Top 10 Biorxiv Papers Today in Cell Biology


2.025 Mikeys
#1. Adaptive reorganization of the cytoplasm upon stress in budding yeast
Guendalina Marini, Elisabeth Nueske, Weihua Leng, Simon Alberti, Gaia Pigino
Yeast cells exposed to stress conditions such as starvation can enter a protective dormant state in which cell division, growth and metabolism are reduced or downregulated. They can remain in that state until nutrients become available again. How cells enter this dormant state and why it is protective is largely unknown. Here we use correlative light and electron microscopy and electron tomography to investigate the ultrastructural changes in the cytoplasm of starved yeast cells. We report that starved yeast cells undergo an extensive cytoplasmic reorganization that involves the formation of both membrane-bound and membraneless organelles. By determining the density of ribosomal particles, we show that the cytoplasm of starved yeast also experiences significant compaction. We further demonstrate that the key enzyme eukaryotic translation initiation factor 2B (eIF2B) polymerizes into large bundles of filaments through a reversible process. We propose that these changes allow yeast cells to store and inhibit proteins, and thus...
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biorxivpreprint: Adaptive reorganization of the cytoplasm upon stress in budding yeast https://t.co/hFm7cx7U1Y #bioRxiv
biorxiv_cellbio: Adaptive reorganization of the cytoplasm upon stress in budding yeast https://t.co/0UvKtFxsuw #biorxiv_cellbio
AnnaBajur: Adaptive #reorganization of the cytoplasm upon stress in budding yeast | well done, Guen, Eli, ⁦@GaiaPigino⁩ and ⁦all the others involved from @mpicbg⁩ 👏👏 https://t.co/3gZcWoUsMQ
mary_munson4: RT @biorxiv_cellbio: Adaptive reorganization of the cytoplasm upon stress in budding yeast https://t.co/0UvKtFxsuw #biorxiv_cellbio
RiboGuy: RT @biorxivpreprint: Adaptive reorganization of the cytoplasm upon stress in budding yeast https://t.co/hFm7cx7U1Y #bioRxiv
Eric_Chevet: RT @biorxiv_cellbio: Adaptive reorganization of the cytoplasm upon stress in budding yeast https://t.co/0UvKtFxsuw #biorxiv_cellbio
BerroLab: RT @biorxiv_cellbio: Adaptive reorganization of the cytoplasm upon stress in budding yeast https://t.co/0UvKtFxsuw #biorxiv_cellbio
1guramritsingh: RT @biorxiv_cellbio: Adaptive reorganization of the cytoplasm upon stress in budding yeast https://t.co/0UvKtFxsuw #biorxiv_cellbio
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Sample Sizes : None.
Authors: 5
Total Words: 11786
Unqiue Words: 3530

2.01 Mikeys
#2. Filament formation by the translation factor eIF2B regulates protein synthesis in starved cells
Elisabeth Nueske, Guendalina Marini, Doris Richter, Weihua Leng, Aliona Bogdanova, Titus M Franzmann, Gaia Pigino, Simon Alberti
Cells exposed to starvation have to adjust their metabolism to conserve energy and protect themselves. Protein synthesis is one of the major energy-consuming processes and as such has to be tightly controlled. The mechanism by which starved cells regulate the process of protein synthesis is largely unknown. Here, we report that the essential translation initiation factor eIF2B forms filaments in starved budding yeast cells. We demonstrate that filamentation is triggered by starvation-induced acidification of the cytosol, which is caused by an influx of protons from the extracellular environment. We show that filament assembly by eIF2B is necessary for rapid and efficient downregulation of translation. Importantly, this mechanism does not require the kinase Gcn2. Furthermore, analysis of site-specific variants of eIF2B suggests that eIF2B assembly results in enzymatically inactive filaments that promote stress survival and fast recovery of cells from starvation. We propose that translation regulation through protein assembly is a...
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Eric_Chevet: Filament formation by the translation factor eIF2B regulates protein synthesis in starved cells https://t.co/ij1KZnNXub
ZidLab: https://t.co/nq6DmO4PTx
MarciniakLab: RT @Eric_Chevet: Filament formation by the translation factor eIF2B regulates protein synthesis in starved cells https://t.co/ij1KZnNXub
Parikki: RT @Eric_Chevet: Filament formation by the translation factor eIF2B regulates protein synthesis in starved cells https://t.co/ij1KZnNXub
gekaragoz: RT @Eric_Chevet: Filament formation by the translation factor eIF2B regulates protein synthesis in starved cells https://t.co/ij1KZnNXub
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Sample Sizes : None.
Authors: 8
Total Words: 13331
Unqiue Words: 3460

