21 research outputs found

    Microscopic Mechanism and Kinetics of Ice Formation at Complex Interfaces: Zooming in on Kaolinite

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    Most ice in nature forms thanks to impurities which boost the exceedingly low nucleation rate of pure supercooled water. However, the microscopic details of ice nucleation on these substances remain largely unknown. Here, we have unraveled the molecular mechanism and the kinetics of ice formation on kaolinite, a clay mineral playing a key role in climate science. We find that the formation of ice at strong supercooling in the presence of this clay is twenty orders of magnitude faster than homogeneous freezing. The critical nucleus is substantially smaller than that found for homogeneous nucleation and, in contrast to the predictions of classical nucleation theory (CNT), it has a strong 2D character. Nonetheless, we show that CNT describes correctly the formation of ice at this complex interface. Kaolinite also promotes the exclusive nucleation of hexagonal ice, as opposed to homogeneous freezing where a mixture of cubic and hexagonal polytypes is observed

    Combining high-resolution scanning tunnelling microscopy and first-principles simulations to identify halogen bonding

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    Scanning tunnelling microscopy (STM) is commonly used to identify on-surface molecular self-assembled structures. However, its limited ability to reveal only the overall shape of molecules and their relative positions is not always enough to fully solve a supramolecular structure. Here, we analyse the assembly of a brominated polycyclic aromatic molecule on Au(111) and demonstrate that standard STM measurements cannot conclusively establish the nature of the intermolecular interactions. By performing high-resolution STM with a CO-functionalised tip, we clearly identify the location of rings and halogen atoms, determining that halogen bonding governs the assemblies. This is supported by density functional theory calculations that predict a stronger interaction energy for halogen rather than hydrogen bonding and by an electron density topology analysis that identifies characteristic features of halogen bonding. A similar approach should be able to solve many complex 2D supramolecular structures, and we predict its increasing use in molecular nanoscience at surfaces

    Impaired phloem loading in zmsweet13a,b,c sucrose transporter triple knock-out mutants in Zea mays

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    Crop yield is critical for human nutrition, yet the underlying machinery that ultimately determines yield potential is still not understood. Crop productivity under ideal conditions is determined by the efficiency with which plants intercept light, convert it into chemical energy, translocate photosynthates and convert these to storage products in harvestable organs (Zhu et al., 2010). In many crops, sucrose is the primary form for translocation inside the conduit (i.e. the phloem). A combination of SWEETmediated efflux from phloem parenchyma and subsequent secondary active sucrose import by SUT sucrose/H+ symporters is thought to create the driving force for pressure gradient-driven phloem transport and retrieval of sucrose leaking along the translocation path (Chen et al., 2015a)

    Lateral organ boundaries 1 is a disease susceptibility gene for citrus bacterial canker disease

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    Citation: Hu, Y., Zhang, J., Jia, H., Sosso, D., Li, T., Frommer, W. B., 
 Jones, J. B. (2014). Lateral organ boundaries 1 is a disease susceptibility gene for citrus bacterial canker disease. Retrieved from http://krex.ksu.eduCitrus bacterial canker (CBC) disease occurs worldwide and incurs considerable costs both from control measures and yield losses. Bacteria that cause CBC require one of six known type III transcription activator-like (TAL) effector genes for the characteristic pustule formation at the site of infection. Here, we show that Xanthomonas citri subspecies citri strain Xcc306, with the type III TAL effector gene pthA4 or with the distinct yet biologically equivalent gene pthAw from strain XccA[superscript w], induces two host genes, CsLOB1 and CsSWEET1, in a TAL effector-dependent manner. CsLOB1 is a member of the Lateral Organ Boundaries (LOB) gene family of transcription factors, and CsSWEET1 is a homolog of the SWEET sugar transporter and rice disease susceptibility gene. Both TAL effectors drive expression of CsLOB1 and CsSWEET1 promoter reporter gene fusions when coexpressed in citrus or Nicotiana benthamiana. Artificially designed TAL effectors directed to sequences in the CsLOB1 promoter region, but not the CsSWEET1 promoter, promoted pustule formation and higher bacterial leaf populations. Three additional distinct TAL effector genes, pthA*, pthB, and pthC, also direct pustule formation and expression of CsLOB1. Unlike pthA4 and pthAw, pthB and pthC do not promote the expression of CsSWEET1. CsLOB1 expression was associated with the expression of genes associated with cell expansion. The results indicate that CBC-inciting species of Xanthomonas exploit a single host disease susceptibility gene by altering the expression of an otherwise developmentally regulated gene using any one of a diverse set of TAL effector genes in the pathogen populations

