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AQA BIOL5 Biology Unit 5 Exam - 22nd June 2011 watch

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    (Original post by N0547)
    Could someone explain the oestrus cycle in a way we could get asked in an exam question?
    Most oestrus cycle questions will come with the graph and will tell you that it is a mammal.
    Learn the steps:
    1. Pituitary gland secretes FSH this stimulates follicles in the ovary to grow and mature.
    2.The follicles secrete oestrogen which builds up the uterus lining and also inhibits FSH and LH. (=Negative Feedback)
    3.Oestrogen levels reach critical point whereby it stimulates a release of FSH and LH causing ovulation. (=Positive Feedback)
    4. LH stimulates the empty follicle to devolp into the corpus luteum, which secretes progesterone, this maintains the uterus lining and inhibits FSH and LH.
    5.Corpus leteum degenerates if it is not fertilised.
    6.No progesterone, so uterus lining breaks down. (=Menstruation)
    7.FSH levels increase...cycle repeats.

    A good question to know the answer to is-How does the pill work?-this will strengthen your understanding of the cycle.

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    (Original post by angel1992)
    basically am stuck on genetics part. If a gene codes for a specific polypeptide chain how can you have different alleles which are the same gene because different alelles have different polypeptide chains( they usually have one amino acid thats different) and that would therefore make them different genes

    Is it that the differences are so small, i.e. one amino acid difference still makes it the same polypeptide chain?

    very confused
    any ideas or explanation would be helpful?
    Gene: length of DNA on a chromosome normally coding for a particular polypeptide
    Allele: one form of a gene. For example,the gene for the shape of pea seeds has two alleles; round and wrinkled

    Essential thing to understand is that genes come in multiple forms, so two different polypeptide sequences will still be the same gene because they code for the same thing.ie. eye colour.
    Thats how I understand it as being.
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    Has everyone started revision for the synoptic? I'm worried because I haven't done anything, don't know how long it will take to get all of that into my head :sigh:

    Chapter 16 is driving me crazy :rant:
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    (Original post by xelaman)
    Gene: length of DNA on a chromosome normally coding for a particular polypeptide
    Allele: one form of a gene. For example,the gene for the shape of pea seeds has two alleles; round and wrinkled

    Essential thing to understand is that genes come in multiple forms, so two different polypeptide sequences will still be the same gene because they code for the same thing.ie. eye colour.
    Thats how I understand it as being.
    yh i get what you mean so therefore the defintion of an allele is based on characteristics rather then focused on the sequence it self.
    hence a gene can code for a number of polypeptide sequences yet the sequences code for the same type of thing so in relative terms they are classed as the same polypeptide(although in essence they are slightly different)
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    (Original post by angel1992)
    yh i get what you mean so therefore the defintion of an allele is based on characteristics rather then focused on the sequence it self.
    hence a gene can code for a number of polypeptide sequences yet the sequences code for the same type of thing so in relative terms they are classed as the same polypeptide(although in essence they are slightly different)
    also another reason why allele is based on charateristics is because if two polypeptide sequences didnt code for the same type of trait then they wouldnt be alleles and so would be different genes
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    Does anyone know the name of the site where Oestrogen combines on the receptor molecule of the transcriptional factor to release the inhibitor molecule?
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    Top tip - what I do for every unit - Print off the Specification and make notes on each topic as you come to each title. Usually leaves me with about 15 pages of all I need to know and in a sensible order, whereas my teacher tends to teach us from all over the syllabus and not chronologically.
    So I'm feeling good about the unit 5 stuff but bricking the synoptic essay. Currently trying to write one for "The causes of disease in Humans", got a few headings to start writing but I'm struggling to actually write it. Not looking forward to this part of the exam.
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    On the june 2010 paper, question 6cii)

    Some of the children in the trial developed cancer. How might the insertion of the DNA
    have caused cancer?

    the mark scheme says:

    Affects tumour suppressor gene;
    Inactivates (tumour suppressor) gene;
    Rate of cell division increased/tumour cells continue to divide;

    Ignore answers relating to oncogenes


    Why ignore answers relating to oncogenes, is it really obvious and i cant see it, its doing my head in!!

    Any help thanks??
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    (Original post by cws121)
    On the june 2010 paper, question 6cii)

    Some of the children in the trial developed cancer. How might the insertion of the DNA
    have caused cancer?

    the mark scheme says:

    Affects tumour suppressor gene;
    Inactivates (tumour suppressor) gene;
    Rate of cell division increased/tumour cells continue to divide;

    Ignore answers relating to oncogenes


    Why ignore answers relating to oncogenes, is it really obvious and i cant see it, its doing my head in!!

