In This Issue
People & Ideas
Rad54’s ATPase activity does not affect accumulation of homologous recombination proteins in repair foci, but influences its dissociation and that of Rad51.
Defining the earliest step of cardiovascular progenitor specification during embryonic stem cell differentiation
Mesp1, the earliest marker of cardiovascular development in vivo, is used to isolate and characterize multipotent cardiovascular progenitors during ESC differentiation.
Distinct ATOH1 and Neurog3 requirements define tuft cells as a new secretory cell type in the intestinal epithelium
Tuft cells represent a fourth type of intestinal secretory cell that constitutes the primary source of endogenous intestinal opioids and are the only epithelial cell that constitutively express cyclooxygenases.
TDRD5 is required for retrotransposon silencing, chromatoid body assembly, and spermiogenesis in mice
Tdrd5-deficient mice develop a functional haploid genome despite spermiogenesis arrest at the round spermatid stage.
Translation of myelin basic protein mRNA in oligodendrocytes is regulated by integrin activation and hnRNP-K
α6β1-integrin interacts with hnRNP-K, an mRNA-binding protein, during oligodendrocyte differentiation to promote translation of MBP mRNA and myelin synthesis.
Phosphorylation of Kvβ2 releases Kv1 channels from microtubules to control their specific distribution at the axonal membrane.
Autocatalytic processing of the Hedgehog ligand from its precursor protein relies on protein disulfide isomerase and ER-associated degradation.
Nup133 links CENP-F, NudE/EL, and the dynein/dynactin complex to anchor centrosomes to the nuclear membrane.
Loss of mitochondrial complex I activity potentiates dopamine neuron death induced by microtubule dysfunction in a Parkinson’s disease model
The combination of microtubule depolymerization and the accumulation of cytosolic dopamine and reactive oxygen species selectively affects survival of dopaminergic neurons.
Kindlin-3–mediated signaling from multiple integrin classes is required for osteoclast-mediated bone resorption
Loss of kindlin-3 impairs activation of β1, β2, and β3 integrin classes, resulting in osteopetrotic defects in osteoclast adhesion and spreading.