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    Home > Biochemistry News > Biotechnology News > The CinB nuclease of wNo-Wolbachia is sufficient to induce cytoplasmic incompatibility in Drosophila

    The CinB nuclease of wNo-Wolbachia is sufficient to induce cytoplasmic incompatibility in Drosophila

    • Last Update: 2022-02-17
    • Source: Internet
    • Author: User
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    Summary

    Wolbachia

    is a specialized intracellular bacterium that can alter the reproduction of its arthropod host, usually through a mechanism called cytoplasmic incompatibility (CI)


    WolbachiaBacteria live inside the cells of many insects


    1) probably the world's most successful bacterial endosymbionts are obligate intracellular alpha-bacteriaPurple wolf poison,Infect~40% of terrestrial arthropod species (2).


    - Induced CI is used in a variety of ways to control mosquito-borne diseases, especially throughAedes aegyptiMosquitoes that transmit dengue virus and other arboviruses


    Wolbachiarelated factors (10–12) CI factor (cif) is encoded by two genetic operons, usually, but not always, found in the two prophage regions (13–15), upstream genes are usually designated ascifAdownstream genescifB(Figure 1A).


    figure 1

    figure 1
    thiswThere are no derived CinA and CinB proteins


    Canadian International Development Agency

    wPipAnd XenawPipBind homologous CiDBwPipAnd CinBwPipA protein with high affinity, but binding does not block the latter's enzymatic active site (10,12) However, co-expression of the cognate CifA protein from each operon in yeast suppressed the toxicity observed when CidB or CinB were expressed by themselves (10) These observations suggest that inhibition is due to CifA factors interfering with CifB enzyme-substrate interactions or enzyme relocalization within cells


    Drosophila melanogasterFor example, female germline expression of CidAwMelor XenawPipSufficient to rescue transgenic CI caused by homologous gene expressioncifA-cifBGenes in the male germline (12,19) In transgenic flies, the enzymatic activity of the CifB enzyme is required for complete CI, as is yeast toxicity (10,12,20) In addition, in Drosophila and yeast, the homologous nucleolarin-α protein inhibits CI and growth inhibition, respectively (18).


    12,14).


    Xena-Simbusystem fromwNoWolbachianatural infectionDrosophila(twenty one) we have previously shownwno infectionD.
    apeDemonstrated embryonic cytology defects in incompatible crosses, similar to those observed with incompatible transgenesD、crossCanadian International Development Agency-cidBorXena-SimbufromwPip (12) However, we have not tested whether GMOXena-SimbuwNoBehavior is similar
    .
    Here we find that this is indeed the case
    .
    Unexpectedly, the expression of the manSimbuwNoTransgenic flies alone are induced to produce strong CI, which is completely rescued by homologsXenawNoExpression in the female germline
    .
    The results show thatXena-SimbuwNoExpression in yeast further demonstrated that the nuclease active site must be intact for toxicity to be observed
    .
    These results suggest that catalytically active CifB is the basic inducer of CI and CifA is the specific rescuer
    .
    Our results also apply to the current model of the CI mechanism
    .
    In particular, they argue against the generality of the 2-1 model, as well as the model in which CifA plays a major role in CI induction
    .
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