Category Archives: alu

The SRP, Alu Elements, and Nudging


I’ve combined the essays about the signal recognition partcle, Alu elements, cytosine deamination, all connected by front-loading. All 11, 465 words of it.
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Alu Behind Learning and Memory?

I’ve been wanting to comment on this article by Mattick and Mehler, but have just been too busy. Luckily, I just ran across a web article that borrows heavily from M&M’s article. I would encourage you to read the whole thing (if you can’t get your hands on M&M’s article, that is). Here are some excerpts:

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More Alu on the Brain

RNA editing, DNA recoding and the evolution of human cognition.

Mattick JS, Mehler MF.

Trends Neurosci. 2008 May;31(5):227-33.

RNA editing appears to be the major mechanism by which environmental signals overwrite encoded genetic information to modify gene function and regulation, particularly in the brain. We suggest that the predominance of Alu elements in the human genome is the result of their evolutionary co-adaptation as a modular substrate for RNA editing, driven by selection for higher-order cognitive function. We show that RNA editing alters transcripts from loci encoding proteins involved in neural cell identity, maturation and function, as well as in DNA repair, implying a role for RNA editing not only in neural transmission and network plasticity but also in brain development, and suggesting that communication of productive changes back to the genome might constitute the molecular basis of long-term memory and higher-order cognition.

Alu Mania

I’ve been talking about Alu elements for weeks now, so I was going to try to change the topic.  But alas, I can’t stop myself.  Here is some more Alu Fun for those similarly intrigued by the manner in which these nifty reformatting devices can facilitate evolution.

First, here is a decent video that outlines the basics of Alu retrotansposition.

Second, remember how it has become clear that the genome has a three-dimensional architecture?

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Nudging the nudge

We have seen that the Alu element is poised to generate binding sites for multiple transcription factors involved in development.  Even more interesting is the manner in which the process of cytosine deamination can easily create several of these transcription factor binding sites.  It’s as if we have two nudges, working together, to facilitate the evolution of primates.

Yet there is more to the story.  Recall that the cytosine deamination events occur at CpG sites.This is simply where a cytosine (C) is followed by a guanine (G).  Why is this?

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It just doesn’t stop!

The title of yet another paper speaks for itself: Alu elements contain many binding sites for transcription factors and may play a role in regulation of developmental processes (Paz Polak and Eytan Domany. BMC Genomics. 2006; 7: 133).

Let’s look at the abstract.

This research suggests that evolution used transposable elements to insert modules of transcription factor binding motifs into promoters and, by means of their presence, assemble higher level regulatory networks. In order to explore this question we focused on Alu elements, which are good potential candidates to be part of the building blocks of regulatory networks for two reasons. First, Alu elements are abundant in the upstream region of the TSS of genes, and second, Alu elements contain dozens of putative BSs for TFs. Some of these BSs were found before and their association with Alu was also reported, whereas in some cases although the BSs were found, the fact that they reside on Alu went unnoticed. Finally, we list here also BSs on Alu that were not identified previously. Our findings imply that the biological pathway on which Alu-mediated regulation appears to have the most significant impact is the development process. Many of the TFs that have binding motifs on Alu are associated with development; moreover, some of these BSs were previously demonstrated to be functional in vivo and essential to regulation of some target genes.

TF stands for transcription factors, proteins that bind to specific DNA sequence to activate the process of gene expression.  TSS stands for transcription start site, the precise point at which the copying of the DNA into an RNA format begins.  BS stands for binding site, the region of the DNA that binds with the transcription factors.

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You too, p53?

p53 has been called the “Guardian of the genome” and is commonly known as a tumor-suppressor gene – a gene that suppresses the formation of cancer.  Normally, the cell expresses low levels of the p53 protein, but if the genome is damaged, p53 levels rise and in turn activate several programs that will arrest the cell cycle and attempt to repair the DNA damage.  If the genome cannot be repaired, p53 will then activate programmed cell death and the cell will die rather than pass on the damage to future generations.

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