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During development of eutherian females, one of the X-chromosomes is silenced. Here, authors show that alleles on the inactive X-chromosome are dynamically expressed along neural differentiation enhancing resilience of female neural tissue.

Japanese researcher plans cache of induced stem cells to supply clinical trials.

Synovial sarcoma (SyS) is a cancer driven by a fusion oncoprotein, SS18::SSX, but the mechanism underlying the oncoprotein-mediated tumorigenesis remains unclear. Here, the authors employ transgenic mouse models and multi-omics to show how SS18:SSX modifies the activity and recruitment of BAF-family chromatin remodeling complexes to drive SyS tumorigenesis.

Rejuvenation and partial reprogramming are two frontier areas in the field of aging. Here, the authors summarize advances in these fields and suggest future directions for research and therapy.

The exfoliation of 2D nanosheets from nonlayered 3D crystals has the potential to generate new 2D materials, but the exfoliation mechanisms remain unclear. Here, the authors identify the important role of intrinsic stacking faults in 3D boron crystals in the liquid-phase exfoliation of 2D boron nanosheets.

Somatic reprogramming involves both transcriptional and epigenetic resetting, but we don’t yet fully understand this process. Here they show that Jdp2, Glis1, Esrrb, and Sall4 can mediate reprogramming by recruiting the NuRD complex to close chromatin, highlighting a potential role in cell fate control.

Morris discusses how single-cell genomics and computational tools expose failure points in reprogramming and guide protocols that improve the fidelity, maturity and purity of engineered cells, advancing their use in regenerative medicine and disease modelling.

Scientists have been reprogramming adult cells into embryonic ones for decades — but they are only now getting to grips with the mechanics.

The Rho signalling pathway is frequently activated in squamous carcinomas. Here, the authors find that the Rho GEF VAV2 is over expressed in both cutaneous and head and neck squamous cell carcinomas and that at the molecular level VAV2 promotes a pro-tumorigenic stem cell-like signalling programme.

Expression of three Yamanaka transcription factors in mouse retinal ganglion cells restores youthful DNA methylation patterns, promotes axon regeneration after injury, and reverses vision loss in a mouse model of glaucoma and in aged mice, suggesting that mammalian tissues retain a record of youthful epigenetic information that can be accessed to improve tissue function.

After heart-treatment claims collapse, researchers caution against a rush to the clinic.

Lentiviral vectors that express a fluorescent reporter and a selectable marker in pluripotent cells improve and simplify isolation of induced pluripotent stem cell lines in mouse and human.

This study identifies and characterizes evolutionarily conserved cytosine methylation patterns related to age across mammals and establishes pan-mammalian epigenetic clocks.

Last year it was reported that a cocktail of four transcription factors — encoded by Oct4, Sox2, Myc and Klf4 — can partly reprogramme mouse somatic cells to an embryonic state, a process that reawakens silenced segments of the genome and restores pluripotency to the somatic cell nucleus. Three groups have now modified this method to generate fully reprogrammed cells that closely resemble embryonic stem cells.

In Myeloiddysplastic syndromes, CEBPA mutations are linked to disease progression and AML. Here, the authors use somatic reprogramming and genome editing to generate isogenic cell lines from an MDS patient, identifying CEBPA bZIP domain disruption as causative for disease progression.

Producing mature epicardium in vitro could allow better understanding of cardiac tissue regeneration. Here, the authors describe how inhibition of mTOR signaling during differentiation of induced pluripotent stem cells yields mature epicardium that can be used to model adult epicardial reactivation.

He showed that specialized cells retain the genes to form an organism.

Changes in chromatin structure impact gene expression programs by modulating accessibility to the transcription machinery. Here, West et al. explore differences in nucleosome occupancy between mammalian pluripotent and somatic cells and uncover regulatory regions likely to play key roles in determining cell identity.

Yamanaka factors can reprogram somatic and cancer cells into induced pluripotent stem cells. Here, the authors show that the induction of these factors in acute myeloid leukemia leads to apoptosis of leukemia cells in vivo, and this is through modulation of chromatin accessibility to apoptotic genes and accompanied by H3K9me3 dysregulation.

Basal Pancreatic Ductal Adenocarcinoma (PDAC) is more aggressive than the classical subtype of pancreatic cancer. Here the authors report that RNA-binding protein LIN28B and its target HMGA2 drive basal PDAC pathogenesis by reducing PP2A methylation and activity, resulting in enhanced protein synthesis and aggressive features.

Graf and colleagues find that B cells exposed to a pulse of C/EBPα and the Yamanaka factors convert into elite-type cells that rapidly and efficiently reprogram into iPSCs, in a process that involves upregulation of Lsd1, Brd4 and Klf4.

Tissue-resident macrophages (TRM) are important mediators of local immunity. Here the authors show that the deficiency or inhibition of a kinase, WNK1, unlinks macrophage colony-stimulating factor signaling and resulted macropinocytosis with the downstream, potentially IRF8-mediated genetic program to bias progenitor differentiation to neutrophil instead of TRM.

Duy and Weise et al. combined human functional integrative genomics with mouse experimental biology to reveal a neuroprogenitor-based genetic subtype of human hydrocephalus with defective neurogenesis and altered brain–fluid biomechanics.

But new leadership’s largesse brings expectations of fast commercial pay-offs.

Cipriano et al. review recent progress in using epigenetic reprogramming to combat age-related deterioration at the cellular, tissue and organismal level, discussing reprogramming strategies and mechanisms, as well as remaining challenges in the field.

Here, Fry and colleagues examine the impact of antigen experience on subsequent CD8⁺ CAR T cell activity during the antileukemia response and show that RUNX2 overexpression enhances antitumor activity of these cells.

Despite being a promising soft material embodied by molecular self-assembly, the formation mechanism of supramolecular gels remains challenging to fully understand. This study describes a block-stacking model to provide molecular and nanoscopic insights.

Loss of epigenetic information is a hallmark of cellular aging. Here, authors examine changes in the epigenetic landscape at three stages of Huntington neurodegenerative disease (HD) in two mouse models and demonstrate accelerated de-repression of developmental genes in HD striatal neurons.

The freshwater planarian S. mediterranea is an important model organism for regeneration research but its use in aging research is little explored and S. mediterranea is commonly referred to as immortal. Here Dai et al. report age-associated physiological and molecular changes in the sexual lineage of S. mediterranea, and global reversal of such changes after regeneration.

The function of transcription factors is conveyed through intrinsically disordered regions (IDRs) containing activation or repression domains, but the lack of quantitative structural ensemble models prevents their mechanistic decoding. Here, the authors use several methods to demonstrate that DNA binding can lead to complex changes in the IDR ensemble and accessibility on the example of the C-terminal IDR of pioneer factor Sox2.

Neural stem cells have a tropism for glioblastoma. Here the authors employ fibroblasts directly reprogrammed into induced neural stem cells and loaded with cytotoxic molecules to migrate to xenotransplanted brain tumours in mice, achieving tumour shrinkage and prolonged survival.

Optineurin is linked to ALS and glaucoma, but the mechanism is unknown. Here, the authors show that optineurin mutation causes deficits in axonal mitochondria transport and neurodegeneration, enhancing of which achieves axon protection and regeneration.

Any TFs other than OCT4 that can individually induce the formation of mouse iPSCs are currently lacking. Here, Xiao et.al. report a single-SALL4-mediated somatic reprogramming method and reveal the underlying mechanism of this process.

Japanese team will use 'iPS' cells to treat patient with degenerative eye disease.

The fall out from the STAP case is still being felt across Japan.