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Review
. 2015 Dec 16:3:79.
doi: 10.3389/fcell.2015.00079. eCollection 2015.

Mechanisms and Regulation of the Mitotic Inheritance of the Golgi Complex

Affiliations
Review

Mechanisms and Regulation of the Mitotic Inheritance of the Golgi Complex

Carmen Valente et al. Front Cell Dev Biol. .

Abstract

In mammalian cells, the Golgi complex is structured in the form of a continuous membranous system composed of stacks connected by tubular bridges: the "Golgi ribbon." At the onset of mitosis, the Golgi complex undergoes a multi-step fragmentation process that is required for its correct partition into the dividing cells. Importantly, inhibition of Golgi disassembly results in cell-cycle arrest at the G2 stage, which indicates that accurate inheritance of the Golgi complex is monitored by a "Golgi mitotic checkpoint." Moreover, mitotic Golgi disassembly correlates with the release of a set of Golgi-localized proteins that acquire specific functions during mitosis, such as mitotic spindle formation and regulation of the spindle checkpoint. Most of these events are regulated by small GTPases of the Arf and Rab families. Here, we review recent studies that are revealing the fundamental mechanisms, the molecular players, and the biological significance of mitotic inheritance of the Golgi complex in mammalian cells. We also briefly comment on how Golgi partitioning is coordinated with mitotic progression.

Keywords: Arf; Rab; cell cycle; golgi complex; mitosis; mitotic spindle.

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Figures

Figure 1
Figure 1
Schematic representation of mitotic partitioning of the Golgi ribbon. This first step of mitotic Golgi fragmentation (i.e., ribbon unlinking) controls G2/M transition and requires the activities of BARS, GRASP55, and GRASP65. These processes also require the activities of several MAP kinase components, as indicated. At the onset of mitosis, these isolated stacks undergo further disassembly in the sequential steps of unstacking and vesiculation. These lead to the formation of the so-called “Golgi haze” during metaphase, where the Golgi membranes are completely fragmented. These processes require the activities of the kinases Plk1 and Cdc2, and their targets GRASP55 and GRASP65. Subsequent events result in dephosphorylation of the kinases that took part in the initial fragmentation, which leads to reassembly of the Golgi ribbon in the daughter cells.

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