I actually did a short research rotation in Jon Widom's lab at the beginning of grad school, 3 years ago. If anyone has any more specific questions regarding the implications of this work, let me know and I'll post something useful.
As the point of this article seems to be for the general enrichment of the/. community with respect to the state of biological sciences, I'll point out an interesting related point.
Genetically engineered knockout mice have existed for nearly 20 years and have been in common usage for more than a decade. While generally extremely useful, knockout mouse technology is limited by the fact that some genes are necessary for survival during development, and hence can't completely knocked out.
The ingenious solution to this problem is to use a variety of genetic tricks to make mosaic mice that are genetic knockouts only in certain tissues. This is accomplished by incorporating special recombination sequences in the DNA flanking your gene of interest. You also integrate a foreign gene encoding a viral-derived recombinase gene that will effectively excise any DNA sequence flanked by the aforementioned recombination sequences. You drive the production of this recombinase gene only in the adult mouse (often in a particular tissue, such as the ear) by including "promoter" sequences upstream of the recombinase that activate transcription only in the tissue of interest.
It's often disappointing for me to read these news releases about 20-year old technology, much in the same way it would be aggravating for many of you to read about the release of a powerful new programming language called Python. Except knockout mice have been around for longer.
Actually, it's a misrepresentation to assume introns are 'parasitic.' There's a good amount of speculation these days that introns actually confer an enormous selective advantage on their bearers, because they could facilitate 'swapping' of exons between genes during replication in a way that permits new genes to arise. Imagine this scenario:
Consider two hypothetical genes with exons "A,B" and "C,D" interspersed by introns "o" with some degree of sequence similarity.
AAAAAAAAoooooooooBBBBBB
and
CCCCCCCCoooooooooDDDDDD
during cell division, the genes are duplicated and some "crossing over" (that is, homologous recombination) occurs between strands in a way that is facilitated by similar sequence. As a result, one copy each of genes "A,B" and "C,D" swap exons and become "A,D" and "C,B"
AAAAAAAAoooooooooBBBBBB
X crossing over of homologous strands
CCCCCCCCoooooooooDDDDDD
Voila! You now have two new genes. Considering the fact that exons are often generalized as acting as discrete, independent units once they are translated into two proteins, you've created two new proteins with a potentially meaningful switcheroo in function. In this way, new proteins can evolve by swapping independent modules.
So don't knock the introns.
At first blush, GeneDesign 2.0 offers nothing over the long-available, free, web-based or local-mirrorable Sequence Manipulation Suite 2 at http://bioinformatics.org/sms2/. When I start on a molecular bio project, I use a mix of SMS2, BLAST, NEB cutter, IDT's web-tools, and other free online tools to accomplish everything I need, and keep track of my thought process in a simple Word document. This suite adds no functionality I don't have free access to already elsewhere.
Slashdot Mirror
I actually did a short research rotation in Jon Widom's lab at the beginning of grad school, 3 years ago. If anyone has any more specific questions regarding the implications of this work, let me know and I'll post something useful.
As the point of this article seems to be for the general enrichment of the /. community with respect to the state of biological sciences, I'll point out an interesting related point.
Genetically engineered knockout mice have existed for nearly 20 years and have been in common usage for more than a decade. While generally extremely useful, knockout mouse technology is limited by the fact that some genes are necessary for survival during development, and hence can't completely knocked out.
The ingenious solution to this problem is to use a variety of genetic tricks to make mosaic mice that are genetic knockouts only in certain tissues. This is accomplished by incorporating special recombination sequences in the DNA flanking your gene of interest. You also integrate a foreign gene encoding a viral-derived recombinase gene that will effectively excise any DNA sequence flanked by the aforementioned recombination sequences. You drive the production of this recombinase gene only in the adult mouse (often in a particular tissue, such as the ear) by including "promoter" sequences upstream of the recombinase that activate transcription only in the tissue of interest.
It's often disappointing for me to read these news releases about 20-year old technology, much in the same way it would be aggravating for many of you to read about the release of a powerful new programming language called Python. Except knockout mice have been around for longer.
Actually, it's a misrepresentation to assume introns are 'parasitic.' There's a good amount of speculation these days that introns actually confer an enormous selective advantage on their bearers, because they could facilitate 'swapping' of exons between genes during replication in a way that permits new genes to arise. Imagine this scenario: Consider two hypothetical genes with exons "A,B" and "C,D" interspersed by introns "o" with some degree of sequence similarity. AAAAAAAAoooooooooBBBBBB and CCCCCCCCoooooooooDDDDDD during cell division, the genes are duplicated and some "crossing over" (that is, homologous recombination) occurs between strands in a way that is facilitated by similar sequence. As a result, one copy each of genes "A,B" and "C,D" swap exons and become "A,D" and "C,B" AAAAAAAAoooooooooBBBBBB X crossing over of homologous strands CCCCCCCCoooooooooDDDDDD Voila! You now have two new genes. Considering the fact that exons are often generalized as acting as discrete, independent units once they are translated into two proteins, you've created two new proteins with a potentially meaningful switcheroo in function. In this way, new proteins can evolve by swapping independent modules. So don't knock the introns.
At first blush, GeneDesign 2.0 offers nothing over the long-available, free, web-based or local-mirrorable Sequence Manipulation Suite 2 at http://bioinformatics.org/sms2/. When I start on a molecular bio project, I use a mix of SMS2, BLAST, NEB cutter, IDT's web-tools, and other free online tools to accomplish everything I need, and keep track of my thought process in a simple Word document. This suite adds no functionality I don't have free access to already elsewhere.