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    Anyone fancy explaining why some of the bread wheat is sterile as it is going through production?
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    (Original post by skatealexia)
    Anyone fancy explaining why some of the bread wheat is sterile as it is going through production?
    the bread wheat is sterile because it does not have an even chromosome number (e.g. 21) or has different chromosomes (e.g. AB)
    this means meiosis cannot take place as the pairing of homogolous chromosomes (formation of bivalents) cannot take place - hence no production or seeds (gametes)

    hope this helps

    mutations double chromosome number to make the bread wheat fertile again
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    (Original post by InvoluntarySlacker)
    I do this with all my bio exams. :facepalm: And I choose to do it with the hardest module. :o:

    Hopefully I have retained most of what I already learnt. I curse the world cup.
    Lol, me too, I'm always like yes I'll definately do biology tonight, but then you don't, and then a few weeks later you realise that your biology exam is 4 days away...story of my life. :p: But just stick with it I guess.

    Yes, truly damn the world cup, I promised myself I wouldn't watch it, but oh no, Steven Gerrard just had to score 4 minutes into the game causing my whole family to scream, obviously I had no choice but to join them. ahaha
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    (Original post by skatealexia)
    Anyone fancy explaining why some of the bread wheat is sterile as it is going through production?
    Because it cannot form any homologous pairs during meiosis. If its AuB, then it cannot form homologous pairs as its only got one copy. But once it doubles due to a mutation, it becomes AuAuBB so can form homologous pairs during meiosis. So it forms a sterile hybrid along the way. The chracterisitc that allows them this is polyploidy, which means that it can contain more than one set of diploid chromosomes in its nucleus.

    Also damn the world cup, im so desperate to watch it yet, ive watched most of the games since the start (half's generally), first exam tomorrow and i just cant revise anymore for it. Plus 3 hours before when i can revise for it.

    Need to go over biology tomorrow evening and tuesday, try and cover all of this unit twice more by memory and then ill be more or less done, just read up on synoptics and hope for the best lol.
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    (Original post by Archen)
    Hey Talon :P
    i'll see you on Wednesday before bio
    we can panic together.
    have fun guessing who i am now :P
    I think I know!
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    Hmmm...there was a genetic question that I came across. Was about yellow, green and yellow-green plants being grown in the light. And the yellow ones died, green ones grew v. tall and the yellow-green ones grew reasonably. It says to explain this.


    I thought it would be due to the yellow plants having the incorrect photosynthetic pigments or accessory pigments for the bright light source, so most of the wavelengths of light are reflected, and they are unable to photosynthesise due to inability to capture light energy, and went on with that argument. Would that get marks also?

    In contrast to the markscheme answer, which just says that the green plants have more cholorophyl, and therefore can photosnthesise, yellow ones have no chlorophyl...?
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    hey Ive just realised there is a good chance of having a big old question on insulin as there's so much on it!!
    so theres the beta cells in the islets of langerhans in the pancreas that produce insulin to lower blood glucose conc. insulin increases liver + muscle cells permeability to glucose, activates glycogenesis and increases rate of respiration to do this.
    how insulin is secreted: high blood glucose conc = more glucose into Beta cell by facilitated diffusion. More glucose is respired so more ATP is produced. the rise in ATP causes K+ ion channels to close, so pot. ions build up inside the Beta cell, making it more +vely charged inside causing depolarisation. depolarisation causes ca2+ channels to open, and ca2+ enters the beta cell causing the vesicles to fuse with the membrane and secrete insulin into the blood by exocytosis

