@article{15266, abstract = {Plant pathogens often exploit a whole range of effectors to facilitate infection. The RXLR effector AVR1 produced by the oomycete plant pathogen Phytophthora infestans suppresses host defense by targeting Sec5. Sec5 is a subunit of the exocyst, a protein complex that is important for mediating polarized exocytosis during plant development and defense against pathogens. The mechanism by which AVR1 manipulates Sec5 functioning is unknown. In this study, we analyzed the effect of AVR1 on Sec5 localization and functioning in the moss Physcomitrium patens. P. patens has four Sec5 homologs. Two (PpSec5b and PpSec5d) were found to interact with AVR1 in yeast-two-hybrid assays while none of the four showed a positive interaction with AVR1ΔT, a truncated version of AVR1. In P. patens lines carrying β-estradiol inducible AVR1 or AVR1ΔT transgenes, expression of AVR1 or AVR1ΔT caused defects in the development of caulonemal protonema cells and abnormal morphology of chloronema cells. Similar phenotypes were observed in Sec5- or Sec6-silenced P. patens lines, suggesting that both AVR1 and AVR1ΔT affect exocyst functioning in P. patens. With respect to Sec5 localization we found no differences between β-estradiol-treated and untreated transgenic AVR1 lines. Sec5 localizes at the plasma membrane in growing caulonema cells, also during pathogen attack, and its subcellular localization is the same, with or without AVR1 in the vicinity.}, author = {Overdijk, Elysa J. R. and Putker, Vera and Smits, Joep and Tang, Han and Bouwmeester, Klaas and Govers, Francine and Ketelaar, Tijs}, issn = {1932-6203}, journal = {PLoS One}, keywords = {Multidisciplinary}, number = {4}, publisher = {Public Library of Science}, title = {{Phytophthora infestans RXLR effector AVR1 disturbs the growth of Physcomitrium patens without affecting Sec5 localization}}, doi = {10.1371/journal.pone.0249637}, volume = {16}, year = {2021}, } @article{7548, abstract = {Although the aggregation of the amyloid-β peptide (Aβ) into amyloid fibrils is a well-established hallmark of Alzheimer’s disease, the complex mechanisms linking this process to neurodegeneration are still incompletely understood. The nematode worm C. elegans is a valuable model organism through which to study these mechanisms because of its simple nervous system and its relatively short lifespan. Standard Aβ-based C. elegans models of Alzheimer’s disease are designed to study the toxic effects of the overexpression of Aβ in the muscle or nervous systems. However, the wide variety of effects associated with the tissue-level overexpression of Aβ makes it difficult to single out and study specific cellular mechanisms related to the onset of Alzheimer’s disease. Here, to better understand how to investigate the early events affecting neuronal signalling, we created a C. elegans model expressing Aβ42, the 42-residue form of Aβ, from a single-copy gene insertion in just one pair of glutamatergic sensory neurons, the BAG neurons. In behavioural assays, we found that the Aβ42-expressing animals displayed a subtle modulation of the response to CO2, compared to controls. Ca2+ imaging revealed that the BAG neurons in young Aβ42-expressing nematodes were activated more strongly than in control animals, and that neuronal activation remained intact until old age. Taken together, our results suggest that Aβ42-expression in this very subtle model of AD is sufficient to modulate the behavioural response but not strong enough to generate significant neurotoxicity, suggesting that slightly more aggressive perturbations will enable effectively studies of the links between the modulation of a physiological response and its associated neurotoxicity.}, author = {Sinnige, Tessa and Ciryam, Prashanth and Casford, Samuel and Dobson, Christopher M. and de Bono, Mario and Vendruscolo, Michele}, issn = {1932-6203}, journal = {PLOS ONE}, number = {5}, publisher = {Public Library of Science}, title = {{Expression of the amyloid-β peptide in a single pair of C. elegans sensory neurons modulates the associated behavioural response}}, doi = {10.1371/journal.pone.0217746}, volume = {14}, year = {2019}, } @article{1029, abstract = {RNA Polymerase II pauses and backtracks during transcription, with many consequences for gene expression and cellular physiology. Here, we show that the energy required to melt double-stranded nucleic acids in the transcription bubble predicts pausing in Saccharomyces cerevisiae far more accurately than nucleosome roadblocks do. In addition, the same energy difference also determines when the RNA polymerase backtracks instead of continuing to move forward. This data-driven model corroborates—in a genome wide and quantitative manner—previous evidence that sequence-dependent thermodynamic features of nucleic acids influence both transcriptional pausing and backtracking.