In the remaining questions section, to test whether the elongated telomeres in lab mice is an adaptive response to the breeding protocol rather than merely a fluke, I would be in favour of adding:
6) Confirmation that the same breeding protocol affects other species than Mus musculus as would be expected under evolutionary theory by causing elongated telomeres and increased rates of tumours relative to their wild conspecifics (e.g. laboratory rats).
7) Identification of locus on which selection is acting in laboratory-bred animals (e.g. hightened systemic expression of telomerase)
8) Does experimentally reducing telomere length (e.g. by inhibiting the expression of telomerase) rescue the 'wild type' phenotypes of reduced tolerance to toxins and higher resistance to tumours?
Jax Lab on "Telomere length in mice" in July 2020
There seems to be only that one "News and Insights" post about this topic since the ep19 aired, so we might consider it somewhat as a rebuttal, esp. because the JRE episode aired in mid-June. Curios wording there (bold by me):
… Greider … observed more than 20 years ago that telomeres in some inbred mouse strains are significantly longer than they are in some wild species. The data indicated that telomere length isn’t a major factor in determining how long the mice live. But some researchers inferred that inbred laboratory strains, because of their controlled breeding regimens and other factors, had developed longer telomeres over time. If true, that inference had the potential to skew cancer and aging research data and the quality of the drugs and therapies ultimately produced based on mouse experiments.
How do you know the assumptions are wrong?
… Length is not determined by whether a mouse is inbred or wild-derived, and it is not affected by how long an inbred strain has been domesticated. … as Greider hypothesized 20 years ago, telomere length does not predict lifespan.
Am I seeing ghosts here, or do they:
- present the details of who "inferred" and who "observed" in the opposite order as presented by the Weinsteins?
- label the "potential to skew … quality of the drugs" as a wrong assumption, without clear arguments (or links to data)?
- end their line of argument by taking down a strawman?
- lead the reader into a longevity and cancer discussion, away from the Weinsteins' (IMHO more important argument) "mice models underestimate chronic drug toxicity" argument?