrocarbons by iron complexes of pyrazine-2-carboxylic acid

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    The reactivity towards H2O2 of the complexes [Fe(pca)2(py)2]·py (1) and Na2{[Fe(pca3)]2O}·2H2O·CH3CN (2) (where pca− is pyrazine-2-carboxylate) and their catalytic activity in the oxidation of hydrocarbons is reported. Addition of H2O2 to 1 results in the formation of a dinuclear Fe(III)–(µ-O)–Fe(III) species characterized spectroscopically and by cyclic voltammetry. By contrast, treatment of 2 with H2O2 results in the formation of mononuclear iron(II) complexes, [Fe(pca)2(solvent)2]. The experimental results indicate that the catalytic activity of the starting complexes 1 and 2 is strongly dependent on the species formed in solution.

    Hypoxia regulates human lung fibroblast proliferation via p53-dependent and -independent pathways

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    <p>Abstract</p> <p>Background</p> <p>Hypoxia induces the proliferation of lung fibroblasts in vivo and in vitro. However, the subcellular interactions between hypoxia and expression of tumor suppressor p53 and cyclin-dependent kinase inhibitors p21 and p27 remain unclear.</p> <p>Methods</p> <p>Normal human lung fibroblasts (NHLF) were cultured in a hypoxic chamber or exposed to desferroxamine (DFX). DNA synthesis was measured using bromodeoxyuridine incorporation, and expression of p53, p21 and p27 was measured using real-time RT-PCR and Western blot analysis.</p> <p>Results</p> <p>DNA synthesis was increased by moderate hypoxia (2% oxygen) but was decreased by severe hypoxia (0.1% oxygen) and DFX. Moderate hypoxia decreased p21 synthesis without affecting p53 synthesis, whereas severe hypoxia and DFX increased synthesis of both p21 and p53. p27 protein expression was decreased by severe hypoxia and DFX. Gene silencing of p21 and p27 promoted DNA synthesis at ambient oxygen concentrations. p21 and p53 gene silencing lessened the decrease in DNA synthesis due to severe hypoxia or DFX exposure. p21 gene silencing prevented increased DNA synthesis in moderate hypoxia. p27 protein expression was significantly increased by p53 gene silencing, and was decreased by wild-type p53 gene transfection.</p> <p>Conclusion</p> <p>These results indicate that in NHLF, severe hypoxia leads to cell cycle arrest via the p53-p21 pathway, but that moderate hypoxia enhances cell proliferation via the p21 pathway in a p53-independent manner. In addition, our results suggest that p27 may be involved in compensating for p53 in cultured NHLF proliferation.</p
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