The phrase "adaptable longevity" is correct and usable in written English.
It can be used to describe the ability of something to maintain its effectiveness or relevance over time while being flexible or adjustable.
Example: "The new software is designed with adaptable longevity, allowing it to evolve with changing user needs and technological advancements."
Alternatives: "flexible durability" or "versatile endurance".
In chronologically aging yeast, the TOR and cAMP/PKA signaling pathways are the two adaptable longevity pathways that govern the life-extending effect of CR [ 5, 6, 60- 62].
Such pathways may regulate yeast longevity irrespective of the number of available calories and may not necessarily overlap (or may only partially overlap) with the adaptable longevity pathways that are under the stringent control of calorie availability.
Synthesized by soil bacteria to inhibit growth of fungal competitors, this macrocyclic lactone provides longevity benefit to yeast, fruit flies and mice by specifically inhibiting TOR (Tor1p in yeast), a nutrient-sensory protein kinase that operates as a master negative regulator of the key adaptable longevity pathway [ 3, 4, 23- 25].
It is likely therefore that some longevity pathways could be "constitutive" or "housekeeping" by nature, i.e., that they: 1) modulate longevity irrespective of the organismal and intra-cellular nutrient and energy status; and 2) do not overlap (or only partially overlap) with the adaptable longevity pathways that are under the stringent control of calorie and/or nutrient availability.
It is plausible therefore that - similar to the proposed above anti-aging mechanism of LCA in yeast - rapamycin in fruit flies can modulate both the housekeeping (TOR-independent) and adaptable (TOR-dependent) longevity pathways.
Our analysis of how LCA influences various longevity-related processes and how it affects the CLS of yeast mutants impaired in the adaptable TOR and cAMP/PKA longevity pathways provided important new insights into mechanisms of longevity regulation, as outlined below.
Hence, one could envision that most, if not all, longevity pathways are "adaptable" by nature, i.e., that they modulate longevity only in response to certain changes in the extracellular and intracellular nutrient and energy status of an organism.
Consistent with our assumption that LCA extends longevity not by modulating the adaptable TOR pathway, lack of Tor1p did not impair the life-extending efficacy of LCA under CR.
Importantly, by eliminating a key nutrient-sensory protein kinase on which the adaptable TOR and cAMP/PKA pathways converge to regulate longevity in a calorie availability-dependent fashion, the rim15 Δ mutation abolishedthe dependence of the anti-aging efficacy of LCA on the number of available calories.
We propose that LCA unveils the anti-aging potential of PKA by activating PKA-dependent phosphorylation of the cytosolic pool of Rim15p, a key nutrient-sensory protein kinase on which the adaptable TOR and cAMP/PKA pathways converge to regulate longevity in a calorie availability-dependent fashion.
The Langendorff perfusion apparatus is highly adaptable and this is reflected not only in the procedure's longevity but also in the number of different applications to which it has been turned.
