Star formation and AGN activity in the most luminous LINERs in the local universe

This work presents the properties of 42 objects in the group of the most luminous, highest star formation rate LINERs at z = 0.04 - 0.11. We obtained long-slit spectroscopy of the nuclear regions for all sources, and FIR data (Herschel and IRAS) for 13 of them. We measured emission line intensities, extinction, stellar populations, stellar masses, ages, AGN luminosities, and star-formation rates. We find considerable differences from other low-redshift LINERs, in terms of extinction, and general similarity to star forming (SF) galaxies. We confirm the existence of such luminous LINERs in the local universe, after being previously detected at z ~ 0.3 by Tommasin et al. (2012). The median stellar mass of these LINERs corresponds to 6 - 7 $\times$ 10$^{10}$M$_{\odot}$ which was found in previous work to correspond to the peak of relative growth rate of stellar populations and therefore for the highest SFRs. Other LINERs although showing similar AGN luminosities have lower SFR. We find that most of these sources have LAGN ~ LSF suggesting co-evolution of black hole and stellar mass. In general among local LINERs being on the main-sequence of SF galaxies is related to their AGN luminosity.Comment: submitted to MNRA

Light-Induced Changes within Photosystem II Protects Microcoleus sp. in Biological Desert Sand Crusts against Excess Light

The filamentous cyanobacterium Microcoleus vaginatus, a major primary producer in desert biological sand crusts, is exposed to frequent hydration (by early morning dew) followed by desiccation during potentially damaging excess light conditions. Nevertheless, its photosynthetic machinery is hardly affected by high light, unlike “model” organisms whereby light-induced oxidative stress leads to photoinactivation of the oxygen-evolving photosystem II (PSII). Field experiments showed a dramatic decline in the fluorescence yield with rising light intensity in both drying and artificially maintained wet plots. Laboratory experiments showed that, contrary to “model” organisms, photosynthesis persists in Microcoleus sp. even at light intensities 2–3 times higher than required to saturate oxygen evolution. This is despite an extensive loss (85–90%) of variable fluorescence and thermoluminescence, representing radiative PSII charge recombination that promotes the generation of damaging singlet oxygen. Light induced loss of variable fluorescence is not inhibited by the electron transfer inhibitors 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), 2,5-dibromo-3-methyl-6-isopropylbenzoquinone (DBMIB), nor the uncoupler carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), thus indicating that reduction of plastoquinone or O2, or lumen acidification essential for non-photochemical quenching (NPQ) are not involved. The rate of QA− re-oxidation in the presence of DCMU is enhanced with time and intensity of illumination. The difference in temperatures required for maximal thermoluminescence emissions from S2/QA− (Q band, 22°C) and S2,3/QB− (B band, 25°C) charge recombinations is considerably smaller in Microcoleus as compared to “model” photosynthetic organisms, thus indicating a significant alteration of the S2/QA− redox potential. We propose that enhancement of non-radiative charge recombination with rising light intensity may reduce harmful radiative recombination events thereby lowering 1O2 generation and oxidative photodamage under excess illumination. This effective photo-protective mechanism was apparently lost during the evolution from the ancestor cyanobacteria to the higher plant chloroplast

Allelic variations in the chpG effector gene within Clavibacter michiganensis populations determine pathogen host range.

Plant pathogenic bacteria often have a narrow host range, which can vary among different isolates within a population. Here, we investigated the host range of the tomato pathogen Clavibacter michiganensis (Cm). We determined the genome sequences of 40 tomato Cm isolates and screened them for pathogenicity on tomato and eggplant. Our screen revealed that out of the tested isolates, five were unable to cause disease on any of the hosts, 33 were exclusively pathogenic on tomato, and two were capable of infecting both tomato and eggplant. Through comparative genomic analyses, we identified that the five non-pathogenic isolates lacked the chp/tomA pathogenicity island, which has previously been associated with virulence in tomato. In addition, we found that the two eggplant-pathogenic isolates encode a unique allelic variant of the putative serine hydrolase chpG (chpGC), an effector that is recognized in eggplant. Introduction of chpGC into a chpG inactivation mutant in the eggplant-non-pathogenic strain Cm101, failed to complement the mutant, which retained its ability to cause disease in eggplant and failed to elicit hypersensitive response (HR). Conversely, introduction of the chpG variant from Cm101 into an eggplant pathogenic Cm isolate (C48), eliminated its pathogenicity on eggplant, and enabled C48 to elicit HR. Our study demonstrates that allelic variation in the chpG effector gene is a key determinant of host range plasticity within Cm populations

Formation of Alkanes by Aerobic Carbon–Carbon Bond Coupling Reactions Catalyzed by a Phosphovanadomolybdic Acid

The valorization of alkanes is possible via carbon–carbon coupling reactions. A series of dialkyl cobalt complexes [(RCH_2)_2Co^(III)(bpy)_2]ClO_4 (R = H, Me, Et, and Ph) were reacted with the H_5PV_2Mo_(10)O_(40) polyoxometalate as a catalyst, leading to a selective oxidative carbon–carbon bond coupling reaction. The reaction is initiated by electron transfer from [(RCH_2)_2Co^(III)(bpy)_2]^+ to H_5PV^V_2Mo_(10)O_(40) to yield an intermediate [(RCH_2)_2Co^(IV)(bpy)_2]^(2+)–H_5PV^(IV)V^VMo_(10)O_(40), as identified by a combination of EPR and X-ray photoelectron spectroscopy experiments. The reaction is catalytic with O_2 as terminal oxidant representing an aerobic C–C bond coupling reaction

Activation of Tm-22 resistance is mediated by a conserved cysteine essential for tobacco mosaic virus movement.