2.0 Mikeys
#3. Germline deletion reveals a non-essential role of the atypical MAPK6/ERK3
Natalia Ronkina, Karin Schuster-Gossler, Florian Hansmann, Heike Kunze-Schumacher, Inga Sandrock, Tatiana Yakovleva, Juri Lafera, Wolfgang Baumgärtner, Andreas Krueger, Immo Prinz, Achim Gossler, Alexey Kotlyarov, Matthias Gaestel
MAPK6/ERK3 is an atypical member of the MAPKs. An essential role has been suggested by the perinatal lethal phenotype of ERK3 knockout mice carrying a lacZ insertion in exon 2 due to pulmonary disfunction and by defects in function, activation and positive selection of T cells. To study the role of ERK3 in vivo, we generated mice carrying a conditional Erk3 allele with exon3 flanked by LoxP sites. Loss of ERK3 protein was validated after deletion of Erk3 in the female germ line using zona pellucida 3 (Zp3)-cre and a clear reduction of the protein kinase MK5 is detected, providing first evidence for the existence of the ERK3/MK5 signaling complex in vivo. In contrast to the previously reported Erk3 knockout phenotype, these mice are viable and fertile, do not display pulmonary hypoplasia, acute respiratory failure, abnormal T cell development, reduction of thymocyte numbers or altered T cells selection. Hence, ERK3 is dispensable for pulmonary and T-cell functions. The perinatal lethality, lung and T-cell defects of the previous...
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KruegerLab: Our first contribution to biorxiv: Germline deletion reveals a non-essential role of the atypical MAPK6/ERK3 https://t.co/eh8x4b3DMb
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Sample Sizes : [105, 105, 5, 5]
Authors: 13
Total Words: 7814
Unqiue Words: 2870

0.0 Mikeys
#4. Impact of chromosome fusions on 3D genome organization and gene expression in budding yeast
Marco Di Stefano, Francesca Di Giovanni, Davide Baù, Lucas B Carey, Marc A. Marti-Renom, Manuel Mendoza
The three-dimensional organization of chromosomes can influence transcription. However, the frequency and magnitude of these effects remains debated. To determine how changes in chromosome positioning affect transcription across thousands of genes with minimal perturbation, we characterized nuclear organization and global gene expression in budding yeast containing chromosome fusions. We used computational modelling and single cell imaging to determine chromosome position and integrated these data with genome-wide transcriptional profiles from RNA sequencing. We find that chromosome fusions dramatically alter 3D nuclear organization without leading to strong genome-wide changes in transcription. However, we observe a mild but significant and reproducible increase in expression of genes near fusion sites. Modeling suggests that this is due to both disruption of telomere-associated silencing and the displacement of genes relative to the nuclear periphery. A 10% decrease in the predicted time a gene spends near the nuclear periphery...
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Sample Sizes : None.
Authors: 6
Total Words: 11540
Unqiue Words: 3109

0.0 Mikeys
#5. The cytoskeleton as a smart composite material: A unified pathway linking microtubules, myosin-II filaments and integrin adhesions
Nisha Mohd Rafiq, Yukako Nishimura, Sergey V. Plotnikov, Visalatchi Thiagarajan, Zhen Zhang, Meenubharathi Natarajan, Shidong Shi, Virgile Viasnoff, Gareth E. Jones, Pakorn Kanchanawong, Alexander D. Bershadsky
The interrelationship between microtubules and the actin cytoskeleton in mechanoregulation of integrin-mediated adhesions is poorly understood. Here, we show that the effects of microtubules on two major types of cell-matrix adhesions, focal adhesions and podosomes, are mediated by KANK family proteins connecting the adhesion protein talin with microtubule tips. Both total microtubule disruption and microtubule uncoupling from adhesions by manipulations with KANKs trigger a massive assembly of myosin-IIA filaments. Myosin-IIA filaments, augmenting the focal adhesions and disrupting the podosomes, are indispensable effectors in the microtubule-dependent regulation of integrin-mediated adhesions. Myosin-IIA filament assembly depends on Rho activation by the RhoGEF, GEF-H1, which is trapped by microtubules when they are connected with integrin-mediated adhesions via KANK proteins but released after their disconnection. Thus, microtubule capturing by integrin-mediated adhesions modulates the GEF-H1-dependent effect of microtubules on...
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mitroe: KANK targets microtubules to FA. Loss of KANK releases GEF-H1 from microtubules leading to RhoA activation https://t.co/fsG5yvtOcv
misslornayoung: The cytoskeleton as a smart composite material: A unified pathway linking microtubules, myosin-II filaments and integrin adhesions https://t.co/Im69B6TiqF
mace_em: The cytoskeleton as a smart composite material: A unified pathway linking microtubules, myosin-II filaments and integrin adhesions https://t.co/43ULwk3R5z
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Sample Sizes : None.
Authors: 11
Total Words: 27516
Unqiue Words: 4594

