Any tips on how yo remember the start and stop codons?
I always get them mixed up when trying to remember them.
Thanks
Please say no lol
Obviously you can’t put a microscope to a base pair and watch it match up, so how do we observe or prove that these things are happening on a sub cellular level?
If I like insert a 10 nucleotide exon with no stop codon in any reading frame AT ALL in between the sequence, will I have more or less amino acids compared to the original? Or does it depend on whether or not it causes a stop codon to occur in between?
- Does the last codon in every mRNA that's being translated have to be one of UAG, UAA, and UGA?
- If mRNA ends, then won't the protein anyway finish, why is a stop codon needed?
- What happens when there is a mutation in transcribing the stop codon? (So mRNA doesn't end with a stop codon)
Basically just that. I'm finished with my Biochem class and am studying further for MCAT's, but I was just struck by how the AUG codon is both for Methionine and a start codon. How can starting every polypeptide with Methionine be advantageous? I assume it *must* be advantageous because of the 64 possible 3 unit combos for codons and only 1 codes for methionine and is a start codon. There must be a reason this evolved that way. Does anyone have ideas/answers? Or is it just a freak coincidence that had no negative impact so it continued that way?
tRNA has the anti-codon and produces the amino acid but it translates from the mRNA which has the codons? Do you use the anti-codon or the codon when reading the chart (the one with AUG = start)?
I was wondering if an ORF is valid if the stop codon overlaps with another start codon.
Start Codon: AUG
Stop Codons: UAG/UAA/UGA
For example:
AUG[xxx][xxx][xxx]UGAUG[yyy][yyy][yyy]UAG
How many ORFs are here?
I was wondering because NCBI's ORF finder does not recognise AUG[xxx][xxx][xxx]UGA as an ORF. Is there a reason for this? Thanks
Edit:
Guess I didn't know what I was asking. The sequence in question is part of the human beta-globin gene:
A:
ATG GGA AAC AGA CGA {ATG ATT GCA TCA GTG TGG AAG TCT CAG GAT CGT TTT AGT TTC TTT TAT TTG CTG TTC ATA ACA ATT GTT TTC TTT TGT TTA ATT CTT GCT TTC TTT TTT TTT CTT CTC CGC AAT TTT TAC TAT TAT ACT TAA} TGC CTT
B:
{ATG GGA AAC AGA CGA ATG ATT GCA TCA GTG TGG AAG TCT CAG GAT CGT TTT AGT TTC TTT TAT TTG CTG TTC ATA ACA ATT GTT TTC TTT TGT TTA ATT CTT GCT TTC TTT TTT TTT CTT CTC CGC AAT TTT TAC TAT TAT ACT TAA} TGC CTT
Based on what ORF finder was returning, why is A not a valid ORF, while B is?
I was wondering if an mRNA molecule could contain more than one start codon(AUG) but only one of the reading Frame gets translated? What im trying to say is can the ribosome differentiate between where to start translation and just a regular AUG codon? I was reading stuff about the Kodak sequence that I was confused about because they didn't put much information in, does AUG only act as a starting point for translation if it is within a Kodak sequence, with any subsequent AUG codons NOT acting as a starting point and instead just encoding methionine? Sorry if I worded that badly, any help is appreciated!
Sorry for all the questions aswell, if its against the rules or its annoying people ill stop, but thanks again!
I used Cre recombinase to excise an exon (i.e. loxP sites in the introns flanking the third exon within my ORF; this exon codes for a functionally essential domain) of my gene of interest. The protein is around 500 AA but the removal of the exon results in a frameshift at codon 74 and ultimately a stop codon at codon 91 (i.e. the protein is missing the last 409 AAs). When I immunostain the cells that express Cre (and should thus have the exon excised) for my GOI, I see a much weaker staining, yet somehow I can still see signal in their nuclei. The genotype of these animals is GOI(flox/-), so I don't see how there could be any partial effect of the excision. The enzyme either excises the one copy in the genome or it doesn't. The antibody is raised against a part of the protein that should not exist upon excision given the frameshift (the C-terminus)
My current hypothesis is that my antibody has a weak but still detectable non-specific staining of neuronal nuclei. In this case the signal wouldn't even be my protein.
