One way that alu sequences are recruited into the functional genome is through a process called exonization.
Lei and Day explain that alu elements actually contain enhancer sequences that facilitate this process.
Ha¨sler and Katharina Strub explain that many alus are found within coding regions of genes. They get there through exonization. This can happen when an alu is inserted in the middle of an intronic region resulting in a new exon. There are several possibilities for alternative splicing in this scenario. Perhaps only the alu sequence itself is included in the new exon or the portion of the intron upstream or downstream could potentially be included. Not all potential splice sites are employed at the same frequency. This is evidence of selection shaping how these genes are alternatively spliced. Another interesting thing is that in every case, some kind of alternative splicing occurs in every gene that contains an exonized alu. The addition of a new exon into a gene would probably involve a frameshift and would be presumably deleterious. So, perhaps unless the original gene is preserved through alternative splicing any new configuration is eliminated through selection.
The exonization process depends on multiple subsequent mutations. These have been mapped out in some cases by Singer and Shmitz in their paper: From Junk to Gene. I wasn't able to look at the whole article yet, because I am waiting for the interlibrary loan but they actually map out the exact sequence of steps involved in the exonization of some particular alu sequences which is pretty amazing.
Since exonization events depend on multiple successive mutations and almost all of the time there will be no benefit for the organism there would need to be a large pool of proliferating alus to draw from in order to explore all of the possibilities. The human genome contains over a million such sequences.
Another area I have been reading about is in the role of alus in RNA editing. Eisenberg explains that in addition to sometimes changing the products of mRNA transcripts, RNA editing may subtly effect the stability of the RNA molecule which in the end would effect expression.
Mattick links alu sequences to the function of memory formation in the human brain. He points out that the ADAR2 protein which is involved in RNA editing binds to alu sequences. ADAR2 is linked to cell signaling pathways involved in memory formation. Mattick believes that this may be a way that an organisms environment and an individual's experiences can shape the way memories are formed.
Gommans and Maas describe RNA editing in terms of evolvability. They argue that selection may favor systems with high levels of diversity and that the drive toward complexity may arise from the need to keep selfish elements under control. They argue that the more complex an organism is, the more resilient it is against the effects of RNA editing. This inevitably leads to tolerance and proliferation of alus that induce RNA editing. This new editing increases the complexity of the organism even more which results in a feedback loop of ascending complexity.
The debate about how much of the noncoding genome is functional is fundamentally misguided. In the case of transposable elements in general and alus in particular, all are in some sense evolutionarily successful or they would not be there at all. But are they functional? I suppose it depends on your perspective. I am reminded of Lane's musings on the troubled birth of the individual. While they generally share the same interests, even the cells in our own body cannot cooperate without mechanisms in place to force them into compliance. All of the genes and other elements in the genome also have a strong incentive to cooperate because if the organism dies then none of them are passed on. But, all elements in the genome must balance these common interests with their own individual interests and unlike rebellious cancerous cells which will never break free, selfish genetic elements are free to evolve and explore ways to pass themselves on. To survive, all elements in the genome must find ways to pass themselves on. So, if a transposable element is recruited by natural selection to perform some function, this element has not lost some kind of battle. From it's perspective, this is the best thing that can happen as being recruited to a task grants the element job security. The same thing happens when a protein coding gene is duplicated. The newly spawned gene must contribute something useful or risk being thrown out by natural selection. Whether you think of the individual in terms of a colony of cells or a group of genes, nothing noteworthy, beautiful or complex can arise without some kind of conflict among the constituent parts. Natural selection does not just magically push life toward complexity. Conflict in the genome isn't about "parasitic" sequences "invading" the genome. Rather, it is about millions of elements cooperating, if reluctantly, to form a cohesive whole. Without conflict, natural selection would have nothing to work with at all.
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