0.0 Mikeys
#6. Mechanosensitive clathrin platforms anchor desmin intermediate filaments in skeletal muscle
Agathe Franck, Jeanne Laine, Gilles Moulay, Michael Trichet, Christel Gentil, Anais Fongy, Anne Bigot, Sofia Benkhelifa-Ziyyat, Emmanuelle Lacene, Mai Thao Bui, Guy Brochier, Pascale Guicheney, Sabrina Sacconi, Vincent Mouly, Norma Beatriz Romero, Catherine Coirault, Marc Bitoun, Stephane Vassilopoulos
Large flat clathrin plaques are stable features of the plasma membrane associated with sites of strong adhesion suggesting that they could also play a role in force transduction. Here, we analyzed how clathrin plaques interact with the cytoskeleton and how they respond to mechanical cues in skeletal muscle myotubes. We show that branched actin networks surrounding clathrin plaques are directly regulated by dynamin 2, anchor intermediate filaments and sequester YAP at the plasma membrane. Dynamin 2, clathrin and desmin intermediate filaments are all required for basal YAP nucleocytoplasmic distribution and efficient nuclear translocation in response to mechanical stimuli. Dynamin 2 mutations that are responsible for centronuclear myopathy in humans disorganize the desmin network and deregulate YAP signaling both in vitro and in vivo. Thus, clathrin plaques and associated dynamin 2 are defined here as a new sensor conveying mechanical cues and integrate cell signaling with cytoskeletal regulation.
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Authors: 18
Total Words: 12074
Unqiue Words: 3490

0.0 Mikeys
#7. RAB6 and microtubules restrict secretion to focal adhesions
Lou Fourriere, Amal Kasri, Nelly Gareil, Sabine Bardin, Jerome Boulanger, Romain Sikora, Gaelle Boncompain, Stephanie Miserey-Lenkei, Franck Perez, Bruno Goud
To ensure their homeostasis and sustain differentiated functions, cells continuously transport diverse cargos to various cell compartments and in particular to the cell surface. Secreted proteins are transported along intracellular routes from the endoplasmic reticulum through the Golgi complex before reaching the plasma membrane along microtubule tracks. Using a synchronized secretion assay, we report here that exocytosis does not occur randomly at the cell surface but on localized hotspots juxtaposed to focal adhesions. Although microtubules are involved, the RAB6-dependent machinery plays an essential role. We observed that, irrespective of the transported cargos, most post-Golgi carriers are positive for RAB6 and that its inactivation leads to a broad reduction of protein secretion. RAB6 may thus be a general regulator of post-Golgi secretion.
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biorxivpreprint: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/ZtdDMZF5hi #bioRxiv
biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
roylelab: Preprint µJC: Fourriere et al. Secretion at focal adhesions visualised with RUSH https://t.co/0NyueUGY8B
WormlockHolmes: Secretory hotspots at focal adhesions depend on RAB6 interactions with ELKS. RAB6 does not appear to have a role in sorting at the golgi using the RUSH system. From G. Boncompain, S. Miserey-Lenkei, F. Pérez @Team_FranckP & B. Goud labs @institut_curie https://t.co/mAklcHp9Id
dhiraj_d_bhatia: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/AmYJ2Hsvil
christlet: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
LauraPicas: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/D4TeQvlypU
JDHL18: RT @roylelab: Preprint µJC: Fourriere et al. Secretion at focal adhesions visualised with RUSH https://t.co/0NyueUGY8B
GoetzJacky: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
IchaJaroslav: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
ERainero_lab: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
Alexis_Lomakin: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
mace_em: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
vickybiotech144: RT @dhiraj_d_bhatia: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/AmYJ2Hsvil
AnnaBajur: RT @roylelab: Preprint µJC: Fourriere et al. Secretion at focal adhesions visualised with RUSH https://t.co/0NyueUGY8B
AnnaBajur: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
Hesso_F_Sci: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
ivaviktorinova: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
CGAlmeidaG: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
jonathanbarrac: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
chiaretta_panda: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
RolandTh1: RT @roylelab: Preprint µJC: Fourriere et al. Secretion at focal adhesions visualised with RUSH https://t.co/0NyueUGY8B
shailajaseethar: RT @biorxiv_cellbio: RAB6 and microtubules restrict secretion to focal adhesions https://t.co/b1k7Kc0mZF #biorxiv_cellbio
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Authors: 10
Total Words: 10124
Unqiue Words: 2775

