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  • Oxford University Press (OUP)  (4)
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  • Oxford University Press (OUP)  (4)
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  • 1
    In: Journal of Economic Entomology, Oxford University Press (OUP), Vol. 114, No. 1 ( 2021-02-09), p. 112-121
    Kurzfassung: Successful application of the sterile insect technique (SIT), an environmentally friendly control technology, mainly depends on mass-rearing of high-quality and high-performance insects. For mass-rearing of insects, the development of artificial diets is a key component. For optimal insect growth and development, sugar is an essential nutrient as it provides energy for flight. To date, few studies have analyzed the effects of different sugar contents on the biological parameters, including the flight capacity of Grapholita molesta, a globally important economic pest. Artificial diets with different sucrose contents (0, 15, and 30 g) were evaluated in two consecutive generations. The insect flight mill was used to study the G. molesta flight capacity. The larval and pupal periods, adult longevity and pupal weight of the first-generation of G. molesta reared on artificial diets with different sucrose contents were significantly different. Insects of the second-generation had a shorter larval period, greater adult longevity, and heavier larvae and pupae in the treatment with 30 g of sucrose than using 15 g. Among the males, strong, medium, and weak flight capacities were recorded and the weakest one was observed in the diet without sucrose. Results showed that the proportion of insects with highest flight capacity increased with increasing sucrose content in insects of the second generation. It can be concluded that sucrose content is a key determinant in the biological traits, including flight capacity of G. molesta, and should be taken into consideration during the mass-rearing of the pest for SIT.
    Materialart: Online-Ressource
    ISSN: 0022-0493 , 1938-291X
    Sprache: Englisch
    Verlag: Oxford University Press (OUP)
    Publikationsdatum: 2021
    ZDB Id: 2477182-X
    ZDB Id: 2030999-5
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 42, No. 1 ( 2014-01-01), p. 458-474
    Materialart: Online-Ressource
    ISSN: 1362-4962 , 0305-1048
    RVK:
    Sprache: Englisch
    Verlag: Oxford University Press (OUP)
    Publikationsdatum: 2014
    ZDB Id: 1472175-2
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    In: Horticulture Research, Oxford University Press (OUP), Vol. 10, No. 4 ( 2023-04-04)
    Kurzfassung: Drought stress is the major abiotic factor that can seriously affect plant growth and crop production. The functions of flavin-containing monooxygenases (FMOs) are known in animals. They add molecular oxygen to lipophilic compounds or produce reactive oxygen species (ROS). However, little information on FMOs in plants is available. Here, we characterized a tomato drought-responsive gene that showed homology to FMO, and it was designated as FMO1. FMO1 was downregulated promptly by drought and ABA treatments. Transgenic functional analysis indicated that RNAi suppression of the expression of FMO1 (FMO1-Ri) improved drought tolerance relative to wild-type (WT) plants, whereas overexpression of FMO1 (FMO1-OE) reduced drought tolerance. The FMO1-Ri plants exhibited lower ABA accumulation, higher levels of antioxidant enzyme activities, and less ROS generation compared with the WT and FMO1-OE plants under drought stress. RNA-seq transcriptional analysis revealed the differential expression levels of many drought-responsive genes that were co-expressed with FMO1, including PP2Cs, PYLs, WRKY, and LEA. Using Y2H screening, we found that FMO1 physically interacted with catalase 2 (CAT2), which is an antioxidant enzyme and confers drought resistance. Our findings suggest that tomato FMO1 negatively regulates tomato drought tolerance in the ABA-dependent pathway and modulates ROS homeostasis by directly binding to SlCAT2.
    Materialart: Online-Ressource
    ISSN: 2052-7276
    Sprache: Englisch
    Verlag: Oxford University Press (OUP)
    Publikationsdatum: 2023
    ZDB Id: 2781828-7
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    Oxford University Press (OUP) ; 2021
    In:  Journal of Molecular Cell Biology Vol. 13, No. 2 ( 2021-05-07), p. 128-140
    In: Journal of Molecular Cell Biology, Oxford University Press (OUP), Vol. 13, No. 2 ( 2021-05-07), p. 128-140
    Kurzfassung: Testosterone deficiency is common in male patients with chronic obstructive pulmonary disease (COPD) and may correlate with the deterioration of COPD. Clinical research suggests that testosterone replacement therapy may slow the COPD progression, but the specific biological pathway remains unclear. In this study, we explored the effect of testosterone on pulmonary inflammation in male COPD rats. The animals were co-treated with lipopolysaccharide (LPS) and cigarette to induce COPD. In COPD rats, nuclear respiratory factor 1 (NRF1) and NF-κB p65 were upregulated. In cigarette smoke extract (CSE)-, LPS-, or the combination of CSE and LPS-treated L132 cells, NRF1 and p65 were also upregulated. Silencing NRF1 resulted in the downregulation of p65. ChIP‒seq, ChIP‒qPCR, and luciferase results showed that NRF1 transcriptionally regulated p65. Both male and female COPD rats showed an upregulated NRF1 level and similar pulmonary morphology. But NRF1 was further upregulated in male castrated rats. Further supplementing testosterone in castrated male rats significantly reduced NRF1, pulmonary lesions, and inflammation. Supplementation of testosterone also reduced the phosphorylation of p65 and IKKβ induced by LPS or CSE in L132 cells. Our results suggest that testosterone plays a protective role in pulmonary epithelial inflammation of COPD through inhibition of NRF1-derived NF-κB signaling and the phosphorylation of p65.
    Materialart: Online-Ressource
    ISSN: 1674-2788 , 1759-4685
    Sprache: Englisch
    Verlag: Oxford University Press (OUP)
    Publikationsdatum: 2021
    ZDB Id: 2500949-7
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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