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    Biologist gather up I need help Pls

    I know that RSV has an v-src gene, which was acquired by its ancestor and subsequently incorporated into its RNA. It nicked the gene which is present in humans know as c-myc.

    C-src encodes for a tyrosine kinase which can interact with cell surface receptors such as EGF-R.


    So my question is: how does RSV having the v-src cause cancer in a host cell?

    Thanks

    2 Comments

    Rous Sarcoma Virus (RSV) contains the viral oncogene v-src. Being a retro virus it uses reverse trasbiption to convert its RNA to cDNA and then inserts into the human genome,however the RSV has acquired the oncogene src into its genome over time.

    A virus has two possible life cycles; lysogenic and lytic. Lysogenic is where the virus is effectly dormant within the cell, divding when the cell undergoes mitosis. The lytic cycle involves the high expression of the viral genes and subsequently the lysis of he cell due to the sheer amount of virus produced. The lysis phase is that associated with active infection.

    So RSV going through the lysis phase will be over expressing its genes including the v-src gene which has now inserted into the human genome. This tyrosine kinase is then able to interact with EGF-receptor prematurely activating it and starting the signal transduction cascade.

    Now if you imagine this happening in almost all cells infected by RSV, you will get uncontrolled growth and proliferation over time leading to sarcoma.

    Hope that helps. Am a bit rusty as exams were over a month ago.

    Original Poster

    Thanks rep+.

    So essentially the transduction of the v-src (oncogene) into the host cell means a higher expression rate of the gene. Therefore more src kinase proteins are floating around the cytoplasm. This then leads to more signaling down the MAPK kinase pathway.

    It makes sense now. My mind was thinking about both the c-src and the v-src but kind of missed out the transcription part. So I was stuck because I couldn't think of the connection between the gene and onset of cancer.

    I have one more question when the v src is inserted into the host DNA, is it under the influence of a different promoter to that of the c src?
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