9 research outputs found

    <i>lin-28</i> mutants can be two stages precocious due to <i>let-7</i> activity.

    No full text
    1<p>All strains are homozygous for null alleles of the genes indicated and carry an integrated transgene of the seam cell marker <i>wIs78(scm::GFP; ajm-1::GFP)</i>. All alleles are null.</p>2<p>Percentage of seam cells synthesizing adult alae by early L3.</p>3<p>n = number of seam cells scored.</p

    Genetic interactions of heterochronic mutants.

    No full text
    1<p>All animals examined were homozygous for null alleles of the genes indicated and carry an integrated transgene <i>wIs78(scm::GFP; ajm-1::GFP)</i> to mark seam cells. All alleles are null.</p>2<p>Seam cell counts were performed on L4 animals except where indicated.</p>3<p>Alae formation was assessed in the early L4 stage.</p>4<p>Strains carrying the <i>let-7</i> mutation additionally contained a linked <i>unc-3</i> mutant allele. They were grown at 15°C to limit constitutive dauer formation that results from the <i>unc-3</i> mutation at higher temperatures in these backgrounds.</p>5<p>Seam cell fusion with no alae formation was observed in the other 85% of animals.</p><p>SEM, standard error of the mean; ND, not determined.</p

    The male tail tip morphogenesis is delayed in let-7 males.

    No full text
    <p>Nomarski images of wild type (A) and <i>let-7</i> null (B) L4 males approximately 8 hours after the L3 molt. The extracellular space between the L4 cuticle and the tail tip in the wildtype indicates the retraction of male tail tip <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002588#pgen.1002588-Nguyen1" target="_blank">[68]</a>. Arrow head, unretracted hypodermis in the <i>let-7</i> mutant.</p

    Catalyst Chemical State during CO Oxidation Reaction on Cu(111) Studied with Ambient-Pressure X‑ray Photoelectron Spectroscopy and Near Edge X‑ray Adsorption Fine Structure Spectroscopy

    No full text
    The chemical structure of a Cu(111) model catalyst during the CO oxidation reaction in the CO+O<sub>2</sub> pressure range of 10–300 mTorr at 298–413 K was studied <i>in situ</i> using surface sensitive X-ray photoelectron and adsorption spectroscopy techniques [X-ray photoelectron spectroscopy (XPS) and near edge X-ray adsorption fine structure spectroscopy (NEXAFS)]. For O<sub>2</sub>:CO partial pressure ratios below 1:3, the surface is covered by chemisorbed O and by a thin (∼1 nm) Cu<sub>2</sub>O layer, which covers completely the surface for ratios above 1:3 between 333 and 413 K. The Cu<sub>2</sub>O film increases in thickness and exceeds the escape depth (∼3–4 nm) of the XPS and NEXAFS photoelectrons used for analysis at 413 K. No CuO formation was detected under the reaction conditions used in this work. The main reaction intermediate was found to be CO<sub>2</sub><sup>δ−</sup>, with a coverage that correlates with the amount of Cu<sub>2</sub>O, suggesting that this phase is the most active for CO oxidation

    A model for the two sequential activities of LIN-28 in specifying cell fates.

    No full text
    <p>Top, Genetic formalisms depicting the two <i>lin-28</i> pathways that regulate the L2-to-L3 and the L3-to-L4 fate transitions. Bottom, A schematic time course depicting the regulatory dynamics during the first three larval stages. LIN-14, LIN-28, HBL-1 and LIN-41 are expressed at the start of larval development and are eventually repressed by the microRNAs lin-4, let-7 and the three let-7 family members miR-48, miR-84, and miR-241 (3 let-7s). The approximate times of LIN-14's two activities are indicated with boxed letters. The relevant times of LIN-28's two activities that correspond to the pathways above are depicted with black lines and circled letters.</p

    <i>lin-28</i> positively regulates <i>hbl-1</i> reporter expression.

