Ultraviolet screening by slug tissue and tight packing of plastids protect photosynthetic sea slugs from photoinhibition.

One of the main mysteries regarding photosynthetic sea slugs is how the slug plastids handle photoinhibition, the constant light-induced damage to Photosystem II of photosynthesis. Recovery from photoinhibition involves proteins encoded by both the nuclear and plastid genomes, and slugs with plastids isolated from the algal nucleus are therefore expected to be incapable of constantly repairing the damage as the plastids inside the slugs grow old. We studied photoinhibition-related properties of the sea slug Elysia timida that ingests its plastids from the green alga Acetabularia acetabulum. Spectral analysis of both the slugs and the algae revealed that there are two ways the slugs use to avoid major photoinhibition of their plastids. Firstly, highly photoinhibitory UV radiation is screened by the slug tissue or mucus before it reaches the plastids. Secondly, the slugs pack the plastids tightly in their thick bodies, and therefore plastids in the outer layers protect the inner ones from photoinhibition. Both properties are expected to greatly improve the longevity of the plastids inside the slugs, as the plastids do not need to repair excessive amounts of damage.

PSI Photoinhibition and Changing CO2 Levels Initiate Retrograde Signals to Modify Nuclear Gene Expression.

Photosystem I (PSI) is a critical component of the photosynthetic machinery in plants. Under conditions of environmental stress, PSI becomes photoinhibited, leading to a redox imbalance in the chloroplast. PSI photoinhibition is caused by an increase in electron pressure within PSI, which damages the iron-sulfur clusters. In this study, we investigated the susceptibility of PSI to photoinhibition in plants at different concentrations of CO2, followed by global gene expression analyses of the differentially treated plants. PSI photoinhibition was induced using a specific illumination protocol that inhibited PSI with minimal effects on PSII. Unexpectedly, the varying CO2 levels combined with the PSI-PI treatment neither increased nor decreased the likelihood of PSI photodamage. All PSI photoinhibition treatments, independent of CO2 levels, upregulated genes generally involved in plant responses to excess iron and downregulated genes involved in iron deficiency. PSI photoinhibition also induced genes encoding photosynthetic proteins that act as electron acceptors from PSI. We propose that PSI photoinhibition causes a release of iron from damaged iron-sulfur clusters, which initiates a retrograde signal from the chloroplast to the nucleus to modify gene expression. In addition, the deprivation of CO2 from the air initiated a signal that induced flavonoid biosynthesis genes, probably via jasmonate production.