The Structure of Alkali Halide Dimers: A Critical Test of Ionic Models and New Ab Initio Results

In semiempirical ionic models a number of adjustable parameters have to be fitted to experimental data of either monomer molecules or crystals. This leads to strong correlations between these constants and prevents a unique test and a clear physical interpretation of the fit parameters. Moreover, it is not clear whether these constants remain unchanged when the model is applied to dimers or larger clusters. It is shown that these correlations can be substantially reduced when reliable information about dimers is available from experiments or ab initio calculations. Starting with Dunham coefficients of the monomer potential determined from microwave measurements, we have calculated the monomer to dimer bond expansion and the bond angle without any additional adjustable parameter. Assuming that the overlap repulsion between nearest neighbors remains unchanged, the bond expansion is mainly determined by the simple Coulomb repulsion between equally charged ions and depends only very little on the effective ion polarizabilities. Deviation of the bond angle from 90° sensitively tests the difference of effective polarizabilities of the two ions. A comparison with previously available data and new ab initio MP2 results presented here for the heavy‐atom containing dimers shows that bond angles can be modeled reasonably well with Seitz–Ruffa corrected Pauling polarizabilities while calculated bond expansions are much too long. This shows that changes of the overlap repulsion term must be considered for reliable predictions of the structure of dimers and larger clusters

Erratum: The Structure of Alkali Halide Dimers: A Critical Test of Ionic Models and New Ab Initio Results

It has come to our attention that some of the ab initio results presented are incorrect due to errors in the Cs and C1 basis sets, and a small error in the binding energy of Rb2F2. The corrected results are presented below for the species that were affected, modifying the results in Table III of the original paper. Only those values which are different from the results of the original Table III are included. Note that some of these results are used for comparison with the ionic models in later tables. In addition, some HF data quoted in Tables V and VI is affected, and the correct values are given in Table II. All the changes in quoted values are small and none of the conclusions drawn in the article are affected, nor are the comparisons with the ionic models significantly affected. However, the error in the C1 basis is what gave rise to the anomalously short M–Cl bond lengths, and the results presented here lead to longer bonds, in somewhat poorer agreement with the experimental results for Cl containing species

A combinatorial TIR1/AFB–Aux/IAA co-receptor system for differential sensing of auxin

The plant hormone auxin regulates virtually every aspect of plant growth and development. Auxin acts by binding the F-box protein transport inhibitor response 1 (TIR1) and promotes the degradation of the AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) transcriptional repressors. Here we show that efficient auxin binding requires assembly of an auxin co-receptor complex consisting of TIR1 and an Aux/IAA protein. Heterologous experiments in yeast and quantitative IAA binding assays using purified proteins showed that different combinations of TIR1 and Aux/IAA proteins form co-receptor complexes with a wide range of auxin-binding affinities. Auxin affinity seems to be largely determined by the Aux/IAA. As there are 6 TIR1/AUXIN SIGNALING F-BOX proteins (AFBs) and 29 Aux/IAA proteins in Arabidopsis thaliana, combinatorial interactions may result in many co-receptors with distinct auxin-sensing properties. We also demonstrate that the AFB5–Aux/IAA co-receptor selectively binds the auxinic herbicide picloram. This co-receptor system broadens the effective concentration range of the hormone and may contribute to the complexity of auxin response

Characterization of the Tomato ARF Gene Family Uncovers a Multi-Levels Post-Transcriptional Regulation Including Alternative Splicing

Background: The phytohormone auxin is involved in a wide range of developmental processes and auxin signaling is known to modulate the expression of target genes via two types of transcriptional regulators, namely, Aux/IAA and Auxin Response Factors (ARF). ARFs play a major role in transcriptional activation or repression through direct binding to the promoter of auxin-responsive genes. The present study aims at gaining better insight on distinctive structural and functional features among ARF proteins. Results: Building on the most updated tomato (Solanum lycopersicon) reference genome sequence, a comprehensive set of ARF genes was identified, extending the total number of family members to 22. Upon correction of structural annotation inconsistencies, renaming the tomato ARF family members provided a consensus nomenclature for all ARF genes across plant species. In silico search predicted the presence of putative target site for small interfering RNAs within twelve Sl-ARFs while sequence analysis of the 59-leader sequences revealed the presence of potential small uORF regulatory elements. Functional characterization carried out by transactivation assay partitioned tomato ARFs into repressors and activators of auxin-dependent gene transcription. Expression studies identified tomato ARFs potentially involved in the fruit set process. Genome-wide expression profiling using RNA-seq revealed that at least one third of the gene family members display alternative splicing mode of regulation during the flower to fruit transition. Moreover, the regulation of several tomato ARF genes by both ethylene and auxin, suggests their potential contribution to the convergence mechanism between the signaling pathways of these two hormones. Conclusion: All together, the data bring new insight on the complexity of the expression control of Sl-ARF genes at the transcriptional and post-transcriptional levels supporting the hypothesis that these transcriptional mediators might represent one of the main components that enable auxin to regulate a wide range of physiological processes in a highly specific and coordinated manner

Beyond an associative conception of automatic self-evaluations: applying the relational responding task to measure self-esteem

