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In mammalian cells, several proteins that are not part of the core replication machinery promote the efficient restart of stalled replication forks, which suggests that fork restart pathways exist. Different models of restart can be envisaged, which involve DNA helicases, nucleases, homologous recombination factors and DNA double-strand breaks.
Ten years ago, the cell biological role of lipid rafts was controversial owing to limited methodology and confusing nomenclature. Through technical advances, our concept of lipid rafts has evolved into that of dynamic nanoscale assemblies that can be stabilized to control signalling and membrane trafficking.
Although necrosis was regarded as an uncontrolled mode of cell death, evidence now shows that it can be highly regulated. The initiation of programmed necrosis (necroptosis) by death receptors requires receptor-interacting protein 1 (RIP1) and RIP3, and its execution involves the active disintegration of mitochondrial, lysosomal and plasma membranes.
Metabolic pathways such as glycolysis and the pentose phosphate pathway communicate to cell cycle and apoptotic effectors, including D-type cyclins, CDKs, APC, p53, caspase 2 and BCL-2 proteins. The importance of this crosstalk is emphasized by the role of metabolic aberrations in the aetiology of disease.
In multicellular organisms, DNA replication adapts to variations in growth conditions, DNA damage and chromatin organization changes associated with cell differentiation. Therefore, only a subset of replication origins is used at each cell cycle, the choice of which is controlled by various factors including epigenetic mechanisms and gene expression.
Non-vesicular lipid transport between intracellular membranes can be mediated by spontaneous lipid transfer or lipid-transfer proteins (LTPs) and is crucial for maintaining the identities of different cellular membranes. Current studies focus on further understanding the mechanisms of non-vesicular lipid transport and elucidating the role of LTPs in intact cells.