Yacoubb's Bio 3+4 Questions

[Irving4Prez]

(by logic, yes) But not every hairy dog will be homozygous dominant, and if we cross heterozygous and heterozygous, we'll end up with a 25% chance of a hairless offspring, which is untrue.

Ah makes sense, thanks mate

[Yacoubb]

Is the purpose of a dihybrid test cross to determine the genotype of the parent who phenotypically expresses the dominant trait at both gene loci under investigation, AND to determine whether two genes are linked/independently assorted?

Thanks

[vox nihili]

Is the purpose of a dihybrid test cross to determine the genotype of the parent who phenotypically expresses the dominant trait at both gene loci under investigation, AND to determine whether two genes are linked/independently assorted?

Thanks

Yeah, it can be used to do both.

[Yacoubb]

Yeah, it can be used to do both.

Thank you. Would it be accurate describe independent assortment as pairs of genes being assorted randomly into gametes independent of the behaviour of other genes? That is, considering the genes are unlinked.

[Bad Student]

Thank you. Would it be accurate describe independent assortment as pairs of genes being assorted randomly into gametes independent of the behaviour of other genes? That is, considering the genes are unlinked.

It would be a bit more accurate to say that the alleles are assorted randomly, not genes.

[Yacoubb]

It would be a bit more accurate to say that the alleles are assorted randomly, not genes.

But the genes do independently assort. I mean, we're talking at the chromosome level here, hence, the gene loci they carry. But I see what you mean. I'd probably mention that pairs of genes (alleles) assort independently of other pairs of genes (alleles). That would probably make up for it Thanks for the input.

[vox nihili]

If you want to be a real pain, it's actually technically the gene loci that assort independently. But yeah, that is an accurate description. It's not accurate to say that the gene loci are on different chromosomes though, because gene loci on the same chromosomes can assort independently, so it is a good definition.

[Yacoubb]

Do we need to know anything about liposomes other than the fact that they are hollow structures used as vectors in gene therapy? I mean, I know that liposomes wrap around a gene, and with the target cell membrane to deliver the gene into the cell. Must I know more?

Retroviruses and adenoviruses - I know that these are both vectors used to transfect cells. But do we need to know, for instance, how retroviruses use reverse transcriptase to create a DNA template from an inserted mRNA strand complementary to the gene of interest, and then how integrase is used to catalyse the incorporation of the gene into the genetic material of the cell.

Also, is it right to say that gene therapy does not involve the integration of a normal functioning allele of a gene into the chromosomal DNA of a cell, and rather just involves the delivery of an allele to a cell through a liposome for instance? I found this to be a logical way of explaining how gene therapy does not involve the removal of a defective allele for a gene.

[simpak]

1.  There really isn't much else to know.

2.  No.  I explained that earlier for interest purposes/explanation purposes you don't have to know it.

3.  There is no requirement for integration in gene therapy but if you want your allele to be maintained through division you would want it to be integrated.  You could still have a gene inserted into the genome elsewhere and have both the defective allele and the functional allele in the genome in completely different places.  For eg your defective allele might be on chromosome 6 but you might insert it into some junk DNA on chromosome 11.  You don't have to remove the defective allele in this case/replace it you can just add to what is already there.  Most of the time your defective allele is going to produce a nonfunctional product.  You would only want to actually eliminate the defective allele specifically if you have a dominant negative.

Let me know if I didn't understand your question correctly as I'm worried I may have misinterpreted.

[Yacoubb]

1.  There really isn't much else to know.

2.  No.  I explained that earlier for interest purposes/explanation purposes you don't have to know it.

3.  There is no requirement for integration in gene therapy but if you want your allele to be maintained through division you would want it to be integrated.  You could still have a gene inserted into the genome elsewhere and have both the defective allele and the functional allele in the genome in completely different places.  For eg your defective allele might be on chromosome 6 but you might insert it into some junk DNA on chromosome 11.  You don't have to remove the defective allele in this case/replace it you can just add to what is already there.  Most of the time your defective allele is going to produce a nonfunctional product.  You would only want to actually eliminate the defective allele specifically if you have a dominant negative.

