Quantitative Dynamics of Chromatin Remodeling during Germ Cell Specification from Mouse Embryonic Stem Cells
Bhaskar Chanda Stem Cell Kurimoto et al. perform careful analyses of chromatin remodeling during mouse germ cell specification from embryonic stem cells. Widespread epigenetic reprogramming events included re-organization of H3K27me3 and bivalent signatures as well as progressive deletion of H3K9me2 throughout the genome, creating a unique foundation for the epigenome of the next generation.
The Long Noncoding RNA Regulates Neuronal Differentiation of Embryonic and Postnatal Neural Stem Cells
Bhaskar Chanda Stem Cell Ramos et al. describe Pinky (Pnky), a neural-specific lncRNA that localizes to the nucleus of neural stem cells (NSCs). Pnky knockdown in NSCs increases neurogenesis. Pnky interacts with splicing regulator PTBP1, and PTBP1 and Pnky regulate the expression and splicing of a core set of transcripts related to neuronal differentiation.
Bhaskar Chanda Stem Cell Luo et al. perform deep RNA sequencing of hematopoietic stem cells (HSCs), identifying previously unannotated long non-coding RNAs (lncRNAs) enriched in this cell population. Functional characterization of several HSC-enriched lncRNAs demonstrated roles in regulating HSC differentiation and self-renewal and revealed genomic binding to hematopoietic transcription factor binding sites.
Bhaskar Chanda Stem Cell Menon, Firth, and colleagues show that TALEN-mediated correction of a novel splice site mutation in the IL-2Rγ gene rescues defective development of mature NK cells from iPSCs derived from a SCID-X1 subject. They demonstrate correction of the aberrant splicing of the IL-2Rγ in T cell precursors.
Elucidating Molecular Phenotypes Caused by the SORL1 Alzheimer’s Disease Genetic Risk Factor Using Human Induced Pluripotent Stem Cells
Bhaskar Chanda Stem Cell Development of late-onset, sporadic Alzheimer’s disease (SAD) has been linked with a range of genetic loci, but determining how variants within these loci contribute to disease progression remains challenging. Using hIPSC-derived neurons from SAD patients and controls, Young et al. link risk and protective variants in the SORL1 gene, an SAD-associated locus, with BDNF-sensitive SORL1 expression, APP processing, and control of amyloid β production.