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Kosuke Sako, Ayako Furukawa, Ryu-Suke Nozawa, Jun-ichi Kurita, Yoshifumi Nishimura, Toru Hirota
Maintenance of ploidy relies on Aurora-B, supported by HP1. Sako et al. report that INCENP binds to HP1 not only through the HP1-binding consensus PVI motif but also its downstream α-helical segment. This unique interface ensures a strong bond with HP1, Aurora-B activity, and mitotic fidelity.
Article
Jason C. Casler, Clare S. Harper, Antoineen J. White, Heidi L. Anderson, Laura L. Lackner
Casler et al. identify that the ER-localized protein Scs2 interacts with a FFAT motif in the C-terminus of the mitochondria–PM tether Num1 to form a tripartite mitochondria–ER–PM contact site. Loss of the Num1–Scs2 interaction severely perturbs mitochondrial division rates. Unexpectedly, they also identify a novel role of mitochondria–ER–PM contact sites in regulating PM PI(4)P metabolism.
Article
Carlo Barnaba, David G. Broadbent, Emily G. Kaminsky, Gloria I. Perez, Jens C. Schmidt
Barnaba, Broabent et al. develop K-FOCUS for high-throughput analysis of autophagy foci in human cells and demonstrate that glucose starvation downregulates autophagy via AMP-activated protein kinase, which prevents phagophore tethering to donor membranes to inhibit autophagosome maturation.
Article
Jennifer E. Gilda, Asrafun Nahar, Dharanibalan Kasiviswanathan, Nadav Tropp, Tamar Gilinski, Tamar Lahav, Dina Alexandrovich, Yael Mandel-Gutfreund, Soyeon Park, Shenhav Shemer
In this study, the authors investigate how cells regulate proteasome content in response to catabolic stimuli in vivo. During cellular adaptation to accelerated proteolysis, muscle cells boost proteasome levels by inducing proteasome subunit genes and assembly chaperones in a two-phase transcriptional program that is controlled by multiple transcription factors.
Article
Kaiden M. Power, Ken C. Nguyen, Andriele Silva, Shaneen Singh, David H. Hall, Christopher Rongo, Maureen M. Barr
Neurodegeneration and ciliary degeneration are caused by mutation of the deglutamylase CCP1/CCPP-1 in humans and C. elegans. The conserved NIMA-related kinase NEKL-4/NEK10 can suppress or promote degeneration in an activity-dependent manner that involves cilia–mitochondria communication and that is independent of glutamylation.
Report
Nassiba Bagdadi, Juliette Wu, Julie Delaroche, Laurence Serre, Christian Delphin, Manon De Andrade, Marion Carcel, Homaira Nawabi, Benoît Pinson, Claire Vérin, Yohann Couté, Sylvie Gory-Fauré, Annie Andrieux, Virginie Stoppin-Mellet, Isabelle Arnal
Bagdadi et al. show that, although usually considered inactive, GDP-bound tubulin polymerizes into remarkably stable microtubules. These results reveal that microtubules possess an intrinsic capacity for stability, independent of accessory proteins. This finding provides novel mechanisms to revisit microtubule dynamics.
Article
Yeongjin David Kim, Hyun Gwan Park, Seunghwan Song, Joohyung Kim, Byoung Ju Lee, Kendal Broadie, Seungbok Lee
Dynamic remodeling of actin cytoskeletal networks is critical for many aspects of presynaptic plasticity. However, it remains poorly defined how presynaptic actin is regulated. Kim et al. demonstrate that the presynaptic Abl-Gef26 and Rut-cAMP-Epac pathways converge on actin-regulatory Rap1-Vav-Rac1 signaling to mediate Gbb/BMP-induced presynaptic growth and activity-induced functional plasticity, respectively.
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Current Issue
Volume 223,
Issue 5,
6 May 2024
Reviews & Opinions
Spotlight
Natalia Elisa Bernardes, Yuh Min Chook
Bernardes and Chook preview work from Yang et al. that reveals that folded WW domains can serve as nuclear localization signals.
Review
Yi-Tang Lee, Mumine Senturk, Youchen Guan, Meng C. Wang
Meng Wang and colleagues review the intricate communication between bacteria and host organelles and the impact of such communication on immune response, aging, and longevity.
Spotlight
Rachel S. Kadzik, David R. Kovar
Rachel Kadzik and David Kovar preview work from Chikireddy and colleagues, which examines how fascin delays cofilin-induced actin filament disassembly and regulates network turnover.

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