The tomato Tm-22 gene was considered to be one of the most durable resistance genes in agriculture, protecting against viruses of the Tobamovirus genus, such as tomato mosaic virus (ToMV) and tobacco mosaic virus (TMV). However, an emerging tobamovirus, tomato brown rugose fruit virus (ToBRFV), has overcome Tm-22 , damaging tomato production worldwide. Tm-22 encodes a nucleotide-binding leucine-rich repeat (NLR) class immune receptor that recognizes its effector, the tobamovirus movement protein (MP). Previously, we found that ToBRFV MP (MPToBRFV ) enabled the virus to overcome Tm-22 -mediated resistance. Yet, it was unknown how Tm-22 remained durable against other tobamoviruses, such as TMV and ToMV, for over 60 years. Here, we show that a conserved cysteine (C68) in the MP of TMV (MPTMV ) plays a dual role in Tm-22 activation and viral movement. Substitution of MPToBRFV amino acid H67 with the corresponding amino acid in MPTMV (C68) activated Tm-22 -mediated resistance. However, replacement of C68 in TMV and ToMV disabled the infectivity of both viruses. Phylogenetic and structural prediction analysis revealed that C68 is conserved among all Solanaceae-infecting tobamoviruses except ToBRFV and localizes to a predicted jelly-roll fold common to various MPs. Cell-to-cell and subcellular movement analysis showed that C68 is required for the movement of TMV by regulating the MP interaction with the endoplasmic reticulum and targeting it to plasmodesmata. The dual role of C68 in viral movement and Tm-22 immune activation could explain how TMV was unable to overcome this resistance for such a long period

Absorption changes in high light-exposed <i>Microcoleus</i> cells.

<p>Cells suspension was exposed to 1500 µmol photons m⁻² s⁻¹ for 40 min followed by 60 min recovery at 50 µmol photons m⁻² s⁻¹, which resulted in the recovery of the Ft–Fo values (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0011000#pone-0011000-g003" target="_blank">Fig. 3B</a>). Elapsed time (min) from the beginning of the experiment is shown in the box. <b>Top panel</b>: Absorptions in the visible range during the entire experiment. <b>Bottom panel</b>: Absorptions changes calculated from the differences between the light exposed and zero time control. O.D.₈₀₀ was used for normalization. Wavelengths are indicated where maximal absorption differences were observed. Differential absorption measurements were made using a Cary 300bio UV-visible spectrophotometer (Varian, Palo Alto, USA). Integration time was set to 0.5 s, the slit to 2 nm and the wavelength increment to 2 nm.</p

A schematic presentation of electron transport within PSII and the resulting TL bands.

<p>The Q_A and Q_B quinones, P₆₈₀ and the Mn cluster S-states are shown. Forward electron transport is represented by plain arrows and back electron transport by blue arrows. Changes in the peak temperature observed in TL experiments can be used as an estimate for the recombination energy of the Q_B⁻S₂/Q_BS₁ and Q_B⁻S₃/Q_BS₂ (B-band) or Q_A⁻S₂/Q_AS₁ (Q-band) redox pairs. To observe the Q band emission, reduction of the Q_B site was blocked by herbicides that bind specifically to this site. The electron released from P₆₈₀ by light excitation at subzero temperatures can reach the Q_A site and, in the presence of herbicides that bind to the Q_B site, recombine upon warming with the oxidized S₂ state by back electron flow producing the Q band. Since the energy gap between Q_A⁻ and P₆₈₀<i>⁺</i> is smaller than that from Q_B⁻ to P₆₈₀<i>⁺</i> (B band), lower activation energy is required for this recombination and thus the Q band is observed at lower temperatures.</p

Loss of variable fluorescence, even in the presence of DCMU, DBMIB and FCCP following excess light treatment.

<p><b>A.</b> Cells suspensions (7.5 µg chl ml⁻¹) were exposed to 2000 µmol photons m⁻² s⁻¹, 2.2 cm optical path, for the indicated times in the presence of 10 µM DCMU, a concentration which completely blocked CO₂-dependent O₂ evolution. Fv was measured after dark adaptation for 2 min using the FL 3000 fluorimeter; optical path 0.5 cm. After 15 min of excess illumination the light intensity was reduced to 50 µmol photons m⁻² s⁻¹ for 50 min. <b>B.</b> Fluorescence emission kinetics of dark-adapted cells in the presence or absence of 10 µM DCMU. The cells were exposed for 950 s to 530 µmol photons m⁻² s⁻¹ of blue light using the IMAG-MAX PAM. Note that in its setup, this light intensity is the maximal but it is not saturating. <b>Insert:</b> Rate of fluorescence decline at the 150–900 s range for cultures exposed to varying light intensities (100–530 µmol photons m⁻² s⁻¹). <b>C</b>. The experiment was performed as in (A), 2000 µmol photons m⁻² s⁻¹, 2.2 cm optical path, but with 10 µg chl ml⁻¹ and 0.15 µM DBMIB instead of DCMU. Note that DBMIB itself is a fluorescence quencher and the procedure used to minimize this effect is explained in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0011000#s4" target="_blank">Materials and Methods</a> section. <b>D.</b> Experiment performed as in (C) but in the presence of 10 µM FCCP.</p