    thennnnn... theres type 1 and type 2 diabetes: type 1: B cells dont produce any insulin. hyperglycaemia = v high blood glucose conc after meals as theres no insulin to lower the conc. hypo = too much insulin injection causes dangerous drop in glucose levels.
    ....then insulin can be produced by GM bacteria: mRNA taken from pancreatic cells, and combine with reverse transcriptase to make cDNA for the insulin gene. the cDNA is then cut using restriction enymes and inserted into a vector (usually a plasmid from bacteria) that has been cut with the same rest. enzyme to ensure they have complimentary sticky ends to each other. Ligase enzyme is then used to seal the sugar/phosphate backbone together to produce recombinant plasmid. The plasmid is transferred into bacterial cells: cells need to be heat shocked and placed in CaCl solution to encourage the membrane's permeability to take up the plasmid. However very few bacteria do take up the recombinant plasmid so those that have need to be identified by replica plating:
    normal plasmid has an ampicillin resistance gene and a tetracycline resistance gene. When the insulin gene is inserted into the plasmid it deactivates the tetracycline resistance gene, so any transformed bacteria wont be able to survive on a medium containing tetracycline. if you first grow the bacteria on a standard nutrient agar medium, they will all survive and reproduce to produce colonies of bacteria. If you then transfer the colonies onto a medium containing ampicillin only the bacteria that have taken up the plasmid will survive. then transfer onto a medium containing tetracycline and only those that havent taken up the plasmid will survive. So the cells that survive on ampicillin medium but not tetracycline are the transformed bacteria. these are then grown on a large scale to produce human insulin
    advantages: no rejection like you would if you extracted insulin from animals, cheaper, large quantities produced and ethical/religous benefits.


    ohh and dont forget theyres the possibility of curing diabetes by growing stem cells into beta cells, which can be inserted into the diabetic pancreas so they have functioning beta cells to produce insulin themselves, rather than needing injections

    phew!! I kind of want there to be a hefty question on insulin after all that!
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    Anyone know a good source for past papers on this topic?

    All the content on this spec was split into like 6 different exams on the old spec.
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    (Original post by tara592)
    hey Ive just realised there is a good chance of having a big old question on insulin as there's so much on it!!
    so theres the beta cells in the islets of langerhans in the pancreas that produce insulin to lower blood glucose conc. insulin increases liver + muscle cells permeability to glucose, activates glycogenesis and increases rate of respiration to do this.
    how insulin is secreted: high blood glucose conc = more glucose into Beta cell by facilitated diffusion. More glucose is respired so more ATP is produced. the rise in ATP causes K+ ion channels to close, so pot. ions build up inside the Beta cell, making it more +vely charged inside causing depolarisation. depolarisation causes ca2+ channels to open, and ca2+ enters the beta cell causing the vesicles to fuse with the membrane and secrete insulin into the blood by exocytosis

    thennnnn... theres type 1 and type 2 diabetes: type 1: B cells dont produce any insulin. hyperglycaemia = v high blood glucose conc after meals as theres no insulin to lower the conc. hypo = too much insulin injection causes dangerous drop in glucose levels.
    ....then insulin can be produced by GM bacteria: mRNA taken from pancreatic cells, and combine with reverse transcriptase to make cDNA for the insulin gene. the cDNA is then cut using restriction enymes and inserted into a vector (usually a plasmid from bacteria) that has been cut with the same rest. enzyme to ensure they have complimentary sticky ends to each other. Ligase enzyme is then used to seal the sugar/phosphate backbone together to produce recombinant plasmid. The plasmid is transferred into bacterial cells: cells need to be heat shocked and placed in CaCl solution to encourage the membrane's permeability to take up the plasmid. However very few bacteria do take up the recombinant plasmid so those that have need to be identified by replica plating:
    normal plasmid has an ampicillin resistance gene and a tetracycline resistance gene. When the insulin gene is inserted into the plasmid it deactivates the tetracycline resistance gene, so any transformed bacteria wont be able to survive on a medium containing tetracycline. if you first grow the bacteria on a standard nutrient agar medium, they will all survive and reproduce to produce colonies of bacteria. If you then transfer the colonies onto a medium containing ampicillin only the bacteria that have taken up the plasmid will survive. then transfer onto a medium containing tetracycline and only those that havent taken up the plasmid will survive. So the cells that survive on ampicillin medium but not tetracycline are the transformed bacteria. these are then grown on a large scale to produce human insulin
    advantages: no rejection like you would if you extracted insulin from animals, cheaper, large quantities produced and ethical/religous benefits.


