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Cardiomyocyte telomeres erode after birth, inducing a cell-cycle arrest that limits the heart’s capacity for regeneration.

People & Ideas

Chang’s work focuses on how cells sense and control their shape and size.



Ping et al. demonstrate that mitochondria-to-plasma membrane anchoring is mediated by Num1 directly interacting with both organelles through two distinct and spatially separated lipid-specific binding domains. These findings suggest a general mechanism for interorganelle tethering.

Mitochondria exert critical functions in lipid metabolism and promote the synthesis of major constituents of cellular membranes, such as phosphatidylethanolamine (PE). Here, Aaltonen et al. demonstrate that two pathways mediate PE synthesis: Ups2–Mdm35–dependent lipid transfer and MICOS-dependent membrane apposition.

The T cell receptor requires force for triggering. Here, Hu and Butte show that T cells generate pushing and pulling forces against an antigen-coated AFM cantilever in an actin-dependent fashion. Exogenous, oscillating forces delivered by the cantilever rescued T cell receptor signaling in the absence of an intact F-actin cytoskeleton. These findings highlight the importance of mechanical forces in T cell activation.

Szabó et al. use computational and experimental approaches to show in vivo that collective migration of neural crest cells (NCCs) depends on spatial confinement imposed by versican, an ECM molecule that inhibits NCC migration and acts as a guiding cue by forming exclusionary boundaries.


Concentrating factors in nuclear bodies is thought to promote efficient gene expression. Tatomer et al. show that the histone locus body (HLB) concentrates pre-mRNA processing factors at replication-dependent histone genes, resulting in optimal 3′ end formation of histone mRNAs coupled with transcription termination.

Aix et al. find that telomere dysfunction is a crucial signal for cardiomyocyte cell-cycle arrest during the postnatal period. After birth, mouse cardiomyocytes undergo telomere shortening. This leads to the appearance of dysfunctional telomeres that activate p21, causing cardiomyocyte cell-cycle withdrawal.

The exact functions of all paxillin family members in mechanosensing and adhesion at invadosomes are unclear. Petropoulos et al. show that redundant and specific activities of paxillin and Hic-5 can couple original adhesion and ECM degradation in invadosomes.

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