Top 7 Biorxiv Papers Today in Cell Biology


2.19 Mikeys
#1. IRE1β negatively regulates IRE1α signaling in response to endoplasmic reticulum stress
Michael J Grey, Eva Cloots, Mariska S Simpson, Nicole LeDuc, Yevgeniy Serebrenik, Heidi De Luca, Delphine De Sutter, Phi Luong, Jay R Thiagarajah, Adrienne W Paton, James C Paton, Markus Seeliger, Sven Eyckerman, Sophie Janssens, Wayne I Lencer
IRE1β is an ER stress sensor uniquely expressed in epithelial cells lining mucosal surfaces. Here, we show that intestinal epithelial cells expressing IRE1β have an attenuated response to ER stress. IRE1β assembles with and blocks activation of the closely related and most evolutionarily ancient stress-sensor IRE1α to suppress stress-induced xbp1 splicing, a key mediator of the unfolded protein response. In comparison, IRE1β has weak xbp1 splicing activity, largely explained by a non-conserved amino acid in the kinase domain that impairs its phosphorylation and restricts oligomerization. This enables IRE1β to act as a dominant negative suppressor of IRE1α. The inhibitory effect is amplified in cells by disrupting an XBP1-dependent feedback loop regulating stress-induced expression of IRE1α. Thus IRE1β functions to negatively regulate IRE1α signaling, perhaps enabling intestinal epithelial cells to manage the response to chronic stress stimuli at the host-environment interface.
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biorxivpreprint: IRE1β negatively regulates IRE1α signaling in response to endoplasmic reticulum stress https://t.co/dSjkRfSpuO #bioRxiv
biorxiv_cellbio: IRE1β negatively regulates IRE1α signaling in response to endoplasmic reticulum stress https://t.co/cVpm45b4mF #biorxiv_cellbio
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Authors: 15
Total Words: 0
Unqiue Words: 0

2.048 Mikeys
#2. Anchoring of actin to the plasma membrane enables tension production in the fission yeast cytokinetic ring
Shuyuan Wang, Ben O'Shaughnessy
The cytokinetic ring generates tensile force that drives cell division, but how tension emerges from the relatively disordered ring organization remains unclear. Long ago a muscle-like sliding filament mechanism was proposed, but evidence for sarcomeric order is lacking. Here we present quantitative evidence that in fission yeast ring tension originates from barbed-end anchoring of actin filaments to the plasma membrane, providing resistance to myosin forces which enables filaments to develop tension. The role of anchoring was highlighted by experiments on isolated fission yeast rings, where sections of ring unanchored from the membrane and shortened ~30-fold faster than normal [Mishra M., et al. (2013) Nat Cell Biol 15(7):853-859]. The dramatically elevated constriction rates are unexplained. Here we present a molecularly explicit simulation of constricting partially anchored rings as studied in these experiments. Simulations accurately reproduced the experimental constriction rates, and showed that following anchor release a...
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biorxivpreprint: Anchoring of actin to the plasma membrane enables tension production in the fission yeast cytokinetic ring https://t.co/ym8VcLDDcA #bioRxiv
biorxiv_cellbio: Anchoring of actin to the plasma membrane enables tension production in the fission yeast cytokinetic ring https://t.co/tBt8tUhxyG #biorxiv_cellbio
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Sample Sizes : None.
Authors: 2
Total Words: 8327
Unqiue Words: 2117

2.025 Mikeys
#3. FSHR-1/GPCR activates the mitochondrial unfolded protein response in Caenorhabditis elegans
Sungjin Kim, Derek Sieburth
The mitochondrial unfolded protein response (UPRmt) is an evolutionarily conserved adaptive response that functions to maintain mitochondrial homeostasis following mitochondrial damage. In C. elegans , the nervous system plays a central role in responding to mitochondrial stress by releasing endocrine signals that act upon distal tissues to activate the UPRmt. The mechanisms by which mitochondrial stress is sensed by neurons and transmitted to distal tissues is not fully understood. Here, we identify a role for the conserved follicle-stimulating hormone G protein coupled receptor (GPCR), FSHR-1, in promoting UPRmt activation. Genetic deficiency of fshr-1 severely attenuates UPRmt activation and organism-wide survival in response to mitochondrial stress. FSHR-1 functions in a common genetic pathway with SPHK-1/sphingosine kinase to promote UPRmt activation, and FSHR-1 regulates the mitochondrial association of SPHK-1 in the intestine. Through tissue-specific rescue assays, we show that FSHR-1 functions in neurons to activate the...
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biorxivpreprint: FSHR-1/GPCR activates the mitochondrial unfolded protein response in Caenorhabditis elegans https://t.co/Xi9rJFrW1R #bioRxiv
biorxiv_cellbio: FSHR-1/GPCR activates the mitochondrial unfolded protein response in Caenorhabditis elegans https://t.co/5y9CTaujRA #biorxiv_cellbio
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Authors: 2
Total Words: 6845
Unqiue Words: 1754