    ohh and dont forget theyres the possibility of curing diabetes by growing stem cells into beta cells, which can be inserted into the diabetic pancreas so they have functioning beta cells to produce insulin themselves, rather than needing injections

    phew!! I kind of want there to be a hefty question on insulin after all that!
    i think the idea is that those that can survive on the first anti-biotic have taken up the plasmid. however some plasmids didnt take up the gene in the first place - in the presence of dna ligase they simply rejoined. to detect those that have taken up the correct plasmid (1 in 100 i think) they are placed on thesecond anti-biotic that our gene would have disrupted. then they die.
    to clarify - all the bacteria on plate 1 & 2 took up the plasmid - but only those that died on plate 2 took up the correct plasmid.
    sorry if thats what you meant but i thought id check!
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    Just came across this past paper question:

    Some drinking water is extracted from the ground. Groundwater is tested for a range of substances including nitrate ions.

    Explain why the prescence of nitrate ions in ground water is a cause for concern.


    Help please!
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    (Original post by ViolinGirl)
    Hmmm...there was a genetic question that I came across. Was about yellow, green and yellow-green plants being grown in the light. And the yellow ones died, green ones grew v. tall and the yellow-green ones grew reasonably. It says to explain this.


    I thought it would be due to the yellow plants having the incorrect photosynthetic pigments or accessory pigments for the bright light source, so most of the wavelengths of light are reflected, and they are unable to photosynthesise due to inability to capture light energy, and went on with that argument. Would that get marks also?

    In contrast to the markscheme answer, which just says that the green plants have more cholorophyl, and therefore can photosnthesise, yellow ones have no chlorophyl...?
    I thought the same Violin but im not sure. Its completely incorrect to assume yellow leaved plants have no chlorophyll, and i wrote pretty much the same as you. The questions etc set by OCR and their answers are so dodgy for this exam =/
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    (Original post by Falcon91)
    I thought the same Violin but im not sure. Its completely incorrect to assume yellow leaved plants have no chlorophyll, and i wrote pretty much the same as you. The questions etc set by OCR and their answers are so dodgy for this exam =/
    why? its makes perfect sense... considering chlorophyll is green...?
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    (Original post by thekooks)
    Just came across this past paper question:

    Some drinking water is extracted from the ground. Groundwater is tested for a range of substances including nitrate ions.

    Explain why the prescence of nitrate ions in ground water is a cause for concern.


    Help please!
    http://www.ext.colostate.edu/pubs/crops/00517.html
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    The colour of the spines on the stems of raspberry plants are controlled by two genes, A/a and B/b. The genes are on different pairs of chromosomes.
    Allele A produces a pink anthocyanin pigment in the spines. Allele B has no effect by itself, but increases the colour produced by allele A to give red spines. Alleles a and b have no effect on spine colour. In the absence of anthocyanin, the spines are green.

    It is an exam question. But i'm confused as in the mark scheme it refers to this as dominant epistasis.
    I thought this is an example of complementary action (epistasis). A codes for some kind of pre pigment, that can then be increased by the prescence of B.

    Isn't dominant epistasis where there is the prescne of a dominant allele at one locus that prevents the expression on alleles at a second locus. So in this case if the prescence of A, meant that regardless of what was present B/b it would still be pink, and if there was a, then B/b can be expressed. Help
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    if in the exam they ask us to a diagram or graph or something and we draw in pencil, will that be scannned and how will it show up since exam papers are scanned and you can onll write in black pen.
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    (Original post by Falcon91)
    I thought the same Violin but im not sure. Its completely incorrect to assume yellow leaved plants have no chlorophyll, and i wrote pretty much the same as you. The questions etc set by OCR and their answers are so dodgy for this exam =/
    i think we are over complicating things again considering this is OCR..
    its not green, so no chlorophyll - just run with it :p:
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    (Original post by ViolinGirl)

