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Study reveals unexpected dialogue between mitotic entrance and exit pathway proteins on yeast spindle pole bodies.

People & Ideas

Fuchs studies how cell death controls stem cell–driven processes.


Bobola previews work from the Schulte laboratory showing that the atypical homeodomain protein MEIS2 facilitates chromatin accessibility of transcriptionally inactive genes in neuronal differentiation.

Elzeneini and Wickström discuss work from Oldenburg et al. on the regulation of adipogenesis by lamin A–mediated control of chromatin.

Serquiña and Ziegelbauer discuss Chiu et al.’s recent finding of a novel strategy for viral ​genome partitioning used by Kaposi’s Sarcoma–associated herpesvirus.

Bezbradica and Schroder preview new work from Kuri et al. that images endogenous ASC dynamics in zebrafish.

Keren and Shemesh preview work from Pontes et al. that elucidates how the mechanical signals of membrane tension interact with the cytoskeleton to determine adhesion positions.


Schmid provides a perspective on exciting new research examining the relationship between signaling and endocytosis in cancer.


Victoria and Zurzolo discuss current evidence for the emerging role of lysosomal damage and tunneling nanotubes in the intercellular propagation of prion and prion-like proteins in neurodegenerative disease.


In Special Collection: Cell Division 2018

The size of mitotic chromosomes is coordinated with cell size. Through an RNAi screen in Caenorhabditis elegans, Ladouceur et al. identify CENP-A and topo-II as factors affecting chromosome length. Quantitative analyses of protein dynamics suggest that CENP-A and topo-II localize and function independently to provide centromeric chromatin structure and determine the length of holocentric mitotic chromosomes.

Many cytokinetic actomyosin ring components undergo dynamic turnover, but its function is unclear. Chew et al. show that continuous actin polymerization ensures crucial F-actin homeostasis during ring contraction, without which ring proteins organize into noncontractile clusters.

Yeast MTs do not appear to undergo the lattice compaction seen in mammalian MTs upon GTP hydrolysis. Binding of the +TIP Bim1, both between and within αβ-tubulin dimers, causes compaction of yeast MTs and their rapid disassembly.

Murley et al. show that sterol transport proteins regulate target-of-rapamycin signaling at membrane contact sites in budding yeast. Ltc3/4 localize to a previously unknown region of the plasma membrane and, with other proteins, inhibit TORC2-Ypk1 signaling. At ER–vacuole contact sites, Ltc1 regulates the formation of sterol-enriched membrane domains that correlate with reduced TORC1 signaling.

Starvation-induced unconventional secretion of Acb1 requires ESCRT-I, -II, and -III and Grh1. Cruz-Garcia et al. report that SOD1 and its mutant form linked to amyotrophic lateral sclerosis are also secreted upon nutrient starvation in a Grh1- and ESCRT-I–, -II–, and -III–dependent process. The authors identify a conserved diacidic motif in Acb1 and SOD1 that is necessary for their export in yeast and human cells.

In motile cilia and flagella, tubulin glycylation is involved in axoneme stabilization. Using a newly developed antibody, Gadadhar et al. now show that glycylation also accumulates in primary cilia, where it controls ciliary length. This suggests an important role for this PTM in primary cilia homeostasis.


PARP1/ARTD1 induces chromatin opening by posttranslational modification of the linker histone H1, but how PARP1 is targeted to physiologically correct gene loci is poorly understood. Hau et al. show that in differentiating neurons, PARP1 is rapidly and specifically recruited to a neuron-specific promoter by the atypical homeodomain protein MEIS2.

Mutations in A-type nuclear lamins cause laminopathies. Oldenburg et al. show that a lipodystrophy-causing lamin A mutation impairs adipogenic gene expression via upregulation of miR-335 through both epigenetic and conformational alterations of the MIR335 locus.

Several human tumor viruses, including Kaposi’s sarcoma–associated herpesvirus (KSHV), maintain their plasmid genomes by tethering them to cellular chromosomes. Chiu et al. identify a viral segregation mechanism: KSHV stably clusters some of its genomes, which are inherited as units. Clustering, as predicted computationally and observed in live cells, rapidly establishes high viral copy numbers in cells.

