Publisher: Rockefeller University Press   (Total: 3 journals)   [Sort alphabetically]

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J. of Cell Biology     Full-text available via subscription   (Followers: 55, SJR: 6.479, CiteScore: 7)
J. of Experimental Medicine     Full-text available via subscription   (Followers: 48, SJR: 8.615, CiteScore: 9)
J. of General Physiology     Full-text available via subscription   (Followers: 4, SJR: 2.623, CiteScore: 3)
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Journal of Cell Biology
Journal Prestige (SJR): 6.479
Citation Impact (citeScore): 7
Number of Followers: 55  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 0021-9525 - ISSN (Online) 1540-8140
Published by Rockefeller University Press Homepage  [3 journals]
  • Dendrite remodeling according to GARP

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      Abstract: Disruptions in membrane trafficking are associated with neurodevelopmental disorders, but underlying pathological mechanisms remain largely unknown. In this issue, O’Brien et al. (2023. J. Cell Biol.https://doi.org/10.1083/jcb.202112108) show how GARP regulates sterol transfer critical for remodeling of dendrites in flies.
      PubDate: Thu, 22 Dec 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202211072
      Issue No: Vol. 222, No. 1 (2022)
       
  • Liquid–liquid phase separation drives herpesvirus assembly in the
           cytoplasm

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      Abstract: Liquid–liquid phase separation (LLPS) has emerged as a fundamental mechanism to compartmentalize biomolecules into membraneless organelles. In this issue, Zhou et al. (2022. J. Cell Biol.https://doi.org/10.1083/jcb.202201088), report that MHV-68 ORF52 undergoes LLPS to form cytoplasmic virion assembly compartments, regulating the spatiotemporal compartmentalization of viral components.
      PubDate: Wed, 21 Dec 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202211015
      Issue No: Vol. 222, No. 1 (2022)
       
  • Cilia bent out of shape over dysfunctional astrocyte mitochondria

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      Abstract: Mitochondrial dysfunction in astrocytes drives neurodegenerative brain pathology. In this issue, Ignatenko et al. (2022. J. Cell. Biol.https://doi.org/10.1083/jcb.202203019) discover a novel connection between cilia and mitochondria in astrocytes, whereby mitochondrial dysfunction leads to abnormal cilia structure and a motile cilia program.
      PubDate: Fri, 16 Dec 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202211123
      Issue No: Vol. 222, No. 1 (2022)
       
  • Clipping EpCAM to release Claudin-7 for the greater good of the epithelial
           barrier

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      Abstract: Maintenance of epithelial barrier function requires dynamic repair and remodeling of tight junctions. In this issue, Higashi et al. (2022. J. Cell Biol.https://doi.org/10.1083/jcb.202204079) demonstrate that the proteolytic cleavage of EpCAM by membrane-anchored serine proteinases releases Claudin-7 to join tight junctions, suggesting a novel mechanism that couples sensing with repair of damaged tight junctions.
      PubDate: Wed, 14 Dec 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202211127
      Issue No: Vol. 222, No. 1 (2022)
       
  • Signal sequences encode information for protein folding in the endoplasmic
           reticulum

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      Abstract: One-third of newly synthesized proteins in mammals are translocated into the endoplasmic reticulum (ER) through the Sec61 translocon. How protein translocation coordinates with chaperone availability in the ER to promote protein folding remains unclear. We find that marginally hydrophobic signal sequences and transmembrane domains cause transient retention at the Sec61 translocon and require the luminal BiP chaperone for efficient protein translocation. Using a substrate-trapping proteomic approach, we identify that nascent proteins bearing marginally hydrophobic signal sequences accumulate on the cytosolic side of the Sec61 translocon. Sec63 is co-translationally recruited to the translocation site and mediates BiP binding to incoming polypeptides. BiP binding not only releases translocationally paused nascent chains but also ensures protein folding in the ER. Increasing hydrophobicity of signal sequences bypasses Sec63/BiP-dependent translocation, but translocated proteins are prone to misfold and aggregate in the ER under limited BiP availability. Thus, the signal sequence–guided protein folding may explain why signal sequences are diverse and use multiple protein translocation pathways.
      PubDate: Fri, 02 Dec 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202203070
      Issue No: Vol. 222, No. 1 (2022)
       