    No full text
    <p>Nomarski and fluorescence micrographs of <i>hbl-1::GFP::hbl-1 3′UTR</i> reporter expression. Early stages are late L1 or early L2. Late stages are L4 or age-matched post-L3 molt <i>lin-28</i> animals. A, wild type. B, <i>mir-48 mir-241; mir-84 (3 let-7s)</i>. C, <i>lin-28; mir-48 mir-241; mir-84 (lin-28; 3 let-7s)</i>. D, a <i>hbl-1::GFP::unc-54 3′UTR</i> reporter in <i>lin-28; mir-48 mir-241; mir-84 (lin-28; 3 let-7s)</i>. Se, seam nuclei. hyp, hyp7 nuclei. All fluorescence images were captured with a 2 sec. exposure time. Scale bar, 10 microns.</p

    Relative contribution of <i>hbl-1</i> and <i>lin-41</i> for the <i>let-7</i> retarded phenotype.

    No full text
    1<p>The <i>let-7</i> mutants were identified by Unc phenotype due to the <i>unc-3</i> mutation.</p>2<p>The precocious alae were assessed at the end of L3–L4 molt or in the early L4 stage of development.</p>3<p>As previously noted, <i>hbl-1(RNAi)</i> causes a proliferation defect in the late L4 which is not interpreted as heterochronic <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002588#pgen.1002588-Lin2" target="_blank">[53]</a>. These divisions were not scored.</p><p>ND, not determined.</p

    Seam cell lineages of animals with altered <i>lin-28</i> activity.

    No full text
    <p>Lineage patterns characteristic of lateral hypodermal seam cells V1, V2, V3, V4 and V6. Left to right: Wild type <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002588#pgen.1002588-Sulston1" target="_blank">[56]</a>. Animals lacking <i>mir-48</i>, <i>mir-84</i>, and <i>mir-241</i> (<i>3 let-7s</i>), or animals carrying a transgene constitutively expressing <i>lin-28</i> (<i>lin-28(gf)</i>) <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002588#pgen.1002588-Moss3" target="_blank">[62]</a>. <i>let-7</i> null mutants, whose defect in these lineages is first visible in the late L4 stage. Two types of seam cell lineages observed in <i>lin-28</i> null mutants <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002588#pgen.1002588-Ambros1" target="_blank">[1]</a>. Seam cell lineages that skip L2 fates in <i>lin-28(low RNAi)</i> animals (see text). Three horizontal lines indicate the time of adult alae formation. Dashed lines indicate variable lineage patterns in <i>lin-28(gf)</i> animals.</p

    Ambient-Pressure Soft X‑ray Absorption Spectroscopy of a Catalyst Surface in Action: Closing the Pressure Gap in the Selective <i>n</i>‑Butane Oxidation over Vanadyl Pyrophosphate

    No full text
    In order to close the pressure gap in the investigation of catalyst surfaces under real operation conditions we have developed a variable-pressure soft X-ray (<i>h</i>ν ≤1.5 keV) absorption cell coupled to a gas analysis system to study the pressure dependency of the electronic and catalytic properties of catalyst surfaces in reactive atmospheres at elevated temperatures. With this setup we investigated the vanadium L<sub>3</sub>-edge and catalytic performance of polycrystalline vanadyl pyrophosphate in the selective oxidation of <i>n</i>-butane to maleic anhydride between 10 and 1000 mbar at 400 °C. As a result, major gas phase and pressure dependent spectral changes are observed at energies attributed to V 2p-3d<sub><i>z</i><sup>2</sup></sub> excitations assigned to vanadium atoms square-pyramidally coordinated to oxygen atoms. This can be interpreted in terms of a shortened vanadyl bond (VO) and an increased vanadium oxidation state with higher pressures. Since this is accompanied by an increasing catalytic activity and selectivity, it indicates that vanadyl oxygen is actively involved in the selective oxidation of the alkane
    corecore