The human p53 gene expresses at least nine different p53 protein isoforms containing different domains of the p53 protein (p53, p53β, p53γ, Δ133p53α, Δ133p53β, Δ133p53γ, Δ40p53α, Δ40p53β and Δ40p53γ) as a result of multiple splicing, alternative initiation of translation and internal promoter usage [ 11- 13].
Both proteins are expressed in multiple splice isoforms – alternative splicing occurs at their N-terminal regions and tissue- and development-specific isoforms have been described in human, rat and mouse (for brief discussion and original references see [21], [22], [23], [3].
Like most of the genes in the human genome (Stamm et al, 2005), p53 gene family members express multiple mRNA variants due to multiple splicing and alternative promoters.
In general, most genes give rise to multiple spliced transcripts by alternative splicing.
The protocadherin gene family has genomic structure similar to IGH and has multiple splicing forms and multiple alternative promoters.
We also considered cases with multiple alternative splice sites, when the number of alternative sites was more than two.
Second, existence of multiple splicing isoforms, particularly those associated with alternative promoters, as well as the use of multiple expression probes for the same gene makes this one-gene vs. one DMR association analysis very challenging.
As several metazoan H2A.Zs contain a conserved intron directly following the start ATG and possess multiple alternative splice acceptors within their second exon, it will be of interest to determine whether generation of alternative splice H2A.Z variants is not unique to O. dioica.
If mechanisms that are specific to multiple alternative splicing decisions (like splicing coordination) are very uncommon or do not rely on sequences located in introns flanking alternate exons, then the sequence composition in the SASS and MASS groups should be similar.