According to dual-process models, implicit self-esteem (SE) is based on automatic self-associations that can be measured with indirect techniques based on an associative conception of implicit cognition (e.g., Implicit Association Test; IAT). However, alternative theoretical proposals (e.g., relational frame theory; RFT) propose that implicit SE might not be based on automatic self-associations, but on implicit propositional self-evaluations that can be captured only with nonassociative implicit measures (e.g., Implicit Relational Assessment Procedure; IRAP). In the present study, both reliability and validity of a new propositional measure of implicit self-esteem (relational responding task; RRT) were assessed, and compared with the SE-IAT and with two self-report scales of self-esteem. In the first study, two alternative self-esteem RRTs (SE-RRT and RSE-RRT) were administered along with a SE-IAT and other scales, to assess reliability and validity issues. The results showed: 1) acceptable, though not optimal, reliability for both RRTs; 2) an adequate support for convergent validity, with significant correlations between implicit and explicit measures of SE; 3) the criterion validity was supported for the RSE-RRT (with significant correlations with all theoretically linked scales), although only partially supported for the SE-RRT (with a significant correlation only with depression; 4) RRTs were not significantly correlated with impression management and self-deception; and 5) incremental validity of implicit propositional SE on depression, controlling for automatic SE associations and explicit self-esteem. In a second study, it was experimentally demonstrated that SE-RRT showed levels of “fakeability” similar to a classical implicit self-esteem measure like the SE-IAT, and considerably lower than SE scales

PMR5, an acetylation protein at the intersection of pectin biosynthesis and defense against fungal pathogens.

Powdery mildew (Golovinomyces cichoracearum), one of the most prolific obligate biotrophic fungal pathogens worldwide, infects its host by penetrating the plant cell wall without activating the plant's innate immune system. The Arabidopsis mutant powdery mildew resistant 5 (pmr5) carries a mutation in a putative pectin acetyltransferase gene that confers enhanced resistance to powdery mildew. Here, we show that heterologously expressed PMR5 protein transfers acetyl groups from [14 C]-acetyl-CoA to oligogalacturonides. Through site-directed mutagenesis, we show that three amino acids within a highly conserved esterase domain in putative PMR5 orthologs are necessary for PMR5 function. A suppressor screen of mutagenized pmr5 seed selecting for increased powdery mildew susceptibility identified two previously characterized genes affecting the acetylation of plant cell wall polysaccharides, RWA2 and TBR. The rwa2 and tbr mutants also suppress powdery mildew disease resistance in pmr6, a mutant defective in a putative pectate lyase gene. Cell wall analysis of pmr5 and pmr6, and their rwa2 and tbr suppressor mutants, demonstrates minor shifts in cellulose and pectin composition. In direct contrast to their increased powdery mildew resistance, both pmr5 and pmr6 plants are highly susceptibile to multiple strains of the generalist necrotroph Botrytis cinerea, and have decreased camalexin production upon infection with B. cinerea. These results illustrate that cell wall composition is intimately connected to fungal disease resistance and outline a potential route for engineering powdery mildew resistance into susceptible crop species

PMR5, an acetylation protein at the intersection of pectin biosynthesis and defense against fungal pathogens.

Powdery mildew (Golovinomyces cichoracearum), one of the most prolific obligate biotrophic fungal pathogens worldwide, infects its host by penetrating the plant cell wall without activating the plant's innate immune system. The Arabidopsis mutant powdery mildew resistant 5 (pmr5) carries a mutation in a putative pectin acetyltransferase gene that confers enhanced resistance to powdery mildew. Here, we show that heterologously expressed PMR5 protein transfers acetyl groups from [14 C]-acetyl-CoA to oligogalacturonides. Through site-directed mutagenesis, we show that three amino acids within a highly conserved esterase domain in putative PMR5 orthologs are necessary for PMR5 function. A suppressor screen of mutagenized pmr5 seed selecting for increased powdery mildew susceptibility identified two previously characterized genes affecting the acetylation of plant cell wall polysaccharides, RWA2 and TBR. The rwa2 and tbr mutants also suppress powdery mildew disease resistance in pmr6, a mutant defective in a putative pectate lyase gene. Cell wall analysis of pmr5 and pmr6, and their rwa2 and tbr suppressor mutants, demonstrates minor shifts in cellulose and pectin composition. In direct contrast to their increased powdery mildew resistance, both pmr5 and pmr6 plants are highly susceptibile to multiple strains of the generalist necrotroph Botrytis cinerea, and have decreased camalexin production upon infection with B. cinerea. These results illustrate that cell wall composition is intimately connected to fungal disease resistance and outline a potential route for engineering powdery mildew resistance into susceptible crop species

Auxin perception and downstream events

Auxin responses have been arbitrarily divided into two categories: genomic and non-genomic effects. Genomic effects are largely mediated by SCF(TIR1/AFB)-Aux/IAA auxin receptor complexes whereas it has been postulated that AUXIN BINDING PROTEIN 1 (ABP1) controls the non-genomic effects. However, the roles of ABP1 in auxin signaling and plant development were recently called into question. In this paper, we present recent progress in understanding the SCF(TIR1/AFB)-Aux/IAA pathway. In more detail, we discuss the current understanding of ABP1 research and provide an updated view of ABP1-related genetic materials. Further, we propose a model in which auxin efflux carriers may play a role in auxin perception and we briefly describe recent insight on processes downstream of auxin perception