4 research outputs found

    An Investigation of the Lethality of Picralima Nitida, Family Apocynaceae in Malaria Vector Control

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    Insecticides resistance and the corresponding health and environmental challenges that arises as a result of the use of synthetic chemical based insecticides prompts the search for better alternative control measures which are more effective, specific in action and less toxic. The 4th instar larvae of Anopheles spp, the vector of the deadly plasmodium were evaluated in this research against aqueous and methanolic leaf extracts of the plant Picralima nitida. Results revealed that aqueous leaf extract of the test plant had a mean mortality of 11 at 24hrs exposure and concentration of 5.0mg/ml. 95% mortality was also recorded at 5.0mg/ml after 48hrs exposure. Methanolic leaf extract had a mean mortality of 7.7 at 48hrs exposure time and same concentration of 5.0mg/ml. however, at 72hrs exposure, (concentration 5.0mg/ml), the mean mortality increased to 19.3 (97% mortality). The Median Lethal Time evaluated using probit analysis at 95% Confidence Limit showed the average lethal time of the test organism Anopheles larvae to the methanolic extract to be 55hrs and 29hrs for the aqueous leaf extract. This result hence supports the fact that leaf extracts of P. nitida can be used as a source of eco-friendly alternatives in the control of mosquito vectors, if developed. Keywords: Resistance, Insecticides, Anopheles spp, Eco-friendly, Larvicidin

    Caenorhabditis elegans NSE3 homolog (MAGE-1) is involved in genome stability and acts in inter-sister recombination during meiosis

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    Melanoma antigen (MAGE) genes encode for a family of proteins that share a common MAGE homology domain. These genes are conserved in eukaryotes and have been linked to a variety of cellular and developmental processes including ubiquitination and oncogenesis in cancer. Current knowledge on the MAGE family of proteins mainly comes from the analysis of yeast and human cell lines, and their functions have not been reported at an organismal level in animals. Caenorhabditis elegans only encodes 1 known MAGE gene member, mage-1 (NSE3 in yeast), forming part of the SMC-5/6 complex. Here, we characterize the role of mage-1/nse-3 in mitosis and meiosis in C. elegans. mage-1/nse-3 has a role in inter-sister recombination repair during meiotic recombination and for preserving chromosomal integrity upon treatment with a variety of DNA-damaging agents. MAGE-1 directly interacts with NSE-1 and NSE-4. In contrast to smc-5, smc-6, and nse-4 mutants which cause the loss of NSE-1 nuclear localization and strong cytoplasmic accumulation, mage-1/nse-3 mutants have a reduced level of NSE-1::GFP, remnant NSE-1::GFP being partially nuclear but largely cytoplasmic. Our data suggest that MAGE-1 is essential for NSE-1 stability and the proper functioning of the SMC-5/6 complex.11Nsciescopu

    Loss of NSE-4 Perturbs Genome Stability and DNA Repair in Caenorhabditis elegans

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    The Structural Maintenance of Chromosomes (SMC) complex plays an important role in maintaining chromosome integrity, in which the SMC5/6 complex occupies a central position by facilitating mitotic and meiotic processes as well as DNA repair. NSE-4 Kleisin is critical for both the organization and function of the SMC5/6 complex, bridging NSE1 and NSE3 (MAGE related) with the head domains of the SMC5 and SMC6 proteins. Despite the conservation in protein sequence, no functional relevance of the NSE-4 homologous protein (NSE-4) in Caenorhabditis elegans has been reported. Here, we demonstrated the essential role of C. elegans NSE-4 in genome maintenance and DNA repair. Our results showed that NSE-4 is essential for the maintenance of chromosomal structure and repair of a range of chemically induced DNA damage. Furthermore, NSE-4 is involved in inter-sister repair during meiosis. NSE-4 localizes on the chromosome and is indispensable for the localization of NSE-1. Collectively, our data from this study provide further insight into the evolutionary conservation and diversification of NSE-4 function in the SMC-5/6 complex
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