Why doesn't the ovarian clock move when the somatic clock does? Germline mitochondrial maintenance as the evolvable setting of reproductive lifespan: the dial hypothesis

Across mammals, maximum lifespan has proven evolutionarily flexible while female reproductive lifespan has not. In humans and in at least four lineages of toothed whales, menopause evolved through the extension of lifespan without any corresponding extension of reproductive span (Ellis et al. 2024), and comparative data across 49 mammal species show reproductive span rising with longevity and then levelling off (Huber & Fieder 2018). The adaptive literature explains why selection tolerates or favors post-reproductive life; it treats the fixity of the ovarian clock itself as an axiom. The mechanistic literature documents an elaborate system of mitochondrial quality control in the female germline, including a metabolic standby in dormant oocytes that keeps reactive oxygen species undetectable (shown directly in frogs and inferred in humans; Rodríguez-Nuevo et al. 2022) and no age-related increase in mitochondrial DNA mutations in human oocytes (Arbeithuber et al. 2025); it does not ask what sets this system's budget. That oocytes protect their mitochondria is well established. The question here is whether the level of that protection is what evolution tunes to set how long a species can reproduce. The dial hypothesis holds that germline mitochondrial maintenance, located in oocyte metabolic quiescence, mitophagy, and organelle-level selection rather than in bottleneck stringency, is the evolvable parameter that sets each species' ovarian expiry, and that menopause marks the completion of a maintenance program whose term selection can tune but has, in menopausal lineages, left at its ancestral setting while extending the soma. The hypothesis distinguishes itself from damage-accumulation accounts by predicting budget-like rather than wear-like signatures, defines the budget by measurable proxies, extends a constraint-based proposal by Monaghan & Ivimey-Cook (2023) into a selectable-parameter framework, proposes that the setting is tuned mainly through gene regulation, and yields five testable comparative and experimental predictions, including that chromosome cohesion decay, the leading rival mechanism, is itself downstream of mitochondrial housekeeping, and that the oocyte's DNA-damage checkpoint responds to mitochondrial state. Earlier accounts treat the term of the egg's mitochondrial protection as a fixed limit; the dial proposes it is an adjustable setting, tuned by selection separately from lifespan.