Dynein orients the spindle by pulling on astral microtubules from the cortex. In Saccharomyces cerevisiae, the microtubule-associated protein She1 specifically inhibits dynein in the mother compartment to promote spindle movements toward the bud. Zhu et al. demonstrate that She1 also stabilizes interpolar microtubules, ensuring spindle integrity during dynein-mediated spindle positioning.

Dynein tethered to the cell cortex generates pulling forces that position the mitotic spindle. To understand the dynamics of this process, Schmidt et al. use fluorescently tagged endogenous dynein and show that two distinct cortical dynein populations together create a robust force-generating system in the polarized one-cell Caenorhabditis elegans embryo.

Events at the fission yeast equivalent of the centrosome, the spindle pole body, determine the timing of mitotic commitment and mitotic exit. Previous work has established that events on Cut12 drive commitment, whereas events on a distinct scaffold, Sid4 drive exit. Chan et al. now show how signaling on Sid4 influences commitment to explain the rationale for using the centrosome as a signaling center; centrosomal signaling supports integration of outputs from distinct inputs.

In Special Collection: Cell Division 2018

How nuclear pore complexes (NPCs) become segregated during mitosis is unclear. Suresh et al. reveal that Nup2 acts as a tether between NPCs and chromatin during mitosis. This effectively links DNA and NPC segregation and ensures accurate NPC inheritance to daughter nuclei.

LINC complexes connect the inner and outer nuclear membrane (ONM) to transduce nucleocytoskeletal force. Ding et al. identify an ONM protein, Kuduk/TMEM258, which modulates the quality of LINC complexes and regulates the nuclear envelope architecture, nuclear positioning, and the development of ovarian follicles.

TRIM37 gene mutations cause muscle–liver–brain–eye (mulibrey) nanism: a rare autosomal recessive, prenatal onset growth disorder. Wang et al. find that TRIM37 ubiquitylates and stabilizes PEX5, the receptor for import of peroxisomal matrix proteins, suggesting that mulibrey nanism is a new peroxisomal biogenesis disorder.

A separation-of-function point mutant in APC is generated that disrupts actin nucleation without affecting APC’s other functions. Genetic analysis using this mutant reveals that APC stimulates actin assembly in living cells and that this activity is critical for microtubule-induced turnover of focal adhesions and directed cell migration.

Copolymerization of nonmuscle myosins IIA and IIB followed by their differential turnover in stress fibers leads to self-sorting of IIA and IIB along the front–rear axis of the cell, thus producing a polarized actin cytoskeleton.

The inflammasome adaptor ASC forms enormous intracellular complexes called specks. Live imaging of endogenous ASC in keratinocytes reveals speck formation dynamics and their lethal effects, as well as macrophages’ engulfment and digestion of the specks left behind by dead cells.

Autosomal-recessive omodysplasia (OMOD1) is caused by mutations in glypican-6. Capurro et al. show that glypican-6 stimulates Hedgehog (Hh) signaling, and reduced Hh signaling may contribute to the pathogenesis of OMOD1.

Acidic clusters act as sorting signals for packaging cargo into clathrin-coated vesicles. Navarro Negredo et al. show that the clathrin adaptor AP-1 subunit µ1 interacts with endogenous acidic cluster cargo as well as with the HIV-1 acidic cluster protein Nef, and they tease out the contribution of this interaction to acidic cluster protein trafficking.

Migrating cells encounter directional cues to reach their destinations, often using G protein–coupled receptors (GPCRs) to interpret such cues. LeBlanc and Lehmann show that two highly conserved domains in the GPCR Tre1 mediate distinct migratory responses in germ cells via separate signaling pathways, one regulating cell polarization and the other directional migration.

In Special Collection: Mechanobiology 2019

Pontes et al. show that plasma membrane mechanics exerts an upstream control during cell motility. Variations in plasma membrane tension orchestrate the behavior of the cell leading edge, with increase–decrease cycles in tension promoting adhesion row positioning.

Microglia can influence the excitatory responses of neurons, but less is known about how these immune cells in the brain may influence inhibitory neurotransmitters. Cantaut-Belarif et al. report that prostaglandin production by Toll-like receptor–stimulated microglia can influence the glycinergic but not GABAergic responses of neurons by altering the lateral diffusion of glycine receptors specifically within the synaptic membrane.

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