  • Glial TGFβ activity promotes neuron survival in peripheral nerves

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      Abstract: Maintaining long, energetically demanding axons throughout the life of an animal is a major challenge for the nervous system. Specialized glia ensheathe axons and support their function and integrity throughout life, but glial support mechanisms remain poorly defined. Here, we identified a collection of secreted and transmembrane molecules required in glia for long-term axon survival in vivo. We showed that the majority of components of the TGFβ superfamily are required in glia for sensory neuron maintenance but not glial ensheathment of axons. In the absence of glial TGFβ signaling, neurons undergo age-dependent degeneration that can be rescued either by genetic blockade of Wallerian degeneration or caspase-dependent death. Blockade of glial TGFβ signaling results in increased ATP in glia that can be mimicked by enhancing glial mitochondrial biogenesis or suppressing glial monocarboxylate transporter function. We propose that glial TGFβ signaling supports axon survival and suppresses neurodegeneration through promoting glial metabolic support of neurons.
      PubDate: Fri, 18 Nov 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202111053
      Issue No: Vol. 222, No. 1 (2022)
       
  • ATM inhibition drives metabolic adaptation via induction of
           macropinocytosis

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      Abstract: Macropinocytosis is a nonspecific endocytic process that may enhance cancer cell survival under nutrient-poor conditions. Ataxia-Telangiectasia mutated (ATM) is a tumor suppressor that has been previously shown to play a role in cellular metabolic reprogramming. We report that the suppression of ATM increases macropinocytosis to promote cancer cell survival in nutrient-poor conditions. Combined inhibition of ATM and macropinocytosis suppressed proliferation and induced cell death both in vitro and in vivo. Supplementation of ATM-inhibited cells with amino acids, branched-chain amino acids (BCAAs) in particular, abrogated macropinocytosis. Analysis of ATM-inhibited cells in vitro demonstrated increased BCAA uptake, and metabolomics of ascites and interstitial fluid from tumors indicated decreased BCAAs in the microenvironment of ATM-inhibited tumors. These data reveal a novel basis of ATM-mediated tumor suppression whereby loss of ATM stimulates protumorigenic uptake of nutrients in part via macropinocytosis to promote cancer cell survival and reveal a potential metabolic vulnerability of ATM-inhibited cells.
      PubDate: Fri, 18 Nov 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202007026
      Issue No: Vol. 222, No. 1 (2022)
       
  • Mitochondrial dysfunction compromises ciliary homeostasis in astrocytes

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      Abstract: Astrocytes, often considered as secondary responders to neurodegeneration, are emerging as primary drivers of brain disease. Here we show that mitochondrial DNA depletion in astrocytes affects their primary cilium, the signaling organelle of a cell. The progressive oxidative phosphorylation deficiency in astrocytes induces FOXJ1 and RFX transcription factors, known as master regulators of motile ciliogenesis. Consequently, a robust gene expression program involving motile cilia components and multiciliated cell differentiation factors are induced. While the affected astrocytes still retain a single cilium, these organelles elongate and become remarkably distorted. The data suggest that chronic activation of the mitochondrial integrated stress response (ISRmt) in astrocytes drives anabolic metabolism and promotes ciliary elongation. Collectively, our evidence indicates that an active signaling axis involving mitochondria and primary cilia exists and that ciliary signaling is part of ISRmt in astrocytes. We propose that metabolic ciliopathy is a novel pathomechanism for mitochondria-related neurodegenerative diseases.
      PubDate: Wed, 16 Nov 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202203019
      Issue No: Vol. 222, No. 1 (2022)
       
  • EpCAM proteolysis and release of complexed claudin-7 repair and maintain
           the tight junction barrier

