Uncovering the functional basis of the reversal of the fecundity/longevity trade-off in a termite

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Reversal of the fecundity/longevity trade-off evolved several times independently with sociality. This provides strong support for the hypothesis that sociality, fecundity and lifespan influence each other during evolution. Our molecular results from the first funding phase indicate convergent evolution at the pathway level. For all studied species, we identified caste-specific, age-related changes in the network along the TOR (target of rapamycin)/IIS (insulin/insulin-like growth factor1 signalling) - juvenile hormone (JH) axis that affects pathways linked to lifespan and fecundity (the TI-J-LiFe network for TOR/IIS-JH-Lifespan Fecundity). Yet details seem to differ between species. In addition, we found for termites a strong signal of age-related transposable element (TE) activity, which we did not detect in the social Hymenoptera. These ‘jumping genes’ have long been hypothesized to play a role in ageing in animals and recently a causal link has been demonstrated. During the second funding phase, we aim to analyse the identified mechanisms in more detail by performing functional experiments in a termite to reveal pathways and networks underlying ageing and the apparent reversal of the fecundity/longevity trade-off. By doing this in termites, we will study the oldest social insects and the largest lineage outside the Hymenoptera that evolved eusociality. We have three Objectives:In a common effort shared across all projects in Focus B ‘Regulators’, we will investigate in Objective 1 the role of protein availability for queen fecundity. In doing so, we will focus on the TOR part of the TI-J-LiFe network. We will test the hypothesis that additional protein increases the fecundity of queens. By undertaking a food-supplement experiment, we will analyse how queen and worker longevity are affected by additional protein sources. Based on results from the first funding phase, we will test in Objective 2 the hypothesis that a change in the regulation of FOXO by Akt in queens can account for an upregulation of IIS signalling without negative consequences on FOXO and its downstream pathways. Here we will concentrate on the IIS-JH-Vitellogenin part of the TI-J-LiFe network. Objective 3 will test the hypothesis that TE activity and caste-specific TE silencing mechanisms contribute to explain longevity differences between queens and workers and the reversal of the fecundity/longevity trade-off. Our studies we will offer insights into mechanisms of ageing and the reversal of the fecundity/longevity trade-off that will help to reveal molecular constraints and lineage specific idiosyncrasies.