Models of Intracellular Transport: Pros and Cons

Abstract

Intracellular transport is one of the most confusing issues in the field of cell biology. Many different models and their combinations have been proposed to explain the experimental data on intracellular transport. Here, we analyse the data related to the mechanisms of endoplasmic reticulum-to-Golgi and intra-Golgi transport from the point of view of the main models of intracellular transport; namely: the vesicular model, the diffusion model, the compartment maturation–progression model, and the kiss-and-run model. This review initially describes our current understanding of Golgi function, while highlighting the recent progress that has been made. It then continues to discuss the outstanding questions and potential avenues for future research with regard to the models of these transport steps. To compare the power of these models, we have applied the method proposed by K. Popper; namely, the formulation of prohibitive observations according to, and the consecutive evaluation of, previous data, on the basis on the new models. The levels to which the different models can explain the experimental observations are different, and to date, the most powerful has been the kiss-and-run model, whereas the least powerful has been the diffusion model.

Tubular ERGIC (t-ERGIC): a SURF4-mediated expressway for ER-to-Golgi transport

“…Whereas studies in yeasts suggest the budding off of COPII-coated vesicles at the ERES as ERto-Golgi carriers (Dancourt and Barlowe, 2010;Kurokawa and Nakano, 2019;Lee et al, 2004), live imaging of mammalian cells has shown COPII coats stably associate with the ER (Mironov and Beznoussenko, 2019;Shomron et al, 2019;Stephens et al, 2000;Westrate et al, 2020). Our RUSH results are in line with the latter observations.…”

Nucleobindin-1 regulates ECM degradation by promoting intra-Golgi trafficking of MMPs

“…Molecular mechanisms of anterograde cargo transport through the Golgi remain a major question in the field of membrane trafficking ( Malhotra et al, 1989 ; Glick and Malhotra, 1998 ; Glick and Luini, 2011 ; Beznoussenko et al, 2014 ; Mironov and Beznoussenko, 2019 ). In this context, there is still a big debate in the field about how anterograde cargo, such as MMPs that arrive in the cis-Golgi, are segregated from retrograde cargo trafficking to the ER ( Glick and Nakano, 2009 ; Mironov and Beznoussenko, 2019 ; Kurokawa et al, 2019 ).…”

Membrane Curvature, Trans-Membrane Area Asymmetry, Budding, Fission and Organelle Geometry

“…For instance, proteins may also affect the local membrane properties as external factors. Membrane-bound proteins such as coatomer (COP) I, COPII, dynamin, clathrin/AP1, clathrin/AP2, AP3, AP4 (reviewed in [ 26 , 33 , 34 , 35 ]), with asymmetric distribution of mass across the bilayer, influence membrane bending in a nonspecific manner due to molecular crowding [ 36 ]. Shallow hydrophobic insertions and strongly curved protein scaffolds appear to be effective generators of the membrane curvature of intracellular organelles [ 37 ].…”