66 research outputs found

    Scotch Pine Deterioration in Michigan Caused by Pine Root Weevil Complex

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    Pine root tip weevil, Hylobius rhizophagus, and pine root collar weevil, H. radicis, attack certain Scotch pine stands simultaneously causing more mortality than expected from either insect alone. Recommendations for curtailing this insect complex include favoring red pine, planting Scotch pine far from brood sources, and avoiding stump culture of Christmas trees

    Michigan\u27s Cooperative Forest Pest Management Program, A Team Approach to Improving Forest Management

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    A forest management team was organized in the late 1970\u27s by cooperative efforts of Michigan\u27s universities. the Michigan Department of Natural Resources, and the USDA Forest Service.The goals were to devise new technologies, transfer available technology, and service and management alternatives to forest land managers in Michigan. The program throughout has emphasized forest management rather than pest management for prevention and control of pests. Dissemination of pest management information has been of importance and new research results have gone directly to land managers for immediate use. The team participates in forest compartmental reviews and helps prescribe management plans for land parcels, thus providing for preventative pest management. Services and management recommendations are provided mostly through forest pest specialists located in the field. They feed back results and problems to researchers and extension specialists of the team for further input. Preventive management information used by by local managers in recent years has nearly paid the cost of the program. Plans are to broaden the team effort by cooperating with organizations and in adjacent states through a computer network system and by other means

    Simulation of How Jack Pine Budworm (Lepidoptera: Tortricidae) Affects Economic Returns From Jack Pine Timber Production in Michigan

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    The impact of jack pine budworm on economic returns from jack pine timber production in Lower Michigan and management actions that might be taken to reduce this impact were evaluated with a simulation model. Results indicate that current jack pine rotation ages arc excessive and should be reduced. Insecticide application is not a viable strategy for reducing jack pine budworm impact

    Life History and Some Habits of a Larch Moth, \u3ci\u3eParalobesia Palliolana\u3c/i\u3e (Lepidoptera: Tortricidae), in Michigan

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    (excerpt) Insect injured shoot tips were discovered in the fall of 1971 on larch (Larix spp.) in a mixed larch provenance plating in Shiawassee County, Michigan. Tortricid larvae collected later from them were reared to maturity and identified as Paralobesia palliolana (McDunnough 1938). McDunnough (1938) described this species as Polychrosis palliolana from insects taken in flight but without definitely associated hosts. The holotype he designated was collected at Milford, Nova Scotia; other specimens he examined were from Quebec and Ottawa, Canada

    Life History and Some Habits of a Larch Moth, \u3ci\u3eParalobesia Palliolana\u3c/i\u3e (Lepidoptera: Tortricidae), in Michigan

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    (excerpt) Insect injured shoot tips were discovered in the fall of 1971 on larch (Larix spp.) in a mixed larch provenance plating in Shiawassee County, Michigan. Tortricid larvae collected later from them were reared to maturity and identified as Paralobesia palliolana (McDunnough 1938). McDunnough (1938) described this species as Polychrosis palliolana from insects taken in flight but without definitely associated hosts. The holotype he designated was collected at Milford, Nova Scotia; other specimens he examined were from Quebec and Ottawa, Canada

    A Plant-Specific Transcription Factor IIB-Related Protein, pBRP2, Is Involved in Endosperm Growth Control

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    General transcription factor IIB (TFIIB) and TFIIB-related factor (BRF), are conserved RNA polymerase II/III (RNAPII/III) selectivity factors that are involved in polymerase recruitment and transcription initiation in eukaryotes. Recent findings have shown that plants have evolved a third type of B-factor, plant-specific TFIIB-related protein 1 (pBRP1), which seems to be involved in RNAPI transcription. Here, we extend the repertoire of B-factors in plants by reporting the characterization of a novel TFIIB-related protein, plant-specific TFIIB-related protein 2 (pBRP2), which is found to date only in the Brassicacea family. Unlike other B-factors that are ubiquitously expressed, PBRP2 expression is restricted to reproductive organs and seeds as shown by RT-PCR, immunofluorescence labelling and GUS staining experiments. Interestingly, pbrp2 loss-of-function specifically affects the development of the syncytial endosperm, with both parental contributions required for wild-type development. pBRP2, is the first B-factor to exhibit cell-specific expression and regulation in eukaryotes, and might play a role in enforcing bi-parental reproduction in angiosperms

    Autoimmunity in Arabidopsis acd11 Is Mediated by Epigenetic Regulation of an Immune Receptor

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    Certain pathogens deliver effectors into plant cells to modify host protein targets and thereby suppress immunity. These target modifications can be detected by intracellular immune receptors, or Resistance (R) proteins, that trigger strong immune responses including localized host cell death. The accelerated cell death 11 (acd11) “lesion mimic” mutant of Arabidopsis thaliana exhibits autoimmune phenotypes such as constitutive defense responses and cell death without pathogen perception. ACD11 encodes a putative sphingosine transfer protein, but its precise role during these processes is unknown. In a screen for lazarus (laz) mutants that suppress acd11 death we identified two genes, LAZ2 and LAZ5. LAZ2 encodes the histone lysine methyltransferase SDG8, previously shown to epigenetically regulate flowering time via modification of histone 3 (H3). LAZ5 encodes an RPS4-like R-protein, defined by several dominant negative alleles. Microarray and chromatin immunoprecipitation analyses showed that LAZ2/SDG8 is required for LAZ5 expression and H3 lysine 36 trimethylation at LAZ5 chromatin to maintain a transcriptionally active state. We hypothesize that LAZ5 triggers cell death in the absence of ACD11, and that cell death in other lesion mimic mutants may also be caused by inappropriate activation of R genes. Moreover, SDG8 is required for basal and R protein-mediated pathogen resistance in Arabidopsis, revealing the importance of chromatin remodeling as a key process in plant innate immunity

    Delineating the molecular and phenotypic spectrum of the SETD1B-related syndrome

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    Purpose: Pathogenic variants in SETD1B have been associated with a syndromic neurodevelopmental disorder including intellectual disability, language delay, and seizures. To date, clinical features have been described for 11 patients with (likely) pathogenic SETD1B sequence variants. This study aims to further delineate the spectrum of the SETD1B-related syndrome based on characterizing an expanded patient cohort. Methods: We perform an in-depth clinical characterization of a cohort of 36 unpublished individuals with SETD1B sequence variants, describing their molecular and phenotypic spectrum. Selected variants were functionally tested using in vitro and genome-wide methylation assays. Results: Our data present evidence for a loss-of-function mechanism of SETD1B variants, resulting in a core clinical phenotype of global developmental delay, language delay including regression, intellectual disability, autism and other behavioral issues, and variable epilepsy phenotypes. Developmental delay appeared to precede seizure onset, suggesting SETD1B dysfunction impacts physiological neurodevelopment even in the absence of epileptic activity. Males are significantly overrepresented and more severely affected, and we speculate that sex-linked traits could affect susceptibility to penetrance and the clinical spectrum of SETD1B variants. Conclusion: Insights from this extensive cohort will facilitate the counseling regarding the molecular and phenotypic landscape of newly diagnosed patients with the SETD1B-related syndrome
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