Are you saying that you had three C13's, one normal and two rings, and only one of the rings underwent apoptosis?

No, Our karyotype shows 46 XX ring13, and we can found extra 13 matterials in the apoptic body.

We just only found apoptic body in the interphase cell, but no anyone in the metaphase cells

Could failure of the chromosomal piece to migrate during mitosis lead to localized apoptosis?

I think it is genetic problem, other than enviroments cause. the abeeration of the chromosome 13 self is the most probability

Thanks stephen mentions

this is an interesting phenomenon.. thanks for reporting it here. Please do update if you come across progress on this topic.

I am aware of elimination of chromosomes in hybrid plants during male meiosis (i guess Brachiaria sp.). but never herd about the apoptosis of single chromosome. this is something new and interesting. all the best "Xianfu Wang"

By localised apoptosis in interphase cells, do you mean the presence of a micronucleus containing chromosome 13 material?

Is this a human patient with an abnormal phenotype? If the case, wouldn't the r(13) have stabilised, giving you a normal 13 and your ring. This makes sense. I guess you have then cultured the material to get metaphase cells, and is it then that you see the apoptotic (?) bodies carrying the chromosome 13 material? Can you describe you FISH findings in a little more detail? How many cells have these additional bodies, and where exactly are they located in the context of the interphase cell structure. What FiSH probes did you use? Centromeric, paints, etc? It is difficult to help without more details.

Could be very interesting though.

In the Pacific oyster Crassostrea gigas, somatic aneuploidy is a rather frequent phenomenon. up to 30% of gill cells can show one more missing chromosomes (2n= 20 in this species). This is not e random phenomenon as chromosome 1, 9, and 10 are preferably lost. See Leitão A, Boudry P, Thiriot-Quiévreux C (2001). Evidence of differential chromosome loss in aneuploid karyotypes of the Pacific oyster Crassostrea gigas. Genome 44 (4) : 735-737.

The mechanisms underlying this phenomenon are unknown.

Thanks for Jon Strefford is interesting in this case. sure. it is a human patient with a abnormoal phenotype. General karyotype shows a 46XX Ring 13. But when we did aCGH, we find 13q13 5mb gain and whole q mosaic gain. the aCGH data was not match the result of the karyotype. so we did FISH study for it. Metaphase cell always is 46xx ring13. it match karyotype fingdings. but we found near 40% of interphase cell has a extra 13q signal and near 15% interphase cell would envelope those signal and it was eliminated out of neuclea.

Thanks for Pierre Boudry's information. I think our case's problem may be telomere lacking of. ring 13 is stable, but if it can't form ring13 and lack of telomere, it's non-stable and will auto-apoptise. I'm trying to detect telomere sequnce of this segments by seqencing and FISH.

Lagged during mitosis chromocomes (as a rule abnormal -acentics, dicentrics) can form separate micronuclei. Micronuclei will auto-apoptise. This is one of the variant micronuclei elimination in cells.

What is the patern on a interphase fish? can we see the abnormal chromosome rejected?

It make me think about some isoparental disomy, when a zygote cell with a trisomy reject one of the extra chromosome, then... we may have two chromosome from the same parent, and it lead to some pathology. (If my plants hybrids could do so in order to corect aneuploidy, it would be great)