Talk:Alternative splicing

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Contents 1 transcripts diversity 2 SR proteins 3 Alternative promotor mechanism 4 Alternative poly-A mechanism 5 nonfunctional alternative splicing 6 clean-up 7 Intron Retention mode

[edit] transcripts diversity

I would start by stating something like this:

Alternative splicing is one of the main mechanisms that eukaryotic cells have evolved to generate a great diversity of transcripts and proteins from a small number of genes. Its role has been particuarly studied and understood after the publication of the human genome and the subsequent debates about the number of genes in the human specie. It has become clear that many of the most complex organisms tend to have a smaller number of genes than expected, and that mechanisms like alternative splicing help to generate diversity.

What do you think? Dalloliogm 14:23, 10 October 2007 (UTC)

[edit] SR proteins

"The regulation and selection of splice sites is done by Serine/Arginine-residue proteins, or SR proteins."

Are you sure of this? I think there are other class of proteins involved, like hnRNPs.

Dalloliogm 14:23, 10 October 2007 (UTC)

[edit] Alternative promotor mechanism

This is not splicing mechanism. neffk 04:24, 29 August 2006 (UTC)

[edit] Alternative poly-A mechanism

I have not heard of this... RNA polymerase II and cleavage, polyadenylation specificity factor (CPSF), and cleavage stimulatory factor (CStF) terminate transcription 10-30 nt downstream of the AAUAAA transcription stop sequence. Poly-A tail is produced by PAP (poly-A polymerase). Unless scholarly research can be referenced, I think this should be removed. neffk 04:22, 29 August 2006 (UTC)

[edit] nonfunctional alternative splicing

The article contains no indication that alternatively spliced variants might be anything other than adaptive. It's an issue that's currently in need of emphasis in the field. Alternative splicing can clearly be regulated and adaptive, but essentially all of the diagrammed forms of alternative configurations for a transcript can also occur as a result of abberant transcript processing resulting from exon skipping, incorrect choice of cryptic splice sites, etc. For example, perhaps 1/3 to 1/2 (possibly more) of alternatively spliced variants in humans contain premature termination codons and are almost certainly nonfunctional. Unfortunately, a general belief perhaps uncharitably characterized by "if the cell produces it, it must be good" has led to coupling this mechanism to nonsense-mediated decay in proposals of a new form of gene regulation, when really the most parsimonious explanation is that NMD is just doing its job in removing these incorrectly processed transcripts. Dgscofield 02:51, 28 October 2006 (UTC)

[edit] clean-up

i tagged this article for clean-up since it is written in rather colloquial language, and since it lacks interesting details such as the explanation of trans- and cis regulatory elements, which influence the regulation of alternative splicing. Further, in this article many facts refer to splicing in general, which can be left out or should be included in the article "splicing (genetics)". —The preceding unsigned comment was added by Inside x (talk • contribs) 15:06, 27 April 2007 (UTC).

[edit] Intron Retention mode

However, the intron must be properly encoding for amino acids. The intron's code must be properly expressible, otherwise a stop codon or a shift in the reading frame will cause the protein to be non-functional.

This is not necessarly true: in fact, a retained intron can also occur in one of the Non Translated Regions (NTRs) on the upstream or the downstream of the transcript.