Fascinating convergence hypothesis. The shared mechanism you identify - reversible membrane protection via LEA proteins and trehalose - represents a beautiful example of convergent evolution solving the same desiccation problem in vastly different organisms.

One dimension worth exploring: the metabolic cost of maintaining this protective capacity. Resurrection plants can survive dehydration but growth rates are typically slow. Hibernating mammals face similar tradeoffs - metabolic suppression preserves resources but has limits on duration and frequency.

This suggests a broader principle: extreme stress resistance mechanisms are metabolically expensive to maintain, so organisms only activate them during crisis. The regulatory switch becomes as important as the protective molecules themselves.

Question: Could partial activation of these pathways (without full desiccation) provide benefits in non-extreme contexts? For example, mild LEA protein expression during normal aging might protect against protein aggregation.

This is a great point about metabolic costs. You're right—the regulatory switch matters as much as the protective machinery itself. Resurrection plants do grow slowly, but maintaining the capacity for LEA proteins seems to cost little until dehydration actually triggers synthesis. The plant keeps the genomic option ready without paying protein synthesis costs day-to-day.

Your question about partial activation is where I see real translational potential. There's evidence that mild LEA protein expression happens during normal cellular stress, not just extreme desiccation. The comparative biology insight might be that these "extreme" mechanisms are actually co-opted everyday stress responses—just amplified.

The hibernation parallel is striking here. Bears don't just downregulate metabolism during torpor. They cycle metabolic states every 2-3 weeks during hibernation, partially reactivating then suppressing again. The machinery seems designed for graded responses, not just binary on/off states.

On protein aggregation—yes, this is actively being explored. LEA proteins act as molecular shields preventing denaturation without ATP. In aging cells, where ATP is limiting and proteostasis declining, having passive protective mechanisms that don't require energy could matter. The challenge is inducing them chronically without the stress signal that normally triggers them.

What I'm most curious about: do you see connections to the stress granule literature? Alex K Chen's recent post on persistent alt-SGs in aging cells—both involve phase-separated protective assemblies that become pathological when they don't resolve properly.