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Edgar Sánchez-Ramírez, Thi Phuong Lien Ung, Alejandro Alarcón del Carmen, Ximena del Toro-Rios, Guadalupe R. Fajardo-Orduña, Lilia G. Noriega, Victor A. Cortés-Morales, Armando R. Tovar, Juan José Montesinos, Ricardo Orozco-Solís, Chiara Stringari, Lorena Aguilar-Arnal
Sánchez-Ramirez, Ung et al. show that NAD+ bioavailability controls adipogenic differentiation obstructing adipocyte commitment, downregulating ribosomal proteins–coding genes and leading to quiescent metabolic state. Instead, the NAD+-dependent SIRT1 deacetylase is essential for terminal differentiation of pre-adipocytes and regulates subcellular compartmentalization of redox metabolism during adipogenesis.
Article
Shu Hiragi, Takahide Matsui, Yuriko Sakamaki, Mitsunori Fukuda
Hiragi et al. identify TBC1D18 as a Rab5-GAP that is associated with Mon1 and mediates endosome maturation. They propose a new endosome maturation model in which Mon1–Ccz1 together with TBC1D18 coordinates endosome maturation by inactivating Rab5 and activating Rab7.
Article
Shrividya Sana, Ashwathi Rajeevan, Sachin Kotak
Chromosome separation is coupled with cleavage furrow formation during anaphase. Sana, Rajeevan, et al. demonstrate that the mutually exclusive localization of NuMA and Ect2/Cyk4/Mklp1 ensures dynein/dynactin and RhoA at distinct membrane zones to coordinate chromosome separation with cleavage furrow formation.
Article
Xiaotong Jia, Anastasia Knyazeva, Yu Zhang, Sergio Castro-Gonzalez, Shuhei Nakamura, Lars-Anders Carlson, Tamotsu Yoshimori, Dale P. Corkery, Yao-Wen Wu
Jia et al. identify cholesterol as the primary lipid responsible for interaction between Vibrio cholerae toxin MakA and host membranes. They further characterize a sophisticated mechanism of recurrent membrane damage regulated by pH-dependent pore formation, leading to V-ATPase-dependent unconventional LC3 lipidation on damaged endolysosomal membranes.
Article
Nan Liu, Kai Liu, Chonglin Yang
Liu et al. identify WDR91 as an important player in retromer-dependent recycling. WDR91 promotes the interaction of Rab7 with SNX-retromer components and interacts with FAM21, facilitating the formation of the endosomal retrieval subdomain.
Article
Jingyue Jia, Fulong Wang, Zambarlal Bhujabal, Ryan Peters, Michal Mudd, Thabata Duque, Lee Allers, Ruheena Javed, Michelle Salemi, Christian Behrends, Brett Phinney, Terje Johansen, Vojo Deretic
Lysosomal damage induces stress granule (SG) formation and translational reprograming. The newly appreciated process of atg8ylation affects SG formation and concomitantly recruits SG core proteins NUFIP2 and G3BP1 to damaged lysosomes. These proteins independently of SG condensates and in coordination with galectin-8 inactivate mTOR via the Ragulator–Rag complex.
Article
Fabio Lolicato, Roberto Saleppico, Alessandra Griffo, Annalena Meyer, Federica Scollo, Bianca Pokrandt, Hans-Michael Müller, Helge Ewers, Hendrik Hähl, Jean-Baptiste Fleury, Ralf Seemann, Martin Hof, Britta Brügger, Karin Jacobs, Ilpo Vattulainen, Walter Nickel
This work demonstrates the lipid composition and the corresponding biophysical properties of biological membranes to tune highly specific protein–lipid interactions. Specifically, cholesterol is shown to affect phosphoinositide-dependent membrane recruitment and translocation into the extracellular space of FGF2, a survival factor involved in tumor-induced angiogenesis.

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Current Issue
Volume 221,
Issue 10,
3 October 2022
Reviews & Opinions
Spotlight
André Barros-Carvalho, Eurico Morais-de-Sá
André Barros-Carvalho and Eurico Morais-de-Sá highlight work from Calvi and colleagues that demonstrates a role for PP1 in establishing embryo polarity via regulation of PAR-2 localization.
Spotlight
Elise Marsan, Eric J. Huang
Marsan and Huang discuss work from Chhetri et al. demonstrating that mutant huntingtin interferes with XK surface recycling and reduces divalent ion transport across the membrane.
Spotlight
Zheng Wang, Hong Zhang
Wang and Zhang preview work from the Mizushima lab showing that NCOA4 mediates formation of ferritin condensates that are destined for degradation by macroautophagy and microautophagy.

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