8 research outputs found

    Biology, Injury, and Control of the European Needle-bending Midge (Diptera: Cecidomyiidae) on Scotch Pine in Michigan

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    Contarinia baeri is univoltine in Michigan. Adults emerge in spring, and females deposit eggs in small clusters in the sheaths of new-growth pine needles. Larvae hatch shortly thereafter and there are three larval instars. Larval feeding causes the needles to at first droop, discolor, and eventually drop, reducing the quality of Christmas trees and occasionally killing shoots. Larvae overwinter on the ground in cocoons, and pupate in spring. Adults were suppressed (\u3e 75% control) with formulations of Pydrin® (fenvalerate) and Tempo® (cyfluthrin) applied within a week after adult emergence

    A Split-Stem Lesion on Young Hybrid \u3ci\u3ePopulus\u3c/i\u3e Trees Caused by the Tarnished Plant Bug, \u3ci\u3eLygus Lineolaris\u3c/i\u3e (Hemiptera: [Heteroptera]: Miridae)

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    The tarnished plant bug, known principally as an agricultural pest, injures young hybrid Populus by feeding on the stems and meristems. Tarnished plant bug eggs, fungi associated with some lesions, and simple mechanical stimuli alone from feeding appeared not to cause lesion formation. Of 20 Populus hybrids tested in a clonal trial, four appeared to be consistently susceptible to lesion injury, with Populus nigra var. betulifolia x trichocarpa the most susceptible. Several clones showed high resistance in the trial but a few were susceptible in other plantings and in host preference tests when caged with tarnished plant bugs. Lesions diminished tenfold on Populus where horseweed, the insect\u27s principal wild host, grew along with susceptible poplars. The tarnished plant bug can be suppressed by ultra-low volume pesticides and cultural manipulation of understory vegetation

    PTBP1 promotes hematopoietic stem cell maintenance and red blood cell development by ensuring sufficient availability of ribosomal constituents.

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    Ribosomopathies constitute a range of disorders associated with defective protein synthesis mainly affecting hematopoietic stem cells (HSCs) and erythroid development. Here, we demonstrate that deletion of poly-pyrimidine-tract-binding protein 1 (PTBP1) in the hematopoietic compartment leads to the development of a ribosomopathy-like condition. Specifically, loss of PTBP1 is associated with decreases in HSC self-renewal, erythroid differentiation, and protein synthesis. Consistent with its function as a splicing regulator, PTBP1 deficiency results in splicing defects in hundreds of genes, and we demonstrate that the up-regulation of a specific isoform of CDC42 partly mimics the protein-synthesis defect associated with loss of PTBP1. Furthermore, PTBP1 deficiency is associated with a marked defect in ribosome biogenesis and a selective reduction in the translation of mRNAs encoding ribosomal proteins. Collectively, this work identifies PTBP1 as a key integrator of ribosomal functions and highlights the broad functional repertoire of RNA-binding proteins
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