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I know that alternative polyadenylation creates different transcript isoforms. My question is whether alternative polyadenylation ever results in differences in the terminal/last exon? The only case I can think where it might be is if the terminal exon is alternatively spliced?

EDIT: I think what I was trying to ask was for a given gene, what factors could cause the transcripts to end in different locations. I drew a picture and it helped me figure it out a little enter image description here Here are 4 transcripts for a given gene, each of which end at a different location. Exon's C and D end in different locations because D is completely different exon than C that is being spliced to exon B. Exon on C and E start at the same location, but exon E is shorter, due to a UTR-Alternative polyA event. Exon B and F start at the same location, but F is shorter due to a Coding APA change. So alternative polyadenylation drives the formation of transcripts 1,3,4 while alternative splicing drives the formation of transcript 2. So I guess to rephrase my question, are there any other biological process that can affect where a transcript ends

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  • $\begingroup$ I am finding it difficult to understand your question. Could you draw a diagram to explain what you mean please? $\endgroup$
    – David
    Commented Jul 10, 2019 at 16:29
  • $\begingroup$ Are you asking if alternative polyadenylation is always associated with alternative splicing of the last exon? $\endgroup$
    – WYSIWYG
    Commented Jul 10, 2019 at 16:30
  • $\begingroup$ @Vinay Swamy: I hope my suggested edit didn't change what you were trying to ask! $\endgroup$
    – tyersome
    Commented Jul 10, 2019 at 16:54

1 Answer 1

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According to a 2011 review1 alterntive polyadenylation sites can be located upstream of the 3'UTR (i.e. within introns or exons). When these sites are used it results in transcripts missing exons at the 3' end and can force alternative splicing. This alters the final protein product.

This figure from that paper may help make this clearer. enter image description here

Figure 1. Schematic Representation of CR-APA and UTR-APA

CR-APA produces mRNA isoforms with distinct C-terminal coding regions, resulting in distinct protein isoforms. UTR-APA produces distinct mRNA isoforms with different-length 3′ UTRs but encodes the same protein. Longer 3′ UTRs usually contain cis-regulatory elements, such as miRNA and/or protein binding sites, which often bring about mRNA instability or translational repression. CR-APA, coding region-alternative polyadenylation; UTR-APA, 3′ UTR-alternative polyadenylation. Light green boxes, untranslated regions; light blue boxes, shared coding regions; dark blue and yellow boxes, unshared coding regions; lines, introns.

Reference:

1: Di Giammartino, D. C., Nishida, K., & Manley, J. L. (2011). Mechanisms and consequences of alternative polyadenylation. Molecular cell, 43(6), 853-866.

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  • $\begingroup$ Alternate splicing can result in the same protein. Perhaps you can add a note below the figure. $\endgroup$
    – WYSIWYG
    Commented Jul 11, 2019 at 5:31
  • $\begingroup$ @WYSIWYG — I'm undoubtedly missing something, but I'm not sure how that relates to the OP 's question or to my answer ... $\endgroup$
    – tyersome
    Commented Jul 12, 2019 at 1:40
  • $\begingroup$ I mean that alternate splicing need not affect just the CDS, it can change the UTRs and can potentially expose cryptic polyadenylation sites, zipcodes etc. See this article, for an example. $\endgroup$
    – WYSIWYG
    Commented Jul 12, 2019 at 15:33
  • $\begingroup$ @WYSIWYG — Sure, but my understanding is that the question is about whether alternative polyadenylation ever alters the protein produced. You seem to be discussing how alternative splicing can affect the transcript. $\endgroup$
    – tyersome
    Commented Jul 12, 2019 at 18:42
  • $\begingroup$ Frankly I didn't understand what OP is asking. They didn't clarify. $\endgroup$
    – WYSIWYG
    Commented Jul 12, 2019 at 19:37

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