February 2016 | Volume 212, No. 4
In This Issue
People & Ideas
- Coupling primary and stem cell–derived cardiomyocytes in an in vitro model of cardiac cell therapy
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.
- MRN, CtIP, and BRCA1 mediate repair of topoisomerase II–DNA adducts
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 suppresses ciliogenesis in proliferating cells by regulating the trichoplein–Aurora A pathway
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.
- Plakophilin-2 loss promotes TGF-β1/p38 MAPK-dependent fibrotic gene expression in cardiomyocytes
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.
- Biophysical changes reduce energetic demand in growth factor–deprived lymphocytes
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 phosphorylation decreases neuronal defects in spinocerebellar ataxia type 3 models
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.