Let me know if I didn't understand your question correctly as I'm worried I may have misinterpreted.

That's fine thank you simpak!

[Bad Student]

It looks like you already know the stuff anyway. My teacher didn't even mention this stuff in class. I learnt all of this stuff from you just now.

[Yacoubb]

It looks like you already know the stuff anyway. My teacher didn't even mention this stuff in class. I learnt all of this stuff from you just now.

Trust me, I feel the same. At times, I feel that I so rapidly went through unit 4 that my knowledge of this unit is superficial. Nevertheless, the topics and concepts are less intricate than unit 3, so I guess its a good unit. Good luck!

[Yacoubb]

Would this be sufficient for describing how apoptosis is an example of signal transduction:

Apoptosis occurs when a specific target cell receives a death signal, triggering a cascade of events (including the activation of caspases, blebbing of the cell) that leads to the cell self-destructing (the response). 

Also, the sample Biology exam seems to suggest that we need to know about action potentials - the question asks to describe how the electrical signal travels across the axon of a post-synaptic neuron. I mean, would I just need to mention that an action potential travels from one node of Ranvier to the next across the myelinated axon. Could someone help me formulate a more appropriate response?

Another question from the sample exam:
A tissue that has been responsive to hormone X may, over time, lose its response to hormone X, even
though the concentration of hormone X remains unchanged.
Based on your understanding of how a hormone controls the functioning of cells, suggest reasons for
this decrease in responsiveness.
Some suggestions:
- The cells have become overstimulated and so no longer respond to hormone X when it binds to specific receptors.
- The reception sites for the ligand molecules have been altered; there is no lock-and-key fit between hormone X and its specific receptor, and thus the effects of hormone X have been reduced.

What else could we mention as suggestions in that regard? Thanks for your help

[Bad Student]

Would this be sufficient for describing how apoptosis is an example of signal transduction:

Apoptosis occurs when a specific target cell receives a death signal, triggering a cascade of events (including the activation of caspases, blebbing of the cell) that leads to the cell self-destructing (the response). 

Also, the sample Biology exam seems to suggest that we need to know about action potentials - the question asks to describe how the electrical signal travels across the axon of a post-synaptic neuron. I mean, would I just need to mention that an action potential travels from one node of Ranvier to the next across the myelinated axon. Could someone help me formulate a more appropriate response?

Another question from the sample exam:
A tissue that has been responsive to hormone X may, over time, lose its response to hormone X, even
though the concentration of hormone X remains unchanged.
Based on your understanding of how a hormone controls the functioning of cells, suggest reasons for
this decrease in responsiveness.
Some suggestions:
- The cells have become overstimulated and so no longer respond to hormone X when it binds to specific receptors.
- The reception sites for the ligand molecules have been altered; there is no lock-and-key fit between hormone X and its specific receptor, and thus the effects of hormone X have been reduced.

What else could we mention as suggestions in that regard? Thanks for your help

The loss of the response to hormone x suggests that some sort of negative feedback witchcraft is going on. This might happen because a substance produced by the binding of hormone x to the receptors alters the shape of the receptors for hormone x.

[Yacoubb]

When discussing how a vaccine confers long-term immunity against a particular pathogen, do I only need to talk about the production of antibodies in the humoral response? Is there a need to discuss a cell-mediated response? Or maybe I can intertwine is subtly and mention that:

1. A specific immune response is coordinated against the pathogen.
2. Memory cells retain memory of the antigenic markers of the pathogen.
3. On subsequent infections caused by the same pathogen, a more rapid, emphatic attack against the pathogen is coordinated.
4. Long term immunity of the individual against the pathogen is conferred.

^ Is this sufficient.