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In a recent paper in Cell Research, Yu et al. show that maternally inherited Yes-associated protein (Yap), a co-activator of TEAD family transcription factors, plays a key role in activating embryonic transcription following fertilization in the mouse.
Wnt morphogens are notoriously elusive proteins. Thanks to a recent study published in Nature, Clevers and colleagues give us a first glimpse of a mammalian Wnt in action in the gut epithelium.
Toll-Like Receptors (TLRs) play critical roles in the early innate immune response to invading pathogens by sensing microorganisms; a number of accessory molecules have been shown to assist microbial recognition by TLRs. In a recent paper in Cell Research, Yang et al. demonstrate that Mex3B is associated with TLR3 in the endosomes and promotes dsRNA binding and proteolytic processing of TLR3, suggesting that Mex3B acts as a coreceptor of TLR3 in response to dsRNA.
A novel approach to gene correction by genome editing shows great promise as a treatment for Duchenne muscular dystrophy (DMD). CRISPR/Cas9 delivered by adeno-associated virus to a mouse model for DMD demonstrated improvement in function and histology.
Non-genetic inheritance is an evocative topic; in the past few years, the debate around potential inheritance of life-time experiences independent of social factors in mammals has become highly prominent due to increasing evidence for phenotypes in the offspring after paternal environmental exposures. Strikingly, two independent studies published in Science newly implicate a special class of RNA, transfer RNA fragments, in the intergenerational effects of paternal dietary intervention.
Pathway choice is a critical event in the repair of DNA double-strand breaks. In a recent paper published in Nature, Orthwein et al. define a mechanism by which homologous recombination is controlled in G1 cells to favor non-homologous end joining.
It is becoming increasingly clear that leukocytes dynamically regulate cancer progression and metastasis, and among leukocytes, granulocytic cells abundantly accumulate in metastatic organs; however, their function in metastasis remains controversial. In a recent report in Nature, Wculek and Malanchi clarify the role of mature neutrophils as mediators of metastatic initiation and provide a targeted approach to prevent the pro-metastatic activity of neutrophils in breast cancer models.
The mammalian target of rapamycin (mTOR), also known as the mechanistic target of rapamycin, is a central cell growth regulating kinase that forms large molecular complexes in all eukaryotic cells. A paper recently published in Science reports the architecture of mTOR complex 1 (mTORC1) and provides molecular insights into the regulation and substrate selectivity of mTORC1.
IgE is commonly known for its role in the Th2 responses, protection against helminth parasites and pathogenesis of allergy. A recent report shows that IgE autoantibodies to dsDNA plays a major role in the pathogenesis of lupus nephritis by exacerbating the interferon-α responses in plasmacytoid dendritic cells.
Reprogramming to pluripotency has thus far required complex procedures involving nuclear transfer, cell fusion or genetic manipulation. Two recent papers from Hongkui Deng's group now show various cell types can be reprogrammed simply by chemicals through an extraembryonic endoderm-like phase instead of the primitive streak-like mesendoderm induced by Yamanaka factors.
The role of oxidative stress in the aging process has been highly debated for decades and remains equivocal. A new study published in Cell Research reports a novel role for the aging-associated SIRT6 deacetylase in the control of oxidative homeostasis in human mesenchymal stem cells.
Macrophages are important innate immune cells with functions in tissue repair and remodeling, induction and resolution of inflammation, as well as elimination of invading pathogens. In a recent study, Schmidt and colleagues describe the open epigenetic landscape of the human inflammatory macrophages, and the transcriptional regulators responsible for their rapid response to environmental signals.
Vitamin C was first suggested to have cancer-fighting properties in the 1930s and has been the subject of controversy ever since. Despite repeated reports of selective cancer cell toxicity induced by high-dose vitamin C treatment in vitro and in mouse models, the mechanism of action has remained elusive.