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      Abstract: TJs maintain the epithelial barrier by regulating paracellular permeability. Since TJs are under dynamically fluctuating intercellular tension, cells must continuously survey and repair any damage. However, the underlying mechanisms allowing cells to sense TJ damage and repair the barrier are not yet fully understood. Here, we showed that proteinases play an important role in the maintenance of the epithelial barrier. At TJ break sites, EpCAM–claudin-7 complexes on the basolateral membrane become accessible to apical membrane-anchored serine proteinases (MASPs) and the MASPs cleave EpCAM. Biochemical data and imaging analysis suggest that claudin-7 released from EpCAM contributes to the rapid repair of damaged TJs. Knockout (KO) of MASPs drastically reduced barrier function and live-imaging of TJ permeability showed that MASPs-KO cells exhibited increased size, duration, and frequency of leaks. Together, our results reveal a novel mechanism of TJ maintenance through the localized proteolysis of EpCAM at TJ leaks, and provide a better understanding of the dynamic regulation of epithelial permeability.
      PubDate: Tue, 15 Nov 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202204079
      Issue No: Vol. 222, No. 1 (2022)
       
  • The Cdc42 GAP Rga6 promotes monopolar outgrowth of spores

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      Abstract: The molecular mechanisms underlying the establishment of the monopolar growth of fission yeast spores have been less characterized. Here, we report that the Cdc42 GTPase-activating protein (GAP) Rga6 is required for promoting monopolar growth during spore germination. The absence of Rga6 increases the number of spores that grow in a bipolar fashion. Rga6 decorates the non-growing cortical region, binds phosphatidylinositol 4,5-bisphosphate, and colocalizes with the phosphatidylinositol 4,5-bisphosphate-binding protein Opy1. Overexpression of Opy1 diminishes the cortical localization of Rga6. The characteristic localization of Rga6 on the cell cortex depends on the C-terminal PBR region of Rga6. Moreover, engineered chimera composed of the Rga6 C-terminal PBR region fused to the GAP domain of Rga3 or Rga4 are sufficient to rescue the spore growth phenotype caused by the absence of Rga6. Hence, our work establishes a paradigm in which the lipid composition of the plasma membrane directs polarized cell growth by specifying the cortical localization of a GAP protein.
      PubDate: Thu, 10 Nov 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202202064
      Issue No: Vol. 222, No. 1 (2022)
       
  • REC drives recombination to repair double-strand breaks in animal mtDNA

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      Abstract: Mechanisms that safeguard mitochondrial DNA (mtDNA) limit the accumulation of mutations linked to mitochondrial and age-related diseases. Yet, pathways that repair double-strand breaks (DSBs) in animal mitochondria are poorly understood. By performing a candidate screen for mtDNA repair proteins, we identify that REC—an MCM helicase that drives meiotic recombination in the nucleus—also localizes to mitochondria in Drosophila. We show that REC repairs mtDNA DSBs by homologous recombination in somatic and germline tissues. Moreover, REC prevents age-associated mtDNA mutations. We further show that MCM8, the human ortholog of REC, also localizes to mitochondria and limits the accumulation of mtDNA mutations. This study provides mechanistic insight into animal mtDNA recombination and demonstrates its importance in safeguarding mtDNA during ageing and evolution.
      PubDate: Thu, 10 Nov 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202201137
      Issue No: Vol. 222, No. 1 (2022)
       
  • The β-cell primary cilium is an autonomous Ca 2+ compartment for
           paracrine GABA signaling

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      Abstract: The primary cilium is an organelle present in most adult mammalian cells that is considered as an antenna for sensing the local microenvironment. Here, we use intact mouse pancreatic islets of Langerhans to investigate signaling properties of the primary cilium in insulin-secreting β-cells. We find that GABAB1 receptors are strongly enriched at the base of the cilium, but are mobilized to more distal locations upon agonist binding. Using cilia-targeted Ca2+ indicators, we find that activation of GABAB1 receptors induces selective Ca2+ influx into primary cilia through a mechanism that requires voltage-dependent Ca2+ channel activation. Islet β-cells utilize cytosolic Ca2+ increases as the main trigger for insulin secretion, yet we find that increases in cytosolic Ca2+ fail to propagate into the cilium, and that this isolation is largely due to enhanced Ca2+ extrusion in the cilium. Our work reveals local GABA action on primary cilia that involves Ca2+ influx and depends on restricted Ca2+ diffusion between the cilium and cytosol.
      PubDate: Wed, 09 Nov 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202108101
      Issue No: Vol. 222, No. 1 (2022)
       
  • V-ATPase/TORC1-mediated ATFS-1 translation directs mitochondrial UPR
           activation in C. elegans

