Tissue specific expression - help

Hi all,

I'm talking in regards to the picture in the link below.

1) When being asked to list the exons present in lymphocytes, do I just add them together? Tried to get a wider reading on this, but just heavily confused on what the question expects me to do.

2) And is there a difference in sum of exons and polyA tail because of something to do with splicing?

https://imgur.com/a/56nYy

Thanks in advance

Reply 1

macpatgh-Sheldon

20

Hi
Firstly, I am not a geneticist only studied genetics as a minor subject in medicine.

I am not sure about part (a)

part (b): I would work out that the disparity exists because one nucleotide is part of the codon that codes for the initiation site, namely AUG, and the amino acid it codes for (namely methionine, a sulphur containing a.a.), breaks off from the nascent polypeptide on the ribosome/mRNA complex.

I wonder if this makes any sense.

M

Reply 2

aneducation

OP

11

Original post by macpatelgh

Hi
Firstly, I am not a geneticist only studied genetics as a minor subject in medicine.

I am not sure about part (a)

part (b): I would work out that the disparity exists because one nucleotide is part of the codon that codes for the initiation site, namely AUG, and the amino acid it codes for (namely methionine, a sulphur containing a.a.), breaks off from the nascent polypeptide on the ribosome/mRNA complex.

I wonder if this makes any sense.

M

Ahhh thank you, yes it makes sense!
Following up from what you said, I really don't get what this question is implying?
https://imgur.com/a/KAXCj

It sounds simple, but I can't get my head around this one, the difference between the mRNA structure would just be the difference in the base pairs for this answer?

If you can, please let me know your input.

Thank you so much!

Reply 3

macpatgh-Sheldon

20

Hi,

Sorry for the delayed answer - I got up like a student today - should have been getting up like at 7.30 a.m. 10 years ago! :smile:

I think the knowledge they are trying to test you on here is your ability to deduce that a resting lymphocyte (presumably NOT one stimulated to ultimately produce antibody [after conversion into a plasma cell in the case of a B lymphocyte]) is NOT going to be actively synthesizing protein (you will probs know that ALL ANTIBODIES, namely IgA [in secretions e.g. tears], IgD,, IgE [active in allergy and in worm infestation)] IgG [small antibody so crosses placenta to infer some immunity to growing baby] and IgM [large molecule with 5 binding sites for Ag] are all Y-shaped proteins with two heavy chains and two light chains of polypeptides connected by disulphide bridges [sorry, getting carried away here by my nerdiness! :h:

]).

On the other hand (and you might know that the liver is the most metabolically active organ in the body), liver cells, being also the cells that synthesize the most protein (e.g. albumin, the clotting factors II, V and VII and X, if I remember right) in the body, so the mRNA in the liver must in some way be actively producing proteins as against a RESTING liver cell, which would not have the mRNA actively synthesizing proteins.

In view of the above, I would presume (and from the detail in your Qs I can tell you are studying genetics! so you will know better than I) that the molecular difference (which is what is asked) involves some change that occurs in the mRNA prior to translation; is this splicing (??) where introns (with NO triplet codes intended as representing actual amino acids) are removed and the exons joined up OR is it some other pre-translational chemical change that occurs between resting mRNA and actively protein-synthesizing RNA?? I recall reading somewhere (in a cell biology book?? - I am not a cytologist, either, just love reading) that mRNA is edited by covalent changes to nucleotides - since tRNA needs to bond with mRNA in a complementary base fashion, this "editing" might be one molecular difference between "resting" and "active" mRNA.

Sorry to go on a bit, but hope this wakes you up even more after getting up before me this morning haha!

M

PS Also google sRNA (small RNA) and snoRNA (small nucleolar RNA), which have a role in control of control of translation (THAT IS ALL I KNOW ABOUT THEM).

(edited 6 years ago)

Reply 4

macpatgh-Sheldon

20

@aneducation

Hi I don't know anywhere near enough about control of transcription to answer this latest Q with any certainty.

However, trying to (almost blindly haha) apply logic to the info given and my limited knowledge, I will try to give you some clues, and hopefully with your superior knowledge of genetics, we can jointly engineer a solution.

part a) the two promoters involved are P1 nd P2 (from earlier Q) - You will need to work out (from the respective nucleotide lengths of each exon??) which way round they are i.e. whether P1 is for liver and P2 for lymphocytes OR vice versa. If badly stuck in an exam on Q like this, you might need to guess; you will have a 50% chance of getting it right, which is better than 0% :smile:

M

Looking at b) now!

Reply 5

macpatgh-Sheldon

20

@aneducation

b) the Q tells you that Silencer 1 is the only silencer that represses liver cells - does this mean that Silencer 2 is not expressed in liver cells? I would predict so. If your answer for Q a) was P1 for liver cells, (e.g.) then I would expect that Silencer1 would influence this same P1 promoter since fine control of transcription, I would predict, could ONLY be achieved if both the promoter and the silencer (having opposite effects) are active in a particular tissue here liver, so that the balance between the two determines finally whether transcription does occur or not AND to what extent (???)

SORRY NOT VERY IMPRESSIVE IS IT?

Reply 6

macpatgh-Sheldon

20

c) and d)

I have managed to locate a few mechanisms of action of repressors summarized below (which of them might be good candidates as answers to parts c) and d), I have no idea at all!

i) competition with activators for same DNA sequence
ii) some repressors are very similar chemically to the activator, but do not have activation domain (so I shuld think they inhibit transcription in a fashion similar to how several drugs (medicines NOT speed or ecstasy!!) act e.g. the treatment of essential hypertension can be undertaken with e.g. ACE (angiotensin converting enzyme) inhibitors like lisinopril, or captopril that are competitive inhibitors of this enzyme.
iii) some repressors binds near the activator and mask its activation domain; the latter then becomes non-viable
iv) some repressors bind to specific sequences of DNA and block coactivator function.

(SOURCE: Cell Biology by T Pollard)

One point worth making: I note that the diagram in the latest Q shows that Silencer 1 is a separate section of the DNA whereas Silencer 2 seems to overlap with the enhancers - could this help you work out c) and d)???

M
Sorry a bit late, but best of luck in your exam today! :smile:

PS I really am very curious what degree you are doing - seems very interesting!

Reply 7

aneducation

OP

11

Original post by macpatelgh

c) and d)

I have managed to locate a few mechanisms of action of repressors summarized below (which of them might be good candidates as answers to parts c) and d), I have no idea at all!

i) competition with activators for same DNA sequence
ii) some repressors are very similar chemically to the activator, but do not have activation domain (so I shuld think they inhibit transcription in a fashion similar to how several drugs (medicines NOT speed or ecstasy!!) act e.g. the treatment of essential hypertension can be undertaken with e.g. ACE (angiotensin converting enzyme) inhibitors like lisinopril, or captopril that are competitive inhibitors of this enzyme.
iii) some repressors binds near the activator and mask its activation domain; the latter then becomes non-viable
iv) some repressors bind to specific sequences of DNA and block coactivator function.

(SOURCE: Cell Biology by T Pollard)

One point worth making: I note that the diagram in the latest Q shows that Silencer 1 is a separate section of the DNA whereas Silencer 2 seems to overlap with the enhancers - could this help you work out c) and d)???

M
Sorry a bit late, but best of luck in your exam today! :smile:

PS I really am very curious what degree you are doing - seems very interesting!