}, author = {Lukacisin, Martin and Landon, Matthieu and Jajoo, Rishi}, issn = {1932-6203}, journal = {PLoS One}, number = {3}, publisher = {Public Library of Science}, title = {{Sequence-specific thermodynamic properties of nucleic acids influence both transcriptional pausing and backtracking in yeast}}, doi = {10.1371/journal.pone.0174066}, volume = {12}, year = {2017}, } @article{682, abstract = {Left-right asymmetry is a fundamental feature of higher-order brain structure; however, the molecular basis of brain asymmetry remains unclear. We recently identified structural and functional asymmetries in mouse hippocampal circuitry that result from the asymmetrical distribution of two distinct populations of pyramidal cell synapses that differ in the density of the NMDA receptor subunit GluRε2 (also known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2 subunits, we previously found that β2-microglobulin-deficient mice, which lack cell surface expression of the vast majority of major histocompatibility complex class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study, we conducted electrophysiological and anatomical analyses on the hippocampal circuitry of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB knockout mice have identical phenotypes suggests that MHCI signals that produce hippocampal asymmetries are transduced through PirB. Our results provide evidence for a critical role of the MHCI/PirB signaling system in the generation of asymmetries in hippocampal circuitry.}, author = {Ukai, Hikari and Kawahara, Aiko and Hirayama, Keiko and Case, Matthew J and Aino, Shotaro and Miyabe, Masahiro and Wakita, Ken and Oogi, Ryohei and Kasayuki, Michiyo and Kawashima, Shihomi and Sugimoto, Shunichi and Chikamatsu, Kanako and Nitta, Noritaka and Koga, Tsuneyuki and Shigemoto, Ryuichi and Takai, Toshiyuki and Ito, Isao}, issn = {1932-6203}, journal = {PLoS One}, number = {6}, publisher = {Public Library of Science}, title = {{PirB regulates asymmetries in hippocampal circuitry}}, doi = {10.1371/journal.pone.0179377}, volume = {12}, year = {2017}, } @article{6142, abstract = {Defining the mutational landscape when individuals of a species grow separately and diverge over many generations can provide insights into trait evolution. A specific example of this involves studying changes associated with domestication where different lines of the same wild stock have been cultivated independently in different standard environments. Whole genome sequence comparison of such lines permits estimation of mutation rates, inference of genes' ancestral states and ancestry of existing strains, and correction of sequencing errors in genome databases. Here we study domestication of the C. elegans Bristol strain as a model, and report the genome sequence of LSJ1 (Bristol), a sibling of the standard C. elegans reference wild type N2 (Bristol). The LSJ1 and N2 lines were cultivated separately from shortly after the Bristol strain was isolated until methods to freeze C. elegans were developed. We find that during this time the two strains have accumulated 1208 genetic differences. We describe phenotypic variation between N2 and LSJ1 in the rate at which embryos develop, the rate of production of eggs, the maturity of eggs at laying, and feeding behavior, all the result of post-isolation changes. We infer the ancestral alleles in the original Bristol isolate and highlight 2038 likely sequencing errors in the original N2 reference genome sequence. Many of these changes modify genome annotation. Our study provides a starting point to further investigate genotype-phenotype association and offers insights into the process of selection as a result of laboratory domestication.}, author = {Weber, Katherine P. and De, Subhajyoti and Kozarewa, Iwanka and Turner, Daniel J. and Babu, M. Madan and de Bono, Mario}, issn = {1932-6203}, journal = {PLoS ONE}, number = {11}, publisher = {Public Library of Science}, title = {{Whole genome sequencing highlights genetic changes associated with laboratory domestication of C. elegans}}, doi = {10.1371/journal.pone.0013922}, volume = {5}, year = {2010}, } @article{11114, abstract = {We present a miniaturized pull-down method for the detection of protein-protein interactions using standard affinity chromatography reagents. Binding events between different proteins, which are color-coded with quantum dots (QDs), are visualized on single affinity chromatography beads by fluorescence microscopy. The use of QDs for single molecule detection allows the simultaneous analysis of multiple protein-protein binding events and reduces the amount of time and material needed to perform a pull-down experiment.}, author = {Schulte, Roberta and Talamas, Jessica and Doucet, Christine and HETZER, Martin W}, issn = {1932-6203}, journal = {PLoS ONE}, keywords = {Multidisciplinary}, number = {4}, publisher = {Public Library of Science}, title = {{Single bead affinity detection (SINBAD) for the analysis of protein-protein interactions}}, doi = {10.1371/journal.pone.0002061}, volume = {3}, year = {2008}, }