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      Abstract: To adapt mitochondrial function to the ever-changing intra- and extracellular environment, multiple mitochondrial stress response (MSR) pathways, including the mitochondrial unfolded protein response (UPRmt), have evolved. However, how the mitochondrial stress signal is sensed and relayed to UPRmt transcription factors, such as ATFS-1 in Caenorhabditis elegans, remains largely unknown. Here, we show that a panel of vacuolar H+-ATPase (v-ATPase) subunits and the target of rapamycin complex 1 (TORC1) activity are essential for the cytosolic relay of mitochondrial stress to ATFS-1 and for the induction of the UPRmt. Mechanistically, mitochondrial stress stimulates v-ATPase/Rheb-dependent TORC1 activation, subsequently promoting ATFS-1 translation. Increased translation of ATFS-1 upon mitochondrial stress furthermore relies on a set of ribosomal components but is independent of GCN-2/PEK-1 signaling. Finally, the v-ATPase and ribosomal subunits are required for mitochondrial surveillance and mitochondrial stress-induced longevity. These results reveal a v-ATPase-TORC1-ATFS-1 signaling pathway that links mitochondrial stress to the UPRmt through intimate crosstalks between multiple organelles.
      PubDate: Mon, 31 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202205045
      Issue No: Vol. 222, No. 1 (2022)
       
  • Real-time imaging of RNA polymerase I activity in living human cells

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      Abstract: RNA polymerase I (Pol I) synthesizes about 60% of cellular RNA by transcribing multiple copies of the ribosomal RNA gene (rDNA). The transcriptional activity of Pol I controls the level of ribosome biogenesis and cell growth. However, there is currently a lack of methods for monitoring Pol I activity in real time. Here, we develop LiveArt (live imaging-based analysis of rDNA transcription) to visualize and quantify the spatiotemporal dynamics of endogenous ribosomal RNA (rRNA) synthesis. LiveArt reveals mitotic silencing and reactivation of rDNA transcription, as well as the transcriptional kinetics of interphase rDNA. Using LiveArt, we identify SRFBP1 as a potential regulator of rRNA synthesis. We show that rDNA transcription occurs in bursts and can be altered by modulating burst duration and amplitude. Importantly, LiveArt is highly effective in the screening application for anticancer drugs targeting Pol I transcription. These approaches pave the way for a deeper understanding of the mechanisms underlying nucleolar functions.
      PubDate: Tue, 25 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202202110
      Issue No: Vol. 222, No. 1 (2022)
       
  • RUFY1 binds Arl8b and mediates endosome-to-TGN CI-M6PR retrieval for cargo
           sorting to lysosomes

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      Abstract: Arl8b, an Arf-like GTP-binding protein, regulates cargo trafficking and positioning of lysosomes. However, it is unknown whether Arl8b regulates lysosomal cargo sorting. Here, we report that Arl8b binds to the Rab4 and Rab14 interaction partner, RUN and FYVE domain-containing protein (RUFY) 1, a known regulator of cargo sorting from recycling endosomes. Arl8b determines RUFY1 endosomal localization through regulating its interaction with Rab14. RUFY1 depletion led to a delay in CI-M6PR retrieval from endosomes to the TGN, resulting in impaired delivery of newly synthesized hydrolases to lysosomes. We identified the dynein-dynactin complex as an RUFY1 interaction partner, and similar to a subset of activating dynein adaptors, the coiled-coil region of RUFY1 was required for interaction with dynein and the ability to mediate dynein-dependent organelle clustering. Our findings suggest that Arl8b and RUFY1 play a novel role on recycling endosomes, from where this machinery regulates endosomes to TGN retrieval of CI-M6PR and, consequently, lysosomal cargo sorting.
      PubDate: Tue, 25 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202108001
      Issue No: Vol. 222, No. 1 (2022)
       
  • Hemicentin-mediated type IV collagen assembly strengthens juxtaposed
           basement membrane linkage