    It is an exam question. But i'm confused as in the mark scheme it refers to this as dominant epistasis.
    I thought this is an example of complementary action (epistasis). A codes for some kind of pre pigment, that can then be increased by the prescence of B.
    the ratio is still 9:4:3 so dominant epistasis?
    there are still only 3 phenotypes
    isnt this what qualifies it as dominant epistasis?

    complementary has the ratio 9:7 doesnt it?
    Complementary gene action (F2 ratio = 9:7): Blocking any step in a sequential enzymatic process can prevent synthesis of the final product of the pathway. Anthocyanin pigment synthesis in sweet peas is an example where blocking either of two steps will prevent pigment formation. Only the double dominant phenotype produces both of the needed enzymes and is able to synthesize the pigment (figure 13.17). The F2 progeny ratio is 9 pigmented (A-B-) to 7 unpigmented (A-bb, aaB-, or aabb) as shown in figure 13.16. Similar results can also be obtained obtained if the products of two independently coded enzymes must interact to yield the final product (figure 13.18). As described in boxed example 13.3 (and in figure 13.16), crossing two strains of sweet peas that are white because of different mutations in the anthocyanin biosynthetic pathway can result in F1 progeny with purple flowers. Please note that some purists do not consider complementary gene action to be an example of epistasis because it involves two steps in the same pathway rather than modification of the effects of one gene by another. However, all four of the textbooks that I have used for this course over a period of six years have included it under epistasis.
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    this was quoted by TX22:


    if in the exam they ask us to a diagram or graph or something and we draw in pencil, will that be scannned and how will it show up since exam papers are scanned and you can onll write in black pen.


    i am curious to this
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    (Original post by ViolinGirl)
    The colour of the spines on the stems of raspberry plants are controlled by two genes, A/a and B/b. The genes are on different pairs of chromosomes.
    Allele A produces a pink anthocyanin pigment in the spines. Allele B has no effect by itself, but increases the colour produced by allele A to give red spines. Alleles a and b have no effect on spine colour. In the absence of anthocyanin, the spines are green.

    It is an exam question. But i'm confused as in the mark scheme it refers to this as dominant epistasis.
    I thought this is an example of complementary action (epistasis). A codes for some kind of pre pigment, that can then be increased by the prescence of B.

    Isn't dominant epistasis where there is the prescne of a dominant allele at one locus that prevents the expression on alleles at a second locus. So in this case if the prescence of A, meant that regardless of what was present B/b it would still be pink, and if there was a, then B/b can be expressed. Help
    This is dominant epistasis. The presence of B masks the presence of A, it stops it from being pink but rather causes it to be red. A has no effect on B, if it did this might be classed as complementary. Its a really poor example of epistasis though.
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    (Original post by george54)
    i think the idea is that those that can survive on the first anti-biotic have taken up the plasmid. however some plasmids didnt take up the gene in the first place - in the presence of dna ligase they simply rejoined. to detect those that have taken up the correct plasmid (1 in 100 i think) they are placed on thesecond anti-biotic that our gene would have disrupted. then they die.
    to clarify - all the bacteria on plate 1 & 2 took up the plasmid - but only those that died on plate 2 took up the correct plasmid.
    sorry if thats what you meant but i thought id check!
    umm yeah I think so...
    so only a few plasmids take up the insulin gene. those that do are no longer resistant to ampicillin because the insulin gene is inserted into the plasmid which deactivates its resistance. But not many plasmids take up the human insulin gene, and even less bacteria take up the plasmids. so you grow the bacteria on standard medium to produce colonies. then grow on tetracycline - any bacteria that have taken up plasmid will survive. then grow on ampicillin - only plasmids that havent taken up insulin gene will grow. so recombinant plasmids will die on ampicillin medium as they dont have the resistance gene. then you compare the 2 to identify transformed bacteria

    is that right?
 
 
 
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