2.009 Mikeys
#4. Human Hepatocyte Nuclear Factor 4-α encodes isoforms with distinct transcriptional functions
Élie Lambert, Jean-Philippe Babeu, Joël Simoneau, Dominique Lévesque, Émilie Jolibois, Michelle S Scott, Francois Boudreau, Francois-Michel Boisvert
HNF4α is a nuclear receptor produced as 12 isoforms from two promoters by alternative splicing. In order to characterize the transcriptional capacities of all 12 HNF4α isoforms, stable lines expressing each isoform were generated. The entire transcriptome associated with each isoform was analyzed as well as their respective interacting proteome. Major differences were noted in the transcriptional function of these isoforms. The α1 and α2 isoforms were the most potent regulators of gene expression while the α3 isoform exhibited significantly reduced activity. The α4, α5 and α6 isoforms, which use an alternative first exon, were characterized for the first time, and showed a greatly reduced transcriptional potential with an inability to recognize the consensus response element of HNF4α. Several transcription factors and coregulators were identified as potential specific partners for certain HNF4α isoforms. An analysis integrating the vast amount of omics data enabled the identification of transcriptional regulatory mechanisms...
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biorxivpreprint: Human Hepatocyte Nuclear Factor 4-α encodes isoforms with distinct transcriptional functions https://t.co/uUfUlQItxF #bioRxiv
biorxiv_cellbio: Human Hepatocyte Nuclear Factor 4-α encodes isoforms with distinct transcriptional functions https://t.co/qutK7o8w7U #biorxiv_cellbio
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Authors: 8
Total Words: 17313
Unqiue Words: 3963

1.997 Mikeys
#5. Krüppel-like factor 2- induced microRNAs: implications for treatment of pulmonary hypertension
Hebah Sindi, Giusy Russomanno, Jo Kyeong Beom, Vahitha B Abdul-Salam, Basma Qazi Chaudhry, Alexander Ainscough, Robert Szulcek, Harm Jan Bogaard, Claire Morgan, Soni Savai Pullamsetti, Mai Alzaydi, Christopher Rhodes, Ekkehard Grünig, Christina Eichstaedt, Martin R Wilkins, Beata Wojciak-Stothard
Flow-activated transcription factor Krüppel-like factor 2 (KLF2) signaling is compromised in pulmonary arterial hypertension (PAH). We aimed to identify KLF2-induced endothelium-protective exosomal microRNAs of potential therapeutic significance. Eight exosomal microRNAs elevated by KLF2 but reduced in PAH were transfected into human pulmonary artery endothelial cells. Of these, only miR-181a-5p and miR-324-5p had anti-apoptotic, anti-inflammatory and anti-proliferative effect on endothelial cells and reduced proliferation of vascular smooth muscle cells in vitro. RNA sequencing of miRNA-transfected HPAECs revealed reduced expression of multiple genes implicated in vascular remodelling, including ETS-1, NOTCH4, ACTA2, TNF-α, IL-1, MMP10, MAPK and NFATC2. KLF2, miR-181a-5p and miR-324-5p were reduced, while their target genes were elevated in blood-derived endothelial colony forming cells and lung tissues from idiopathic and heritable PAH patients with disabling KLF2 mutation and Sugen/hypoxia mice. Supplementation of miR-181a-5p...
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biorxivpreprint: Krüppel-like factor 2- induced microRNAs: implications for treatment of pulmonary hypertension https://t.co/e4oRaYIPHn #bioRxiv
biorxiv_cellbio: Krüppel-like factor 2- induced microRNAs: implications for treatment of pulmonary hypertension https://t.co/9wJArWJvMT #biorxiv_cellbio
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Sample Sizes : [14, 12, 6, 3, 6]
Authors: 16
Total Words: 10656
Unqiue Words: 3361

1.931 Mikeys
#6. Control of the Endo-Lysosome Homeostasis by the Paracaspase MALT1 regulates Glioma Cell Survival
Kathryn A Jacobs, Gwennan André-Grégoire, Clément Maghe, Ying Li, An Thys, Elizabeth Harford-Wright, Kilian Trillet, Tiphaine Douanne, Jean-Sébastien Frénel, Nicolas Bidère, Julie Gavard
Glioblastoma is one of the most lethal forms of adult cancer with a median survival of around 15 months. A potential treatment strategy involves targeting glioblastoma stem-like cells (GSC), which constitute a cell autonomous reservoir of aberrant cells able to initiate, maintain, and repopulate the tumor mass. Here, we report that the expression of the paracaspase mucosa-associated lymphoid tissue l (MALT1), a protease previously linked to antigen receptor-mediated NF-κB activation and B-cell lymphoma survival, inversely correlates with patient probability of survival. The knockdown of MALT1 largely impaired the expansion of patient-derived stem-like cells in vitro, and this could be recapitulated with pharmacological inhibitors, in vitro and in vivo. Blocking MALT1 protease activity increases the endo-lysosome abundance, impaired autophagic flux, and culminates in lysosomal-mediated death, concomitantly with mTOR inactivation and dispersion from lysosomes. These findings place MALT1 as a new druggable target involved in...
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Authors: 11
Total Words: 0
Unqiue Words: 0

1.931 Mikeys
#7. Integrin-dependent YAP signaling requires LAMTOR1 mediated delivery of Src to the plasma membrane
Daniel Bouvard, Marc Block, Molly Brunner, Théo Ziegelmeyer, Dominique Lallemand, Mylène Pezet, Genevieve Chevalier, Philippe Rondé, Bernhard M Wehrle-Haller
YAP signaling has emerged as an important signaling pathway involved in several normal and pathological processes. While main upstream effectors regulating its activity have been extensively studied, the interplay with other cellular processes has been far less analyzed. Here, we identified the LAMTOR complex as a new important regulator of YAP signaling. We uncovered that p18/LAMTOR1 is required for the recycling of Src on late endosomes to the cell periphery, and consequently to activate a signaling cascade that eventually controls YAP nuclear shuttling. Moreover, p18/LAMTOR1 positives late endosomes distribution is controlled by β1 integrins, extracellular matrix stiffness and cell contractility. This likely relies on the targeting of microtubules to β1 positive focal adhesion via ILK. Altogether our findings identify the late endosomal recycling pathway as a major regulator of YAP.
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Authors: 9
Total Words: 12880
Unqiue Words: 3062

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