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      Abstract: Basement membrane (BM) matrices surround and separate most tissues. However, through poorly understood mechanisms, BMs of adjacent tissue can also stably link to support organ structure and function. Using endogenous knock-in fluorescent proteins, conditional RNAi, optogenetics, and quantitative live imaging, we identified extracellular matrix proteins mediating a BM linkage (B-LINK) between the uterine utse and epidermal seam cell BMs in Caenorhabditis elegans that supports the uterus during egg-laying. We found that hemicentin is secreted by the utse and promotes fibulin-1 assembly to jointly initiate the B-LINK. During egg-laying, however, both proteins’ levels decline and are not required for B-LINK maintenance. Instead, we discovered that hemicentin recruits ADAMTS9/20, which facilitates the assembly of high levels of type IV collagen that sustains the B-LINK during the mechanically active egg-laying period. This work reveals mechanisms underlying BM–BM linkage maturation and identifies a crucial function for hemicentin and fibulin-1 in initiating attachment and type IV collagen in strengthening this specialized form of tissue linkage.
      PubDate: Tue, 25 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202112096
      Issue No: Vol. 222, No. 1 (2022)
       
  • APC/C Cdc20 -mediated degradation of Clb4 prompts astral microtubule
           stabilization at anaphase onset

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      Abstract: Key for accurate chromosome partitioning to the offspring is the ability of mitotic spindle microtubules to respond to different molecular signals and remodel their dynamics accordingly. Spindle microtubules are conventionally divided into three classes: kinetochore, interpolar, and astral microtubules (kMTs, iMTs, and aMTs, respectively). Among all, aMT regulation remains elusive. Here, we show that aMT dynamics are tightly regulated. aMTs remain unstable up to metaphase and are stabilized at anaphase onset. This switch in aMT dynamics, important for proper spindle orientation, specifically requires the degradation of the mitotic cyclin Clb4 by the Anaphase Promoting Complex bound to its activator subunit Cdc20 (APC/CCdc20). These data highlight a unique role for mitotic cyclin Clb4 in controlling aMT regulating factors, of which Kip2 is a prime candidate, provide a framework to understand aMT regulation in vertebrates, and uncover mechanistic principles of how the APC/CCdc20 choreographs the timing of late mitotic events by sequentially impacting on the three classes of spindle microtubules.
      PubDate: Fri, 21 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202203089
      Issue No: Vol. 222, No. 1 (2022)
       
  • Liquid–liquid phase separation mediates the formation of herpesvirus
           assembly compartments

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      Abstract: Virus assembly, which takes place during the late stage of viral replication, is essential for virus propagation. However, the underlying mechanisms remain poorly understood, especially for viruses with complicated structures. Here, we use correlative light and electron microscopy to examine the formation of cytoplasmic virion assembly compartments (cVACs) during infection by a γ-herpesvirus. These cVACs are membraneless organelles with liquid-like properties. Formation of cVACs during virus infection is mediated by ORF52, an abundant tegument protein. ORF52 undergoes liquid–liquid phase separation (LLPS), which is promoted by both DNA and RNA. Disrupting ORF52 phase separation blocks cVACs formation and virion production. These results demonstrate that phase separation of ORF52 is critical for cVACs formation. Our work defines herpesvirus cVACs as membraneless compartments that are generated through a process of LLPS mediated by a tegument protein and adds to the cellular processes that are facilitated by phase separation.
      PubDate: Mon, 17 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202201088
      Issue No: Vol. 222, No. 1 (2022)
       
  • Force tuning through regulation of clathrin-dependent integrin endocytosis

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      Abstract: Integrin endocytosis is essential for many fundamental cellular processes. Whether and how the internalization impacts cellular mechanics remains elusive. Whereas previous studies reported the contribution of the integrin activator, talin, in force development, the involvement of inhibitors is less documented. We identified ICAP-1 as an integrin inhibitor involved in mechanotransduction by co-working with NME2 to control clathrin-mediated endocytosis of integrins at the edge of focal adhesions (FA). Loss of ICAP-1 enables β3-integrin-mediated force generation independently of β1 integrin. β3-integrin-mediated forces were associated with a decrease in β3 integrin dynamics stemming from their reduced diffusion within adhesion sites and slow turnover of FA. The decrease in β3 integrin dynamics correlated with a defect in integrin endocytosis. ICAP-1 acts as an adaptor for clathrin-dependent endocytosis of integrins. ICAP-1 controls integrin endocytosis by interacting with NME2, a key regulator of dynamin-dependent clathrin-coated pits fission. Control of clathrin-mediated integrin endocytosis by an inhibitor is an unprecedented mechanism to tune forces at FA.
      PubDate: Mon, 17 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202004025
      Issue No: Vol. 222, No. 1 (2022)
       
