Figure 1

Evolution of the endomembrane system, mitochondrion, and eukaryote cell size. A - F. Model for evolution of the endomembrane system in response to imbalances in plasma membrane activities. Archaeal cells, containing co-translationally active ribosomes, are exposed to an environmental stressor (here exemplified by external H₂O₂, orange background, although UV radiation and/or desiccation may provide additional sources of stress). The plasma membrane was particularly affected by this external injury. As a result of the peripheral damage, a vesicle carrying molecular components (e.g., ribosomes) pinched off from the plasma membrane and accumulated in the inner cell, giving rise to the proto-ER. H₂O₂ that infiltrated the cell was cleared by enzymes (e.g., catalases and peroxidases). This generated a protected intracellular zone (white) that allowed proliferation of the proto-ER and associated ribosomes, while H₂O₂-damaged co-translational targeting gradually disappeared from the plasma membrane. Vesicular traffic, scaffolded by the incipient cytoskeleton (microtubule-organizing center and microtubules in red), emerged as an exocytic avenue to target ER-synthesized proteins to the plasma membrane (E and F). G - K. Putative model for early events in mitochondrial evolution. In a biofilm, archaeal and alphaprotobacterial cells are juxtaposed in a syntrophic association (arrows). Fusogenic and membrane remodeling activities necessary for cell-cell fusions during archaeal mating allowed the capture and retention of the alphaproteobacterium precursor of mitochondria. Environmental O₂ (blue background) penetrates the cells and is photo-activated to ROS by UV. Alphaproteobacterial aerobic respiration clears the intracellular O₂ (white zones). Intracellular mitochondria propagate and deliver ATP to the cytoplasm (J and H). Increase in cell size (E, F and J, K) emerges as a crucial eukaryotic strategy to counterbalance the influx of oxygenic species.