Here are my notes on the Titia De Lange, Vicki Lundblead, and Elizabeth Blackburn book TELOMERES (2nd Edition).
From Chapter 5, Modeling Cancer and Aging in the Telomere-Deficient Mouse (Chapter contributed by Wong (Harvard), Chang, and DePinho (Harvard).
After describing how mice null for the telomere transcription gene were created
Telomere length determination in mTerc -/- mice confirmed a steady decline in telomere length at a rate of approx 120 base pairs per cell division, a rate analogous to the attrition rate in primary human cells lacking detectable telomerase.
They developed mice with shorter and shorter telomeres to examine what happens near the "end game."
... revealed chromosomal end-to-end fusion with loss of telomere repeats at the junction , in accord with significant reductions in telomere length in this model.
Subsequent analysis established a link between telomere dysfunction and complex cytogenetic rearrangements, including non reciprocal translocations - a common feature of human cancer.
Subsequent random breakage will generate broken chromosomes in the daughter cells capable of fusing to other free chromosomal ends.. (me evolutioin?)
It appears that decline in telomere length, rather than absence of telomerase activity per se, is the most important parameter dictating chromosomal integrity ..
These results further highlight the fact that telomerase persevere genome stability primarily by maintaining telomere structure and averting (damage)...
The late generation mTerc -/- males experienced progressive marked testicular atrophy, stemming from apoptopic germ cell depletion, and ... Females showed a decrease in the number of oocytes on ovulation and impaired capacity of most fertilized embryos to progress beyond early development.
Reconstitution of telomerase activity in later-generation mTerc -1- mice increases telomere lengths preferentially at the shortest telomeres, and is associated with the striking rescue of pathologies associated with telomere dysfunction.