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Microtubule-associated proteins 1A/1B light chain 3B (hereafter referred to as LC3) is a protein that in humans is encoded by the MAP1LC3B gene. [5] LC3 is a central protein in the autophagy pathway where it functions in autophagy substrate selection and autophagosome biogenesis. LC3 is the most widely used marker of autophagosomes. [6]
The completed autophagosome then fuses with a lysosome through the actions of multiple proteins, including SNAREs [72] [73] and UVRAG. [74] Following the fusion LC3 is retained on the vesicle's inner side and degraded along with the cargo, while the LC3 molecules attached to the outer side are cleaved off by Atg4 and recycled. [75]
LC3 cleavage is required for the terminal fusion of an autophagosome with its target membrane. LC3 is commonly used as a marker of autophagosomes in immunocytochemistry , because it is the essential part of the vesicle and stays associated until the last moment before its fusion.
Since lipids are hydrophobic molecules, they need to be solubilized before their metabolism can begin. Lipid metabolism often begins with hydrolysis, [7] which occurs with the help of various enzymes in the digestive system. [2] Lipid metabolism also occurs in plants, though the processes differ in some ways when compared to animals. [8]
Primary metabolism in a plant comprises all metabolic pathways that are essential to the plant's survival. Primary metabolites are compounds that are directly involved in the growth and development of a plant whereas secondary metabolites are compounds produced in other metabolic pathways that, although important, are not essential to the functioning of the plant.
Programmed cell death (PCD; sometimes referred to as cellular suicide [1]) is the death of a cell as a result of events inside of a cell, such as apoptosis or autophagy. [2] [3] PCD is carried out in a biological process, which usually confers advantage during an organism's lifecycle.
The transient conjugation of Atg8 to the membrane lipid phosphatidylethanolamine is essential for phagophore expansion as its mutation leads to defects in autophagosome formation. [9] It is distributed symmetrically on both sides of the autophagosome and it is assumed that there is a quantitative correlation between the amount of Atg8 and the ...
The effect of Bafilomycin on autophagosome-lysosome fusion is complex and time dependent in each cell line. [8] [24] In neurons, an increase in the autophagosome marker LC3-II has been seen with Bafilomycin treatment. This occurs as autophagosomes fail to fuse with lysosomes, which normally stimulates the degradation of LC3-II. [25]