Sea Slugs Evolved a New Organelle to Steal and Power Photosynthesis in Animal Cells

For over a century, biologists have puzzled over how certain sea slugs maintain stolen chloroplasts—the photosynthesis machinery from algae—alive and active inside animal cells for up to a year without access to the algal nuclear genes that normally sustain them. This landmark study in Cell provides the first mechanistic explanation: a novel, host-derived organelle called the kleptosome.

Using the Sacoglossan sea slug Elysia crispata as their primary model, researchers first confirmed these animals survive starvation dramatically longer than the non-photosynthetic sea slug Aplysia californica (nearly four months vs. three to four weeks). Metabolic analyses showed both species activate normal starvation responses (mTOR inactivation, global transcriptional downregulation) within one week of food withdrawal, yet E. crispata maintains active chloroplast gene expression and intact thylakoid membranes throughout. Notably, slug-encoded nuclear genes show no upregulation of photosynthesis-support programs, challenging prior horizontal gene transfer hypotheses.

Click chemistry labeling of newly synthesized proteins in live slugs, followed by chloroplast isolation and proteomics, revealed that the vast majority of proteins associated with isolated chloroplasts were slug-derived rather than algal—and were enriched in endocytosis and phagosome markers, particularly Rab7a. This led to the discovery that each stolen chloroplast resides within its own distinct host-membrane-enclosed compartment. The researchers named these kleptosomes and confirmed their identity using membrane dyes and markers for phagosomes and phagolysosomes (P2X4, VHA, NPC-2, Rab7).

Whole-organelle patch-clamp electrophysiology demonstrated that kleptosomes possess an ion-impermeable membrane distinct from the porous outer chloroplast membrane, and that luminal ATP activates inwardly-rectifying currents via the P2X4 receptor. The slug's own P2X4 channel (eP2X4) was cloned, expressed heterologously, and shown to recapitulate native kleptosome electrophysiology. Critically, pharmacological blockade of P2X4 with 5-BDBD reduced net photosynthetic oxygen production by 62%, without affecting respiratory oxygen consumption, establishing that kleptosome ion channel activity directly supports chloroplast photosynthesis.

During prolonged starvation (beyond four weeks), slugs turn orange as chlorophyll autofluorescence disappears, photosynthesis ceases, and photosystem gene expression collapses. The team demonstrated this reflects active, lysosome-mediated digestion of chloroplasts—a process involving Rab7-positive kleptosome fusion with lysosomes—rather than passive decay. Fed slugs maintain kleptosomes with bright far-red chlorophyll fluorescence and intact thylakoid ultrastructure, while starved slugs show degraded chloroplasts accumulating near lipid droplets. Convergent evolution of this organellar system was identified in corals and anemones, broadening the biological significance of the findings.

This study reframes kleptoplasty not as an unresolved curiosity but as a bona fide, mechanistically grounded example of organelle evolution in real time—illuminating how host cells can domesticate foreign organelles for dual metabolic functions.