🚀 go-pugleaf

> 
> By the way, although mature sperm are haploid, the precursor cells
> aren't; permanent infertility shouldn't result from a system that
> attacks aneuploid cells. Mature eggs are diploid as far as I know, only
> "kicking" the second chromosome set upon fertilisation. I may be under a
> misapprehension there, though; anyone with more knowledge care to comment?
> 

I believe it to be the case. However, megakaryocytes are polyploid all
along. Killing all megakaryocytes would lead to death by haemorrage 
within a week or so.
As mentionned previously, dividing cells would pass through various
apparent states of aneuploidy, too, so there would have to be a way to
avoid killing them.
Lastly, chromosomic superstructures (like telomeres and centromeres, 
which would be the most obvious recognised features) are already used
for other functions (mainly regulation of the cell cycle, senescence
and apoptosis, but probably also as-yet-udiscovered roles). That is, 
for example, what prevent cells from undergoing division if they do 
not have 2 sets of chromatids (well, meiosis excepted). Or what 
triggers senescence. As stated upper in the thread, ploidy is already
one of the most tightly regulated feature in mammalian cells, so 
probably not the target of choice as any "sensor" system would have 
to not disrupt existing interactions. 
Tricky, and potentially very dangerous.
Sensing the deletion of specific antiocogenes or the duplication of
protooncogenes as you suggest would probably be safer.

-- 
PiLS