Tuesday, 27 May 2014

Movie Science : X-men days of future past

I'm sure I've mentioned it before but the X-men cartoon and comics of the 90s probably bare a lot of the blame for me being a biologist. As such I still have a soft spot for them and was very impressed when I came out of the cinema having watched the latest instalment "Days of Future Past". Yes. I'm a big fan of the original comic storyline as well.

In terms of the science, I just have to accept that "mutant" is a license to do whatever you want, biology and physics be damned and I'm not complaining when it looks so cool. What I did find curious though was a bit of genetics in the film in which a character said they could detect people who could have mutant children or have grandchildren that could be mutants. This got me thinking, the films and comics often refer to a gene called the "x-gene" which seems to be the super awesome gene that results in all the mutant powers. I'm guessing it must be a transcription factor. The fact humans can have mutant children means the mutation is either spontaneous (a random mutation in the parent's germ line) or recessive (the mutant has to have two x-genes to be a mutant). But the grandchildren thing strikes me as odd because if it is recessive then you wouldn't necessarily have to wait an extra generation to get the mutant child. Unless two separate recessive mutant genes are required eg "x-gene" and "Z-gene". This might help explain why the mutants are so rare as well as the major variety in powers (maybe the other Z-gene encodes an epigenetic remodelling factor?).
That or the screenwriters didn't really consider the genetic implications of that sentence. In true Marvel tradition I'm providing a "no-prize" in case they need let off the hook.

If the genetics didn't make any sense on first read, hopefully this diagrams will help. Be warned it gets far too geeky from here on out.

Saturday, 10 May 2014

Mutant Fail

This song pretty much sums up the discovery I made on Friday.

Basically the Drosophila mutant I have (and have been performing various experiments with) is still being expressed, Which isn't great news when you've been assuming it is a null mutant (a mutation with no expression of functional protein).
The mutant is missing the first two exons and has lost it's original start (ATG) site but annoyingly it has chosen to pick up an alternate start site. This gets more tricky as there are two that are close together


If it has picked the first one then I should still be ok as it is out of frame has 8 nonsense amino acids and then hits a STOP codon. The problem is that the second one is in frame and would happily make the remainder of the protein that contains at least one domain that is vital to its function.
The unfortunate thing is that I have no way of telling which start site is being used without an antibody (which I don't have). If anyone knows of a way to do so - I'm all ears. The best I can come up with is to clone the mutant cDNA into a GFP vector and see what is expressed. Not a great experiment as the only thing it can confirm is whether a truncated protein is being produced,

Ultimately I need to make a genuine null mutant which is what my priority has to be. Somewhat worrying with 11 months left on my contract but I may as well get on with it.

In an attempt to see a positive in this revelation - it may at least explain the lack of a phenotype in the mutant I have been using. Maybe the real deal will have a phenotype that rewards the mutant making!