UC San Diego

Embryos develop in dynamic environments and are subject to myriad stressors – both biotic and abiotic. Among those stressors are encounters with pathogens and toxic molecules. The systems for sensing and responding to the environment include a robust suite of molecular machinery that protects the cell, and a heterogeneous population of immune cells that mount coordinated responses. Establishing a whole-animal echinoderm embryo model to address embryo-environment interactions and how stressors influence such systems is the focus of this dissertation work.

Accomplishing this task began with identifying a need for a sea urchin model species that grew more rapidly that other commonly used echinoderms, and establishing a comparable developmental staging scheme and culturing practices for rearing animals in the lab. The painted white urchin, Lytechinus pictus, was a clear choice for the optimal model.

Generating molecular tools was also essential, and yielded a fully sequenced genome with chromosomal resolution and transcriptomic tools pooled across developmental stages. To assess the quality of these molecular resources I annotated the suite of ATP-binding cassette transporters (ABCs). ABCs are expressed in, and play important roles in handling of toxic molecules as well as in the differentiation and migration of, immune cells.

In addition to the ABCs, I combed the genome for other components involved in immunity – including cytokines, transcription factors, enzymes, effectors, and signal mediators. This suite of annotations establishes a foundation of potential targets of exposure in the immune system. From there, I challenged sea urchin larvae with bacterial infection and characterized the first phenotypic responses of an echinoderm model of immunosuppression.

The outcome of this research is a series of tools and resources that open doors for future investigation. With a reliable, dose-dependent model of immunosuppression and complimentary molecular tools in a rapidly developing echinoderm species, it is now possible to address the influence of toxic molecules on whole-animal immune responses. It is also possible to investigate how early life exposures alter later life health or the health of subsequent generations. Finally, we can begin to tease apart the cross-talk of developmental and protective systems in the embryo contributing to environmental sensing and signaling.