Issues

Dinet and Michelot discuss work from Wang et al. demonstrating that pollen tube pH gradients regulate the localization and activity of two ADF/cofilin isoforms, providing spatial control over actin networks.

Jetter and Ackerman preview work from Tan and colleagues which shows that δ-catenin controls the astrocyte–neuron cadherin interactions that regulate layer-specific astrocyte morphogenesis.

Bourdais et al. have discovered that MRCKβ activates cortial myosin II rings to facilitate both spindle rotation in the egg and paternal nucleus migration in the zygote.

Wei et al. discuss new findings from the Avinoam lab regarding the mechanisms of large secretory vesicle exocytosis and provide a comparison with the fusion of small endocrine vesicles.

S-acylation is one of the most frequent posttranslational modifications that regulates diverse cellular processes. Anwar and van der Goot discuss the complexity and disease implications of this highly regulated reversible lipidation.

Delage et al. provide a primer on light sheet fluorescence microscopy to guide biologists through the specific challenges of this 3D imaging technique.

This study reveals that functional specification and cooperation of ADF isovariants with different pH sensitivities enable the coordination of the actin cytoskeleton with the cytosolic pH gradient to support pollen tube growth.

How human cells sense chromatin bridges to delay completion of cytokinesis (abscission) is unknown. Petsalaki et al. show that Topoisomerase IIα–DNA covalent complexes are formed on “knotted” DNA and promote recruitment of downstream factors to chromatin bridges to activate the abscission checkpoint and prevent chromatin breakage.

Qi et al. report a novel UHRF1 function as a nuclear protein catalyzing EG5 polyubiquitination for proper spindle architecture and faithful genomic transmission, which is independent of its roles in epigenetics and DNA damage repair. These findings reveal a previously unknown mechanism of UHRF1 controlling mitotic spindle architecture and chromosome behavior.

Gaspary et al. use a forward genetics approach in yeast to identify two RNA-binding proteins, Rie1 and Sgn1, which form a complex that promotes the meiotic cell fate decision. This complex acts posttranscriptionally to enhance translation of the master transcriptional regulator of meiosis, IME1, under starvation conditions.

Bourdais et al. reveal that in mouse oocytes, the kinase MRCK, a Cdc42 effector, promotes ring-shaped myosin II activation and membrane bulging over the meiotic spindle and in the sperm fertilization cone. They further show that the MRCK/myosin II pathway promotes spindle rotation for polar body emission and male pronucleus centration.

During Drosophila border cell migration, the B-type lamin, Lam, maintains nuclear envelope integrity, stabilizes the lead cell protrusion, and promotes cluster invasion between nurse cells. The nucleus may function as a wedge to promote this collective, confined in vivo movement.

Metastatic spread of ovarian cancer is associated with multicellular spheroids shed from the primary tumor into the peritoneal cavity. Pawar et al. show that overactive matriptase activates a PAR-2/PI3K/Akt/MMP9 signaling axis to enhance spheroid dissemination and metastasis.

Huang et al. report that ZRANB1, an OTU family DUB, ubiquitinates and represses SLC7A11 expression as an E3 ubiquitin ligase and that ZRANB1 inhibits glutathione (GSH) synthesis through SLC7A11 degradation, leading to elevated lipid peroxidation and ferroptosis.

Drosophila border cells are an excellent model to study fundamental cell behaviors. Torres et al show that elevated and localized Src activity in border cells induces cannibalism of neighboring cells by aberrantly activating phagocytosis with implications for the role of Src in cancer progression.

Melanoma cells exist in a bidirectional communication unit with lesional keratinocytes. In this niche, melanoma cells hijack keratinocyte signaling, causing them to produce promigratory chemokines through the downregulation of keratinocyte desmosomal cadherin Dsg1, leading to increased migration in vitro and an associated epidermal spread in vivo.

Biton et al. elucidate how large secretory vesicles in Drosophila larval salivary glands employ a distinct machinery comprised of branched actin, myosin-II, and BAR-domain proteins to control fusion pore dynamics. This process facilitates a unique mode of exocytosis, which maintains apical membrane homeostasis during secretion.

Pfitzner, Zivkovic, et al. characterize a novel membrane-bound ESCRT-III copolymer initiated by Vps60. They show that Vps60-based copolymers are in vitro spatially and biochemically distinct from classical Snf7-based ESCRT-III filaments. Different behavior of both ESCRT-III filaments in cells furthermore suggests potential diverse functions in vivo.

Legal et al. use cryo-electron tomography to study the tips of motile cilia. They reveal novel structural features of the central pair, expand on the functional role of CEP104/FAP256, and identify potential new proteins that are important for the stability of the ciliary tip.

Chatzifrangkeskou et al. show that c-Jun N-terminal kinase (JNK) is found at the base of motile and primary cilia, in association with the basal bodies. In multiciliated cells, JNK is involved in ciliogenesis and the ciliary function through the regulation of the actin network.

Tan et al. show that δ-catenin, previously thought to be neuron specific, is expressed by astrocytes and required both in astrocytes and neurons to control astrocyte morphogenesis. Furthermore, they provide evidence demonstrating how the cadherin–δ-catenin adhesion complex controls astrocyte morphology in a layer-specific manner.

Zeng et al. show that sexually dimorphic cholinergic synaptic transmission occurring at neuromuscular junctions in C. elegans is mediated by the sex-differential abundance of CaMKII, leading to sexually dimorphic locomotion behaviors.

In this Report, which replaces the previous retracted version, the authors show that G3BP is an effector of SG assembly, and that Ras signaling contributes to this process by regulating G3BP dephosphorylation.