In article <1998Aug20.123428.29969 at jarvis.cs.toronto.edu>, bae at cs.toronto.edu
says...
>>In article <6rh6dv$qug$1 at ostrich.cybercomm.net>,
>Jennifer Ann Petersen <jennifer at jenniferpetersen.com> wrote:
>>Beverly Erlebacher wrote in message
>><1998Aug19.135543.14736 at jarvis.cs.toronto.edu>...
>>>Note that the telomerase knock-out mice had normal life spans for *six*
>>>*generations* of steadily decreasing telomere length. THe only apparent
>>>effect was that the sixth generation was sterile.
>>>>What did the mice die from?
>>I don't remember if the paper said, but the important point is that the
>life span was no different from that of the mouse strain that the knock-out
>line originated from. I don't know what lab mice normally die of. Boredom?
This paper gives some insight into cause of death in mice, Nippon Eiseigaku
Zasshi 1996 Jul;51(2):569-578 "[Senescence-accelerated mouse (SAM): with
special reference to
age-associated pathologies and their modulation]".
Actually mus musculus and some other mice have an alternative mechanism for
regulating telomeric length, (Proc Natl Acad Sci U S A 1998 Jul
21;95(15):8648-8653 "Telomere length regulation in mice is linked to a novel
chromosome locus.")
No valid conclusions regarding telomeric shortening and life span can be
drawn from this study. Other studies determining the effects of the gene(s)
from chromosome 2 and their interaction with both telomerase and the
telomeres need to be conducted to help sort out how telomeric length is
regulated.
Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.
http://home.earthlink.net/~excelife/index.html