    Étude fonctionnelle de deux gĂšnes PPR dans le dĂ©veloppement du grain chez le maĂŻs (Zea Mays)

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    Les graines de cĂ©rĂ©ales reprĂ©sentent une ressource majeure pour l agroalimentaire, l industrie chimique et la production alternative d Ă©nergie. Parmi les cĂ©rĂ©ales, le maĂŻs prĂ©sente le rendement le plus Ă©levĂ© mais face Ă  une demande toujours plus forte, la comprĂ©hension des mĂ©canismes molĂ©culaires du dĂ©veloppement du grain apparaĂźt donc comme un enjeu Ă©conomique primordial. Nous prĂ©sentons dans ce manuscrit la caractĂ©risation phĂ©notypique et molĂ©culaire de deux mutants du grain de maĂŻs : le mutant PPR8522 (embryon anormal, mutation lĂ©tale) et le mutant PPR2263 (grain miniature). Les 2 gĂšnes mutĂ©s ont Ă©tĂ© identifiĂ©s et codent pour des protĂ©ines Ă  motifs PPR (Pentatricopeptide Repeat). Ces derniĂšres sont connues pour ĂȘtre impliquĂ©es dans la maturation des ARN organellaires. Le gĂšne PPR8522 a Ă©tĂ© identifiĂ© par la technique de transposon tagging et confirmĂ© par cartographie fine. La protĂ©ine PPR8522 est adressĂ©e aux plastes et apparaĂźt nĂ©cessaire pour la transcription d une majoritĂ© de gĂšnes chloroplastiques. Des plantules mutantes (obtenues par sauvetage d embryon ) prĂ©sentent un phĂ©notype albinos liĂ© Ă  l absence de chloroplastes fonctionnels. La mutation PPR2263 responsable du phĂ©notype grain miniature a Ă©tĂ© aussi identifiĂ©e par transposon tagging et confirmĂ© par complĂ©mentation via transgenese du mutant. La protĂ©ine PPR2263 prĂ©sente un adressage mitochondrial et un domaine DYW, suggĂ©rant un rĂŽle dans l Ă©dition des ARN. Les plantes mutantes se caractĂ©risent par une croissance ralentie et une taille rĂ©duite.The maize kernel is at the heart of research efforts geared to elucidate the molecular mechanisms governing its development and the accumulation of oil and starch in its two major compartments, embryo and endosperm. Here, we present the molecular and phenotypic characterisation of two maize kernel mutants, the embryo-specific PPR8522 and the miniature PPR2263 mutant. Despite dissimilar phenotypes both mutations concerned genes coding for pentatricopeptide repeat (PPR) proteins predicted to act in organellar RNA processing. The gene responsible for the embryo-lethal phenotype of PPR8522 was identified by transposon tagging and confirmed by fine mapping. PPR8522 contains 10 PPR motifs, is targeted to plastids and required for the transcription of nearly all plastid-encoded genes. Mutant embryos deviate as early as the 3-cell stage from normal development but can be rescued in vitro in certain genetic backgrounds. Rescued mutant plantlets have an albino lethal phenotype due to a substantial cellular desorganisation of their plastids including a total lack of thylakoid stacks. The mutation responsible for the miniature kernel phenotype of PPR2263 was identified by a novel cDNA transposon display technique. The cloning was confirmed by transgenic complementation via Agrobacterium-mediated maize transformation. PPR2263 contains 10 PPR motifs, a mitochondrial-targeting sequence and a DYW domain, suggesting a role in organellar RNA editing. Mutant plants hardly ever reach sexual maturity and are characterised by slow growth.LYON-ENS Sciences (693872304) / SudocSudocFranceItalyFRI

    PPR2263, a DYW-Subgroup Pentatricopeptide Repeat Protein, Is Required for Mitochondrial nad5 and cob Transcript Editing, Mitochondrion Biogenesis, and Maize Growth

