10/ This suggests the idea that transgenerational effects are can be just a delayed cost of intergenerational benefits. We discuss a TE/small-RNA-based “multigenerational trade-off” hypothesis that could generate these patterns and reconcile previous work. The end.

9/ Result: the genotype with short-term F1 gains but F3 costs can still win and nearly fix in the population, because selection mostly “sees” the immediate advantage before the debt comes due

6/ Then we looked at great-grand-offspring (F3).
Here, the story flips
Descendants of starved ancestors showed:
⬇️ lifetime reproduction
⬇️ λ
⬇️ survival
The F1 benefits are paid for by F3

5/ But their direct offspring (F1) did surprisingly well – regardless of whether they were starved or well-fed:
⬆️ reproduce earlier
⬆️ higher λ
⬆️ better survival in at least some environments
Short-term starvation of parents - better offspring - looks like starved parents invest more per offspring

4/ First, the obvious: starved worms (P0) paid a price
⬇️ lifetime reproduction
⬇️ rate-sensitive fitness λ
⬇️ survival
Reproduced later, produced fewer offspring overall

3/ We looked intergenerational and transgenerational effects of larval starvation in C. elegans

1/ Evolutionary trade-offs between intergenerational and transgenerational fitness effects

Transgenerational / intergeneration fitness effects can be adaptive, but they can also trade-off with each other:

New work led by Isaac Harris, preprint:

tinyurl.com/yp2b6tjm

4/6
Our analytical model shows DR-driven lifespan extension evolves because DR suppresses fertility—this strengthens selection against mortality compared to full feeding environment

Works with different genes acting in different environments, or when gene expression differs between environments 📉

2/6
Classic theories say dietary restriction (DR) extends life by shifting resources from reproduction to survival or improving cellular housekeeping.

But we tricked C. elegans into reproducing under DR (using food odour). Surprisingly, their survival stayed just as high!

Why does eating less extend lifespan? 🧬

Mutation accumulation underpins evolution of lifespan extension by dietary restriction

We often think about saving energy or recycling waste - but we show how evolution acting on mutation load can generate longer life on low food 🧵

🔗 tinyurl.com/jn5ryhxv

We consider both ‘hyperfunction’ and ‘hypofunction’ routes for the evolution of ageing and suggest that both are equally likely but there is not enough empirical data yet to make strong conclusions regarding the relative importance of either route 4/5

We suggest DST and DTA make unique testable predictions, and while DST is a special case of AP, DTA is broader, and ageing evolves under DTA via both MA and AP alleles 3/5

We discuss the relationships between ‘ultimate’ population genetic theories such as Mutation Accumulation (MA) and Antagonistic Pleiotropy (AP), and ‘proximate’ Disposable Soma theory (DST) and DTA and propose a general hierarchical model from genes to vital rates 2/5

Why do organisms age? We attempted to present a unified overview of evolutionary genetic and physiological theories of ageing, with a focus on emerging evolutionary physiological theory – developmental theory of ageing (DTA): bit.ly/4c59xiG  1/5

Germline removal increased stress resistance in both sexes, but increased lifespan only in males, and only when high costs of mating were excluded (above). Germline removal reduced growth but more so in females. Germline maintenance seems costlier for males than for females. 2/2

How does germline removal affect lifespan in females and males? There are theoretical arguments to suggest that germline is more costly to maintain in males, we tested this in C. remanei 1/2: www.biorxiv.org/content/10.1...

Germline mutation rate is elevated in young and old parents in Caenorhabditis remanei
academic.oup.com/evlett/advan...