rules for alternative splicing

Another potential source of progress in this direction is provided by the evidence showing that cooperativity and synergy between distinct and relatively low affinity RBPs can build specificity.

Recalling that the first splicing events to be documented involved the use of alternative splice sites led some to anticipate the contribution of alternative splicing to biological complexity. In 2001, the discovery that only 25,000 genes were required to produce a human being came as a surprise because less complex organisms such as worms and flies have a similar number of genes. One recent surprise was the finding that mutations in splicing factors categorized as “constitutive” or “generic” could also impact splice site selection.

One pathway that may produce genomic change in germ cells is transcription-associated genomic instability, a process driven by R-loops that is stimulated when the level of RBPs drops (work pioneered by the group of Andrés Aguilera in Sevilla, Spain). Based on recent studies in yeast and viral systems, another emerging feature of RBP function may be that these proteins are themselves controlled by increasing or decreasing levels of transcripts, not unlike the recently documented sponging effects of noncoding RNAs on miRNA function.The last 20 years have witnessed a convergence of efforts aimed at understanding how genes produce biological complexity. Although our knowledged of the diversity of these molecular mechanisms is guaranteed to expand, let us hope that this quest will be more rapid than in other fields; in 2011, 10 years after the human genome was sequenced, more than 75% of protein research focused on the 10% of proteins that were known before the genome was sequenced (based on an analysis by Aled Edwards in Toronto, Canada).Projecting what the field will look like 20 years from now is an uncomfortable exercise, in part because our funding agencies have trained us not to plan more than five years in advance. When the pre-mRNA has been transcribed from the DNA, it includes several introns and exons. Following the initial success of using complex sets of known regulatory elements to identify tissue-specific regulatory programs (Ben Blencowe and Brendan Frey groups in Toronto, Canada), future efforts aimed at uncovering the splicing code will undoubtedly evolve to integrate data from transcription elongation speed, signaling input, levels of RBPs and transcripts that compete for their binding.Another challenging area deals with repetitive or repeat-derived sequences which constitute more than 50% of the human genome. Because the biological functions of at least one-third of these RBPs are unknown or were inferred from homologs, we can anticipate that many more RBPs will be implicated in splicing control. The current limitations of RNA sequencing technologies have prevented an assessment of the contribution of most repetitive elements, including the highly polymorphic minisatellites (VNTRs), to the function of splice variants and to biological complexity. Alternative splicing is an integral component of biodiversity.

method cells use to create many proteins from the same strand of DNA Another critical task is to continue describing the role of alternative splicing in disease and aging, and how the production of splice variants is modulated by our environment, including our microbiomes.

Interestingly, alternative splicing is also prevalent in testis, and gene expression profiles exhibited by brain, cerebellum, and testis are most similar to each other as compared with other tissues. Although most cases involve elements and factors bound in the immediate vicinity of the regulated splice sites, additional molecular strategies may soon include many more examples of longer range interactions mediated by proteins, and possibly stabilized by higher order structure of the pre-mRNA, or vice-versa.

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rules for alternative splicing