On the cover
A cultured hippocampal neuron is stained for the neuronal marker MAP2 (green) and F-actin (red), which preferentially labels dendritic spines. Liu et al. reveal that the cytoplasmic C-terminal domain of Neuroligin 1 promotes synapse formation by binding to spine-associated Rap GTPase-activating protein (SPAR) to induce LIMK1/cofilin-mediated actin reorganization.Image © 2016 Liu et al.
See page 449.
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Coupling of stronger primary and weaker stem cell–derived cardiomyocytes results in junctional substrate adhesions that maintain structural integrity but impair force transmission and this may contribute to the limited efficacy of cell therapy in vivo.
Analyses in Xenopus egg extracts show that the MRN complex, CtIP, BRCA1, and the interaction between CtIP and BRCA1 are required for the removal of Top2–DNA adducts, forsubsequent resection of Top2-adducted double-strand break ends, and for cellular resistance to etoposide during genomic DNA replication.
Ndel1, a protein located at the subdistal appendage of mother centriole, functions as an upstream regulator of the trichoplein–Aurora A pathway that suppresses ciliogenesis in proliferating cells.
Loss of the desmosome armadillo protein Plakophilin-2 in neonatal cardiomyocytes results in decreased stability and expression of the cytoskeletal linker protein Desmoplakin, which causes activation of a TGF-β1/p38 MAPK signaling cascade and induces expression of fibrotic genes.
Changes to the biophysical properties of lymphocytes are identified as an adaptive response to acute nutrient stress that occurs before the induction of autophagy.
Neuroligin 1 regulates spines and synaptic plasticity via LIMK1/cofilin-mediated actin reorganization
The C-terminal domain of NLG1 is sufficient to enhance spine and synapse number and to modulate synaptic plasticity, and it exerts these effects via its interaction with SPAR and the subsequent activation of LIMK1/cofilin-mediated actin reorganization.
Ataxin-3, the protein involved in spinocerebellar ataxia type 3 or Machado-Joseph disease, causes dendritic and synapse loss in cultured neurons when expanded, and mutation of phosphorylation site S12 reduces aggregation, neuronal loss, and synapse loss.