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ORF- open reading frame???


soconfused

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It's the stretch of DNA after a start codon that doesn't contain any stop codons. So everything between a start codon and the next stop codon. This may contain one gene only, it maybe contain several genes, such as in operons in bacteria, or it may contain a gene and noncoding material, such is in most of our genes.

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  • 3 weeks later...

Well...it's really only relevant to mRNA so it is not really an intron/exon issue. The ORF relates to the start sequence of protein coding in mRNA...so introns and exons don't come into it at this stage.

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  • 3 weeks later...
It's the stretch of DNA after a start codon that doesn't contain any stop codons. So everything between a start codon and the next stop codon. This may contain one gene only, it maybe contain several genes, such as in operons in bacteria, or it may contain a gene and noncoding material, such is in most of our genes.

 

Ah I think you are confusing stop codon with terminator here. An operon can contain several ORFs, but not the other way round. A gene ends with its stop codon :)

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  • 1 month later...
but is there any difference between ORF and reading frame?

 

well that depends on what you are asking... are you asking the difference between open reading frames and reading frames?

 

or one of the other meanings or ORF?

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do the open reading frame and reading frame mean the same thing?

I suppose that an ORF have the potential to encode a protein?

 

am I right?

 

thanks

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  • 2 months later...
  • 3 months later...

as nucleotides are read in triplets called codons, each genetic sequence has 6 ways of reading it: three forward, and three backward.

 

For example, two of the reading frames for the genetic sequence atgccatagacttaa are shown below, and either reading frame can be read from left-to-right or from right-to-left.

 

.........................<-- or -->

.....................tgc...cat...aga...ctt

...................|----|----|-----|----|

.................a t g c c a t a g a c t t a a

.................|___|____|____|____|___|

..................atg...cca...tag...act...taa

...........................<-- or -->

 

i'm pretty sure that 'open' denotes, out of the possible reading frames, the one that is actually used. for example

 

3'-atgccatagacttaa-5'

 

has the following reading frames:

 

(reading 3'-->5')

 

atg cca tag act taa

tgc cat aga ctt

gcc ata gac tta

 

(reading 5'-->3')

aat tca gat acc gta

ttc aga tac cgt

caa cag ata ccg

 

however, atg cca tag act taa is the only reading which results in a translatable genetic sequence, ie it starts with a start codon (atg) and ends with a stop codon (taa), therefore it is the 'open' reading frame, as it is the reading frame that will be to manufacture the protien.

 

eukaryiotic genes generally only have one open reading frame per gene, however bacterial and viral genes can have more than one open reading frame, and the reading frames can overlap; for example:

 

..........3'-->5' ORF

....|-----------------|

3'-atgccataatggacttaacgtaaacgtatacggggactgta-5'

..............||_____________|..........................|

..............|.....3'-->5' ORF.............................|

..............|_______________________________|

............................5'-->3' ORF

 

Note that all the ORFs start in atg and end in taa, despite the fact they are read in different directions, and also that the reading frames are staggered (ie, one of the 3'-->5' frames is a nucleotide behind a the other). In the above case, there would be two promoters off to the 3' direction, and one off to the 5' to activate the variouse ORFs.

 

 

the reading frame used (ie, the open reading frame) is usually determined by the promoter: most promoters initiate transcription starting x nucleotides away, so if we imagine a promoter with the sequence CCCC which initiates transcription 7 nucleotides away, then

 

CCCCccgtctgatgcagggggtcetc

 

will result in this ORF (codons marked by | pipes)

 

CCCCccgtctg|atg|cag|ggg|gtcetc

 

whereas, if we shift the promoter along one by deleting the fist nucleotide after it (underlined above) we get a completely different ORF.

 

CCCCcgtctga|tgc|agg|ggg|tcetc

 

which is called a frame shift, and is how the deletion/insertion of a single nucleotide can have such a profound effect.

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  • 1 month later...

That was a kool explanation for the ORF's.

 

But how can you prove this...

 

..... that all the ORFs start in atg and end in taa, despite the fact they are read in different directions......

 

I have never found that the ORF'f start in ATG and end in TAA. PLease clarify...

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atg is a start codon, and taa is a stop codon. i didnt mean to say that all ORFs start and end in atg and taa, (as there are other start/stop codons), but all the ORFs in my example did -- ie, they are all legitimate genes, with a start and a stop codon.

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Ok. Thnks

One more question.

 

You hav also mentioned about the frame shift mutations and IN/DELs.

 

If these mutations can cause a profound effect on the proteins formation, then how is it so that our body tends to reduce the effects and also repair it??

OR

Is it that it is not repaired but the redundancy of the genetic code hides the effects of mutations ?

 

Please source relevant links if poss.

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[if the number of bases indel'd is not divisible by three, then] the reading frame is disturbed and the resulting gene generally codes for an entirely different protein, with different amino acids and a different length than the original gene. Insertions or deletions are therefore rare in coding regions, but rather frequent in noncoding regions.When occurring in coding regions, indels can occasionally change the reading frame of a gene and make another ORF of the same gene accessible. Such mutations can lead to acquisition of new gene functions. Viruses make extensive use of this possibility. They often encode several proteins from a single gene by using overlapping ORFs
From Basic concepts of molecular evolution, by Anne-Mieke Vandamme (pdf)

 

Basically, the frame-shift caused by indels is so profound that the gene product is completely changed; if the gene was a vital one, then its function will be lost and the cell will be non-viable (ie it will die). Thats how the body keeps its number of indels in functioning regions of dna low.

 

redundancy would probably allow a gene product to survive an indel event. In addition, there are a variety of ways in which the genome can be repaired if an indel event occoures during DNA replication. presumably by the exsicion-repair mechanism would recognise the indel in the new strand, as the indel would likely cause a warping in the double helix (as one strand would have an extra nucleotide): more about dna proof-reading is here (scroll down to the highlighted bits)

 

If an indel event occours in a coding region outside of DNA synthesys -- which is relatively unlikely -- i think its just a case of whats called masterly inaction*: 'if the cell can survive the indel, then it will, and its not a problem: else, it will die, and the problem will have gone away'.

 

Although it appears that this approach is not 100% effective, and can cause genetic defects1

 

----------------------------------------------------------------------

*masterly inaction: the act of cunningly desciding to solve a problem by doing absolutely nothing at all about it. not to be confused with lazyness, which is superficially similar but rarely actually solves the problem, whereas masterly inaction does.

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