  • The GARP complex prevents sterol accumulation at the trans-Golgi network
           during dendrite remodeling

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      Abstract: Membrane trafficking is essential for sculpting neuronal morphology. The GARP and EARP complexes are conserved tethers that regulate vesicle trafficking in the secretory and endolysosomal pathways, respectively. Both complexes contain the Vps51, Vps52, and Vps53 proteins, and a complex-specific protein: Vps54 in GARP and Vps50 in EARP. In Drosophila, we find that both complexes are required for dendrite morphogenesis during developmental remodeling of multidendritic class IV da (c4da) neurons. Having found that sterol accumulates at the trans-Golgi network (TGN) in Vps54KO/KO neurons, we investigated genes that regulate sterols and related lipids at the TGN. Overexpression of oxysterol binding protein (Osbp) or knockdown of the PI4K four wheel drive (fwd) exacerbates the Vps54KO/KO phenotype, whereas eliminating one allele of Osbp rescues it, suggesting that excess sterol accumulation at the TGN is, in part, responsible for inhibiting dendrite regrowth. These findings distinguish the GARP and EARP complexes in neurodevelopment and implicate vesicle trafficking and lipid transfer pathways in dendrite morphogenesis.
      PubDate: Fri, 14 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202112108
      Issue No: Vol. 222, No. 1 (2022)
       
  • Convergence of secretory, endosomal, and autophagic routes in
           trans-Golgi–associated lysosomes

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      Abstract: At the trans-Golgi, complex traffic connections exist to the endolysosomal system additional to the main Golgi-to–plasma membrane secretory route. Here, we investigated three hits in a Drosophila screen displaying secretory cargo accumulation in autophagic vesicles: ESCRT-III component Vps20, SNARE-binding Rop, and lysosomal pump subunit VhaPPA1-1. We found that Vps20, Rop, and lysosomal markers localize near the trans-Golgi. Furthermore, we document that the vicinity of the trans-Golgi is the main cellular location for lysosomes and that early, late, and recycling endosomes associate as well with a trans-Golgi–associated degradative compartment where basal microautophagy of secretory cargo and other materials occurs. Disruption of this compartment causes cargo accumulation in our hits, including Munc18 homolog Rop, required with Syx1 and Syx4 for Rab11-mediated endosomal recycling. Finally, besides basal microautophagy, we show that the trans-Golgi–associated degradative compartment contributes to the growth of autophagic vesicles in developmental and starvation-induced macroautophagy. Our results argue that the fly trans-Golgi is the gravitational center of the whole endomembrane system.
      PubDate: Fri, 14 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202203045
      Issue No: Vol. 222, No. 1 (2022)
       
  • β-heavy-spectrin stabilizes the constricting contractile ring during
           cytokinesis

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      Abstract: Cytokinesis requires the constriction of an actomyosin-based contractile ring and involves multiple F-actin crosslinkers. We show that partial depletion of the C. elegans cytokinetic formin generates contractile rings with low F-actin levels that constrict but are structurally fragile, and we use this background to investigate the roles of the crosslinkers plastin/PLST-1 and β-heavy-spectrin/SMA-1 during ring constriction. We show that the removal of PLST-1 or SMA-1 has opposite effects on the structural integrity of fragile rings. PLST-1 loss reduces cortical tension that resists ring constriction and makes fragile rings less prone to ruptures and regressions, whereas SMA-1 loss exacerbates structural defects, leading to frequent ruptures and cytokinesis failure. Fragile rings without SMA-1 or containing a shorter SMA-1, repeatedly rupture at the same site, and SMA-1::GFP accumulates at repair sites in fragile rings and in rings cut by laser microsurgery. These results establish that β-heavy-spectrin stabilizes the constricting ring and reveals the importance of β-heavy-spectrin size for network connectivity at low F-actin density.
      PubDate: Tue, 11 Oct 2022 00:00:00 GMT
      DOI: 10.1083/jcb.202202024
      Issue No: Vol. 222, No. 1 (2022)
       
 
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