The architecture and evolution of host control in a microbial symbiosis

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

Endosymbiosis is fundamental to the origin of complex life, enabling evolutionary innovation and functional compartmentalization by the merger of once independent lineages into singular units. Endosymbiont cells live inside the cells of their host, and thus hosts have evolved to regulate and control their symbionts, but the underlying molecular mechanisms are not understood. In particular, how the architecture of host control has evolved to provide both ecological flexibility and evolutionary robustness is unknown.

We focus here on two newly discovered putative mechanisms of control that the host Paramecium bursaria (PB) uses to manipulate its Chlorella (CH) endosymbionts. Specifically, we hypothesise that the PB arginine-to-polyamine pathway acts as a provisioning-type positive control lever on endosymbionts, whereas the PB chitin processing pathway acts as a sanction-type negative control lever through endosymbiont digestion. We predict that such an integrated multi-layered host control architecture enables both precise modulation of endosymbionts by hosts (i.e., plasticity) and enhanced evolutionary robustness.

We test these ideas using RNAi knockdown experiments. We will knockdown either the PB arginine-to-polyamine pathway, the PB chitin processing pathway, or both, and measure the effects upon host growth, plasticity and fitness using established methods. In tandem, we will use a combination of photochemistry, RNAseq and LC-MS metabolomic analyses to understand the cellular impacts of disrupting host control on both PB and CH. We will use experimental evolution to understand the longer-term impacts of disrupting single or multiple control mechanisms for the symbiosis and mechanisms of compensatory evolution to mitigate deleterious effects of host control disruption. We will again use multi-omics methods to gain a detailed mechanistic understanding the molecular mechanisms enabling the evolutionary robustness of symbiosis.