    Any help thanks??
    What is the DNA/gene? Really need the rest of the question to help.
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    (Original post by jayt)
    Top tip - what I do for every unit - Print off the Specification and make notes on each topic as you come to each title. Usually leaves me with about 15 pages of all I need to know and in a sensible order, whereas my teacher tends to teach us from all over the syllabus and not chronologically.
    So I'm feeling good about the unit 5 stuff but bricking the synoptic essay. Currently trying to write one for "The causes of disease in Humans", got a few headings to start writing but I'm struggling to actually write it. Not looking forward to this part of the exam.
    Thank you i think im gonna try this!
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    hey i have a question about chapter 16 which is one long chapter
    anyway, dna that is produced by reverse transcriptase, how is this dna that isolated inserted into a vector. I know the dna isolated by restiction endonucleases can inserted into a vector because its done using the same restriction endonucleases from which it was produced. However dna isolated by reverse transcriptase wasnt isolated in this way so how is it inserted into a vector if insertion involves restriction endonucleases?? :s
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    (Original post by cws121)
    On the june 2010 paper, question 6cii)

    Some of the children in the trial developed cancer. How might the insertion of the DNA
    have caused cancer?

    the mark scheme says:

    Affects tumour suppressor gene;
    Inactivates (tumour suppressor) gene;
    Rate of cell division increased/tumour cells continue to divide;

    Ignore answers relating to oncogenes


    Why ignore answers relating to oncogenes, is it really obvious and i cant see it, its doing my head in!!

    Any help thanks??
    I was going to ask the exact same question! because they can both mutate, resulting in uncontrollable cell division (cancer)... ? hmmm
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    (Original post by tehsponge)
    What is the DNA/gene? Really need the rest of the question to help.
    SCID is a severe inherited disease. People who are affected have no immunity.
    Doctors carried out a trial using gene therapy to treat children with SCID.
    The doctors who carried out the trial obtained stem cells from each child’s umbilical
    cord.

    The doctors mixed the stem cells with viruses. The viruses had been genetically
    modified to contain alleles of a gene producing full immunity. The doctors then injected this mixture into the child’s bone marrow.
    The viruses that the doctors used had RNA as their genetic material. When these
    viruses infect cells, they pass their RNA and two viral enzymes into the host cells.

    The other viral enzyme is called integrase. Integrase inserts the DNA copy anywhere in the DNA of the host cell. It may even insert the DNA copy in one of the host cell’s genes.

    This is basically the stem of the question, and i can see any hints why it would be tumour suppresor genes rather than ocagenes.
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    (Original post by cws121)
    On the june 2010 paper, question 6cii)

    Some of the children in the trial developed cancer. How might the insertion of the DNA
    have caused cancer?

    the mark scheme says:

    Affects tumour suppressor gene;
    Inactivates (tumour suppressor) gene;
    Rate of cell division increased/tumour cells continue to divide;

    Ignore answers relating to oncogenes


    Why ignore answers relating to oncogenes, is it really obvious and i cant see it, its doing my head in!!

    Any help thanks??
    Oncogenes (or proto-oncogenes) make tumour cells grow. Tumour suppressor genes inhibit tumour growth.

    If you stop tumour supressor genes working e.g. by putting another gene in there, there's nothing to stop cell growth, so you get uncontrollable growth i.e. cancer.

    If you stop oncogenes working, then there's nothing driving the cell growth... So you don't get uncontrollable cell growth... So there is no cancer.

    Hope this helped
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    unit 5 topic 10 notes, hope you'll find useful ..

    http://www.thestudentroom.co.uk/show...IOL5%29&page=6
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    browsing through last yrs thread posts 109 found unit 5 topic 10 notes, hope you'll find usefull ..

    http://www.thestudentroom.co.uk/show...IOL5%29&page=6
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    unit 5 topic 10 notes, hope you'll find useful ..

    http://www.thestudentroom.co.uk/show...IOL5%29&page=6
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    (Original post by student777)
    Oncogenes (or proto-oncogenes) make tumour cells grow. Tumour suppressor genes inhibit tumour growth.

    If you stop tumour supressor genes working e.g. by putting another gene in there, there's nothing to stop cell growth, so you get uncontrollable growth i.e. cancer.

    If you stop oncogenes working, then there's nothing driving the cell growth... So you don't get uncontrollable cell growth... So there is no cancer.

    Hope this helped
    No...proto-oncogenes mutate into oncogenes which speed up cell division. The question doesn't say anything about stopping oncogenes working
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    hey i have a question about chapter 16 which is one long chapter
    anyway, dna that is produced by reverse transcriptase, how is this dna that isolated inserted into a vector. I know the dna isolated by restiction endonucleases can inserted into a vector because its done using the same restriction endonucleases from which it was produced. However dna isolated by reverse transcriptase wasnt isolated in this way so how is it inserted into a vector if insertion involves restriction endonucleases?? :s
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    (Original post by cws121)
    SCID is a severe inherited disease. People who are affected have no immunity.
    Doctors carried out a trial using gene therapy to treat children with SCID.
    The doctors who carried out the trial obtained stem cells from each child’s umbilical
    cord.

    The doctors mixed the stem cells with viruses. The viruses had been genetically
    modified to contain alleles of a gene producing full immunity. The doctors then injected this mixture into the child’s bone marrow.
    The viruses that the doctors used had RNA as their genetic material. When these
    viruses infect cells, they pass their RNA and two viral enzymes into the host cells.

    The other viral enzyme is called integrase. Integrase inserts the DNA copy anywhere in the DNA of the host cell. It may even insert the DNA copy in one of the host cell’s genes.

    This is basically the stem of the question, and i can see any hints why it would be tumour suppresor genes rather than ocagenes.
    Yeah...I would have mentioned them both, as they both could be the cause of the cancer... Maybe check the examiners report?
 
 
 
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