I'm also wondering if it's possible that other translation products could be synthesized off of this mRNA with the missing exon, specifically from a later ATG that would allow the gene product to include the region my antibody binds. The ATG of the actual ORF is at around the 500th base of the transcript and the earliest ATG that is in the correct frame for the synthesis of a gene product containing the epitope is at around base 1000 of the mRNA. Is it possible that protein fragments are being made from this "other" ATG?
tl;dr Can protein fragments be made from non-ORF ATGs? This would explain why immunostaining gives a signal when the epitope should not be translated given a genetic manipulation.
Does anyone know how far you have to get from the ribosome binding site (i.e. 5' cap) before an ATG cannot mediate translation initiation?
Edit: fixed a couple details that didn't make sense as clarified by /u/iayork
Because of translation and stuff
If gene S has three in frame start codons pre-S1, pre-S2, and S and a missense mutation occurs in S2.
Then, one of those unaffected start codons will be used and translation would happen anyway from the beginning to the end including S2?
The explanation says " it is likely that one of the other two start codons could be used, translation would start, and protein structure would be unaffected"
But in my mind, if S2 start codon is affected, only S1 codon and S codon will be read ..... isn't it?
how can the prtein structure be unaffected?
Wikipedia says that nonsense mutations are caused by a mutation creating an end codon causing a protein to end prematurely. (https://en.wikipedia.org/wiki/Nonsense_mutation) but it says nothing about start codon mutation.
It also says that in order to start DNA transcription nearby DNA sequences are required in addition to the start codon so this type of mutation would be more common than a nonsense mutation. (https://en.wikipedia.org/wiki/Genetic_code#Start.2Fstop_codons)
I'm curious as to whether this type of mutation exists because it doesn't have a wiki page.
Evolutionists don't like talking about thorny problems in biochemical evolution. It is no wonder molecular biologists don't get along with evolutionary biologists.
Note how two scientists in the same University are in open conflict: molecular biologist James Shapiro vs. evolutionary biologist Jerry Coyne.
The following material is unfortunately technical, but that is why I love teaching creation to students familiar with molecular biology, they appreciate the problems for Darwinism at the molecular level.
The triplet code is widely billed as follows:
http://sabeerhassan.files.wordpress.com/2013/01/figure-09-08.jpg
Notice Methionine is coded by AUG/ATG. AUG/ATG is also traditionally viewed as the start codon. But the problem is that the supposed universal genetic code really isn't universal!
In the case of alternate start codons: http://en.wikipedia.org/wiki/Start_codon#Alternative_start_codons
GUG/GTG as an alternate start codon which normally codes for Valine results in Metheonine and UUG/TTG which normally codes for Leucine codes for Metheonine.
So how did alternate start codons evolve? Er, one day a cell was happily coding GUG/GTG for Valine and UUG/TTG for Leucine then spontaneously decides to code them for Methionine? Wouldn't that like blow apart a protein especially leucine-rich or valine-rich proteins?
http://en.wikipedia.org/wiki/Leucine-rich_repeat
But this wouldn't be a problem if alternative start codon machinery pops into place at the same time to prevent such a disaster -- Metheonine would only coded for Valine GUG/GTG codon and Leucine UUG/TTG codons if the codons are acting as alternate start codons.
Wait! That's the other problem. How do we get transcription machinery to recognize GTG (valine) and TTG (leucine) in DNA as alternate start codons instead of ATG (methionine).
But that is exactly the problem for evolution, all the interdependent features have to be in place at the same time lest the changes become lethal. It would seem in the case of the emergence of alternate start codons, a miracle of special creation is needed since gradual evolution would fail.
