Golgi apparatus self-organizes into the characteristic shape via postmitotic reassembly dynamics

Tachikawa, Masashi; Mochizuki, Atsushi

doi:10.1073/pnas.1619264114

Cited by 52 publications

(78 citation statements)

References 37 publications

(45 reference statements)

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“…Furthermore, computational simulation has implicated self-organizing properties of Golgi cisternae during reassembly processes (Tachikawa and Mochizuki, 2017).…”

Section: Discussionmentioning

confidence: 99%

A Missense Mutation in the NSF Gene Causes Abnormal Golgi Morphology in Arabidopsis thaliana

Tanabashi

Shoda

Saito

et al. 2018

Cell Struct. Funct.

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The Golgi apparatus is a key station of glycosylation and membrane traffic. It consists of stacked cisternae in most eukaryotes. However, the mechanisms how the Golgi stacks are formed and maintained are still obscure. The model plant Arabidopsis thaliana provides a nice system to observe Golgi structures by light microscopy, because the Golgi in A. thaliana is in the form of mini-stacks that are distributed throughout the cytoplasm. To obtain a clue to understand the molecular basis of Golgi morphology, we took a forward-genetic approach to isolate A. thaliana mutants that show abnormal structures of the Golgi under a confocal microscope. In the present report, we describe characterization of one of such mutants, named #46-3. The #46-3 mutant showed pleiotropic Golgi phenotypes. The Golgi size was in majority smaller than the wild type, but varied from very small ones, sometimes without clear association of cis and trans cisternae, to abnormally large ones under a confocal microscope.At the ultrastructual level by electron microscopy, queer-shaped large Golgi stacks were occasionally observed. By positional mapping, genome sequencing, and complementation and allelism tests, we linked the mutant phenotype to the missense mutation D374N in the NSF gene, encoding the N-ethylmaleimide-sensitive factor (NSF), a key component of membrane fusion. This residue is near the ATP-binding site of NSF, which is very well conserved in eukaryotes, suggesting that the biochemical function of NSF is important for maintaining the normal morphology of the Golgi.3

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“…Furthermore, computational simulation has implicated self-organizing properties of Golgi cisternae during reassembly processes (Tachikawa and Mochizuki, 2017).…”

Section: Discussionmentioning

confidence: 99%

A Missense Mutation in the NSF Gene Causes Abnormal Golgi Morphology in Arabidopsis thaliana

Tanabashi

Shoda

Saito

et al. 2018

Cell Struct. Funct.

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“…1E-G). Zippering was assessed using two parameters: rostral-caudal distance of closing neural folds and caudal zipper point angle (Galea et al, 2017) (Fig. 1H,I).…”

Section: Zinc Deficiency Disrupts Inflection Of the Neural Foldsmentioning

confidence: 99%

Zinc deficiency causes neural tube defects through attenuation of p53 ubiquitylation

Zhang

Niswander

2018

Development

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Micronutrition is essential for neural tube closure, and zinc deficiency is associated with human neural tube defects. Here, we modeled zinc deficiency in mouse embryos, and used live imaging and molecular studies to determine how zinc deficiency affects neural tube closure. Embryos cultured with the zinc chelator TPEN failed to close the neural tube and showed excess apoptosis. TPEN-induced p53 protein stabilization in vivo and in neuroepithelial cell cultures and apoptosis was dependent on p53. Mechanistically, zinc deficiency resulted in disrupted interaction between p53 and the zinc-dependent E3 ubiquitin ligase Mdm2, and greatly reduced p53 ubiquitylation. Overexpression of human CHIP, a zinc-independent E3 ubiquitin ligase that targets p53, relieved TPEN-induced p53 stabilization and reduced apoptosis. Expression of p53 pro-apoptotic target genes was upregulated by zinc deficiency. Correspondingly, embryos cultured with p53 transcriptional activity inhibitor pifithrin-α could overcome TPEN-induced apoptosis and failure of neural tube closure. Our studies indicate that zinc deficiency disrupts neural tube closure through decreased p53 ubiquitylation, increased p53 stabilization and excess apoptosis.

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“…Simulating macromolecule stability and interactions in a eukaryotic-like cell requires a large effort for the presence of localized and pervasive structures (Neri et al 2013;Smith et al 2014;Unterberger and Holzapfel 2014;Mak et al 2015Mak et al , 2016Gao et al 2015;Nguyen et al 2016;Popov et al 2016;Reddy and Sansom 2016;Chavent et al 2016;Foffano et al 2016;Niesen et al 2017;Tachikawa and Mochizuki 2017). Future investigations will be devoted to simulating dynamical processes involving the cytoskeleton and the membranes, such as the trafficking of macromolecules and vesicles to their sub-cellular localization (Miller et al 2016).…”

Section: Toward Realistic Molecular Simulations Of Cellular Eventsmentioning

confidence: 99%

Molecular simulations of cellular processes

Trovato

Fumagalli

2017

Biophys Rev

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It is, nowadays, possible to simulate biological processes in conditions that mimic the different cellular compartments. Several groups have performed these calculations using molecular models that vary in performance and accuracy. In many cases, the atomistic degrees of freedom have been eliminated, sacrificing both structural complexity and chemical specificity to be able to explore slow processes. In this review, we will discuss the insights gained from computer simulations on macromolecule diffusion, nuclear body formation, and processes involving the genetic material inside cell-mimicking spaces. We will also discuss the challenges to generate new models suitable for the simulations of biological processes on a cell scale and for cellcycle-long times, including non-equilibrium events such as the co-translational folding, misfolding, and aggregation of proteins. A prominent role will be played by the wise choice of the structural simplifications and, simultaneously, of a relatively complex energetic description. These challenging tasks will rely on the integration of experimental and computational methods, achieved through the application of efficient algorithms.

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Golgi apparatus self-organizes into the characteristic shape via postmitotic reassembly dynamics

Cited by 52 publications

References 37 publications

A Missense Mutation in the <i>NSF</i> Gene Causes Abnormal Golgi Morphology in <i>Arabidopsis thaliana</i>

A Missense Mutation in the <i>NSF</i> Gene Causes Abnormal Golgi Morphology in <i>Arabidopsis thaliana</i>

Zinc deficiency causes neural tube defects through attenuation of p53 ubiquitylation

Molecular simulations of cellular processes

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