Cell cycle maintenance and biogenesis of the Golgi complex

How organelle identity is established and maintained, and how organelles di vide and partition between daughter cells, are central questions of organel le biology. For the membrane-bound organelles of the secretory and endocyti c pathways [including the endoplasmic reticulum (ER), Golgi complete, lysos omes, and endosomes], answering these questions has proved difficult becaus e these organelles undergo continuous exchange of material. As a result, ma ny "resident" proteins are not localized to a single site, organelle bounda ries overlap, and when interorganellar membrane flow is interrupted, organe lle structure is altered. The existence and identity of these organelles, t herefore, appears to be a product of the dynamic processes of membrane traf ficking and sorting. This is particularly true for the Golgi complex, which resides and functions at the crossroads of the secretory pathway. The Golg i receives newly synthesized proteins from the ER, covalently modifies them , and then distributes them to various final destinations within the cell. In addition, the Golgi recycles selected components back to the ER. These a ctivities result from the Golgi's distinctive membranes, which are organize d as polarized stacks (cis to trans) of flattened cisternae surrounded by t ubules and vesicles. Golgi membranes are highly dynamic despite their chara cteristic organization and morphology, undergoing rapid disassembly and rea ssembly during mitosis and in response to perturbations in membrane traffic king pathways. How Golgi membranes fragment and disperse under these condit ions is only beginning to be clarified, but is central to understanding the mechanism(s) underlying Golgi identity and biogenesis. Recent work, discus sed in this review, suggests that membrane recycling pathways operating bet ween the Golgi and ER play an indispensable role in Golgi maintenance and b iogenesis, with the Golgi dispersing and reforming through the intermediary of the ER both in mitosis and in interphase when membrane cycling pathways are disrupted.