0.0 Mikeys
#8. Local Enrichment of HP1alpha at Telomeres Alters Their Structure and Regulation of Telomere Protection
Tracy T Chow, Xiaoyu Shi, Jen-Hsuan Wei, Juan Guan, Guido Stadler, Bo Huang, Elizabeth H Blackburn
Enhanced telomere maintenance is evident in malignant cancers. While telomeres are thought to be inherently heterochromatic, detailed mechanisms of how epigenetic modifications impact telomere protection and structures are largely unknown in human cancers. Here we develop a molecular tethering approach to experimentally enrich heterochromatin protein HP1α specifically at telomeres. This results in increased deposition of H3K9me3 at cancer cell telomeres. Telomere extension by telomerase is attenuated, and damage-induced foci at telomeres are reduced, indicating augmentation of telomere stability. Super resolution STORM imaging shows an unexpected increase in irregularity of telomeric structure. Telomere-tethered chromo shadow domain (CSD) mutant I165A of HP1α abrogates both the inhibition of telomere extension and the irregularity of telomeric structure, suggesting the involvement of at least one HP1α-ligand in mediating these effects. This work presents a new approach to specifically manipulate the epigenetic status locally at...
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biorxivpreprint: Local Enrichment of HP1alpha at Telomeres Alters Their Structure and Regulation of Telomere Protection https://t.co/AQlKjZXebO #bioRxiv
biorxiv_cellbio: Local Enrichment of HP1alpha at Telomeres Alters Their Structure and Regulation of Telomere Protection https://t.co/GbVSCqX7B2 #biorxiv_cellbio
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Authors: 7
Total Words: 13202
Unqiue Words: 4706

0.0 Mikeys
#9. SSU72 phosphatase is a telomere replication terminator
Jose Miguel Escandell, Edison Samir Mascarenhas Carvalho, Maria Gallo-Fernandez, Clara Reis, Samah Matmati, Ines Matias Luis, Isabel Abreu, Stephane Coulon, Miguel Godinho Ferreira
Telomeres, the protective ends of eukaryotic chromosomes, are replicated through concerted actions by conventional DNA polymerases and telomerase, though the regulation of this process is not fully understood. Telomere replication requires (C)-Stn1-Ten1, a telomere ssDNA-binding complex that is homologous to RPA. Here, we show that the evolutionarily conserved phosphatase Ssu72 is responsible for terminating the cycle of telomere replication in fission yeast. Ssu72 controls the recruitment of Stn1 to telomeres by regulating Stn1 phosphorylation at S74, a residue that lies within the conserved OB fold domain. Consequently, ssu72Δ mutants are defective in telomere replication and exhibit long 3′ overhangs, which are indicative of defective lagging strand DNA synthesis. We also show that hSSU72 regulates telomerase activation in human cells by controlling the recruitment of hSTN1 to telomeres. Thus, in this study, we demonstrate a previously unknown yet conserved role for the phosphatase SSU72, whereby this enzyme controls telomere...
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ehelegam: The first preprint from my friend and colleague Edison Carvalho from @PGCD_IGC @IGCiencia @MGodinhoFerr lab https://t.co/RHq3Uk1Vg3
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Authors: 9
Total Words: 13744
Unqiue Words: 4047

0.0 Mikeys
#10. Inducing controlled cell cycle arrest and re-entry during asexual proliferation of Plasmodium falciparum malaria parasites.
Riette A Van Biljon, Jandeli Niemand, Roelof DJ van Wyk, Katherine Clark, Bianca Brider, Clarissa Abrie, Hilde Von Gruning, Werner Smidt, Annel Smit, Janette Reader, Heather Painter, Manuel Llinas, Christian Doerig, Lyn-Marie Birkholtz
The life cycle of the malaria parasite Plasmodium falciparum is tightly regulated, oscillating between stages of intense proliferation and quiescence. Cyclic 48-hour asexual replication of Plasmodium is markedly different from cell division in higher eukaryotes, and mechanistically poorly understood. Here, we report tight synchronisation of malaria parasites during the early phases of its cell cycle by exposure to DL-α-difluoromethylornithine (DFMO), which results in the depletion of polyamines. This induces an inescapable cell cycle arrest in G1 (~15 hours post-invasion) by blocking G1/S transition. Cell cycle-arrested parasites enter a quiescent G0-like state but, upon addition of exogenous polyamines, re-initiate their cell cycle in a coordinated fashion. This ability to halt malaria parasites at a specific point in their cell cycle, and to subsequently trigger re-entry into the cell cycle, provides a valuable framework to investigate cell cycle regulation in these parasites. We therefore used gene expression analyses to show...
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biorxivpreprint: Inducing controlled cell cycle arrest and re-entry during asexual proliferation of Plasmodium falciparum malaria parasites. https://t.co/R1Gs44Dv33 #bioRxiv
biorxiv_cellbio: Inducing controlled cell cycle arrest and re-entry during asexual proliferation of Plasmodium falciparum malaria parasites. https://t.co/aJedUjJ4Kl #biorxiv_cellbio
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Sample Sizes : [100, 4, 6, 4, 91]
Authors: 14
Total Words: 10405
Unqiue Words: 3414

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