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Alexandra Colin, Gaëlle Letort, Nitzan Razin, Maria Almonacid, Wylie Ahmed, Timo Betz, Marie-Emilie Terret, Nir S. Gov, Raphaël Voituriez, Zoher Gueroui, Marie-Hélène Verlhac
Nucleus centering in mouse oocytes depends on a gradient of actin-positive vesicle persistence. Modeling coupled to 3D simulations and experimental testing of predictions coming from the simulations demonstrate that this gradient nonspecifically centers large objects during prophase I and meiosis I in oocytes.
Sandra Sofía Edwards-Jorquera, Floris Bosveld, Yohanns A. Bellaïche, Ana-María Lennon-Duménil, Ana-María Lennon-Duménil, Álvaro Glavic, Álvaro Glavic
The authors show the dual regulation of phagosomal degradation and migration of Drosophila macrophages by Trpml, a lysosomal calcium channel. Trpml promotes cell migration by activating actomyosin contractility but supports phagosomal degradation through a myosin-independent mechanism.
Arnaud Rondelet, Yu-Chih Lin, Divya Singh, Arthur T. Porfetye, Harish C. Thakur, Andreas Hecker, Pia Brinkert, Nadine Schmidt, Shweta Bendre, Franziska Müller, Lisa Mazul, Per O. Widlund, Tanja Bange, Michael Hiller, Ingrid R. Vetter, Alexander W. Bird
Clathrin stabilizes microtubules and promotes chromosome alignment during mitosis. Rondelet et al. show that the clathrin–adaptor interaction mechanism is repurposed to recruit GTSE1 to the spindle, which inhibits the microtubule depolymerase MCAK and promotes chromosome alignment by stabilizing nonkinetochore microtubules.
Sofia Cunha-Silva, Mariana Osswald, Jana Goemann, João Barbosa, Luis M. Santos, Pedro Resende, Tanja Bange, Cristina Ferrás, Claudio E. Sunkel, Carlos Conde
The spindle assembly checkpoint requires recruitment of Mad1-C-Mad2 to unattached kinetochores but also Mad1 binding to Megator/Tpr at nuclear pore complexes during interphase. Cunha-Silva et al. provide evidence that this spatiotemporal redistribution is due to Mps1-mediated dissociation of Mad1 from Megator/Tpr during prophase, which is critical for Mad1-C-Mad2 accumulation at unattached kinetochores and for the accuracy of chromosome segregation in vivo.
Wei Wang, Alba Zuidema, Lisa te Molder, Leila Nahidiazar, Liesbeth Hoekman, Thomas Schmidt, Stefano Coppola, Arnoud Sonnenberg
This study reveals a novel role of hemidesmosomes in resisting actomyosin-generated cellular tension, which is dependent on mechanical coupling of focal adhesions to hemidesmosomes and inhibition of mechanosensitive signaling. Furthermore, through their ability to influence cellular tension, hemidesmosomes also control the localization of αvβ5 in flat clathrin lattices.
Min Lee, Yen-Chen Liu, Chen Chen, Chi-Huan Lu, Shao-Tzu Lu, Tzyy-Nan Huang, Meng-Tsung Hsu, Yi-Ping Hsueh, Pei-Lin Cheng
Lee et al. show that the local abundance of the chloride importer NKCC1 and timely emergence of GABAergic inhibition are modulated by proteasome distribution, mediated through interactions of proteasomes with the proteasome adaptor Ecm29 and the axon initial segment scaffold protein ankyrin G.
Guendalina Rossi, Dante Lepore, Lillian Kenner, Alexander B. Czuchra, Melissa Plooster, Adam Frost, Mary Munson, Patrick Brennwald
Rossi et al. describe a novel assay for exocyst in-vesicle tethering. In this assay, gain-of-function mutants in the Exo70 subunit of the exocyst, which bypass Rho/Cdc42 activation in vivo, stimulate vesicle tethering. Single-particle EM studies reveal a structural change responsible for the gain of function.

Related Articles from Rockefeller University Press

Current Issue
Volume 219,
Issue 1,
January 6, 2020
Reviews & Opinions
Christophe Leterrier
Christophe Leterrier previews work from Lee et al. that describes a mechanism by which NKCC1 levels are regulated in GABAergic neurons.
Jeevisha Bajaj, Emily Diaz, Tannishtha Reya
Bajaj et al. review how cancers originate, how their heterogeneity is linked to cancer stem cells, and the signals fundamental to driving these processes.
Alexander Buffone, Jr., Valerie M. Weaver
Buffone and Weaver discuss how the structure of the backbones and glycans of the tumor glycocalyx governs cell–matrix interactions and directs cancer progression.

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