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    International audienceRNA editing plays an important role in organelle gene expression in various organisms, including flowering plants, changing the nucleotide information at precise sites. Here, we present evidence that the maize (Zea mays) nuclear gene Pentatricopeptide repeat 2263 (PPR2263) encoding a DYW domain-containing PPR protein is required for RNA editing in the mitochondrial NADH dehydrogenase5 (nad5) and cytochrome b (cob) transcripts at the nad5-1550 and cob-908 sites, respectively. Its putative ortholog, MITOCHONDRIAL EDITING FACTOR29, fulfills the same role in Arabidopsis thaliana. Both the maize and the Arabidopsis proteins show preferential localization to mitochondria but are also detected in chloroplasts. In maize, the corresponding ppr2263 mutation causes growth defects in kernels and seedlings. Embryo and endosperm growth are reduced, leading to the production of small but viable kernels. Mutant plants have narrower and shorter leaves, exhibit a strong delay in flowering time, and generally do not reach sexual maturity. Whereas mutant chloroplasts do not have major defects, mutant mitochondria lack complex III and are characterized by a compromised ultrastructure, increased transcript levels, and the induction of alternative oxidase. The results suggest that mitochondrial RNA editing at the cob-908 site is necessary for mitochondrion biogenesis, cell division, and plant growth in maize

    Combining high-resolution scanning tunnelling microscopy and first-principles simulations to identify halogen bonding

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    Scanning tunnelling microscopy (STM) is commonly used to identify on-surface molecular self-assembled structures. However, its limited ability to reveal only the overall shape of molecules and their relative positions is not always enough to fully solve a supramolecular structure. Here, we analyse the assembly of a brominated polycyclic aromatic molecule on Au(111) and demonstrate that standard STM measurements cannot conclusively establish the nature of the intermolecular interactions. By performing high-resolution STM with a CO-functionalised tip, we clearly identify the location of rings and halogen atoms, determining that halogen bonding governs the assemblies. This is supported by density functional theory calculations that predict a stronger interaction energy for halogen rather than hydrogen bonding and by an electron density topology analysis that identifies characteristic features of halogen bonding. A similar approach should be able to solve many complex 2D supramolecular structures, and we predict its increasing use in molecular nanoscience at surfaces

    Sugar Partitioning between Ustilago maydis and Its Host Zea mays L during Infection

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    The basidiomycete Ustilago maydis causes smut disease in maize (Zea mays) by infecting all plant aerial tissues. The infection causes leaf chlorosis and stimulates the plant to produce nutrient-rich niches (i.e. tumors), where the fungus can proliferate and complete its life cycle. Previous studies have recorded high accumulation of soluble sugars and starch within these tumors. Using interdisciplinary approaches, we found that the sugar accumulation within tumors coincided with the differential expression of plant sugars will eventually be exported transporters and the proton/sucrose symporter Sucrose Transporter1. To accumulate plant sugars, the fungus deploys its own set of sugar transporters, generating a sugar gradient within the fungal cytosol, recorded by expressing a cytosolic glucose (Glc) Forster resonance energy transfer sensor. Our measurements indicated likely elevated Glc levels in hyphal tips during infection. Growing infected plants under dark conditions led to decreased plant sugar levels and loss of the fungal tip Glc gradient, supporting a tight link between fungal sugar acquisition and host supplies. Finally, the fungal infection causes a strong imbalance in plant sugar distribution, ultimately impacting seed set and yield

    PPR8522 encodes a chloroplast-targeted pentatricopeptide repeat protein necessary for maize embryogenesis and vegetative development

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    International audienceThe pentatricopeptide repeat (PPR) domain is an RNA binding domain allowing members of the PPR superfamily to participate in post-transcriptional processing of organellar RNA. Loss of PPR8522 from maize (Zea mays) confers an embryo-specific (emb) phenotype. The emb8522 mutation was isolated in an active Mutator (Mu) population and co-segregation analysis revealed that it was tightly linked to a MuDR insertion in the first exon of PPR8522. Independent evidence that disruption of PPR8522 caused the emb phenotype was provided by fine mapping to a region of 116kb containing no other gene than PPR8522 and complementation of the emb8522 mutant by a PPR8522 cDNA. The deduced PPR8522 amino acid sequence of 832 amino acids contains 10 PPR repeats and a chloroplast target peptide, the function of which was experimentally demonstrated by transient expression in Nicotiana benthamiana. Whereas mutant endosperm is apparently normal, mutant embryos deviate from normal development as early as 3 days after pollination, are reduced in size, exhibit more or less severe morphological aberrations depending on the genetic background, and generally do not germinate. The emb8522 mutation is the first to associate the loss of a PPR gene with an embryo-lethal phenotype in maize. Analyses of mutant plantlets generated by embryo-rescue experiments indicate that emb8522 also affects vegetative plant growth and chloroplast development. The loss of chloroplast transcription dependent on plastid-encoded RNA polymerase is the likely cause for the lack of an organized thylakoid network and an albino, seedling-lethal phenotype
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