Unusual Pseudogap-like Features Observed in Iron Oxypnictide Superconductors

We have performed a temperature-dependent angle-integrated laser photoemission study of iron oxypnictide superconductors LaFeAsO:F and LaFePO:F exhibiting critical transition temperatures (Tc's) of 26 K and 5 K, respectively. We find that high-Tc LaFeAsO:F exhibits a temperature-dependent pseudogap-like feature extending over ~0.1 eV about the Fermi level at 250 K, whereas such a feature is absent in low-Tc LaFePO:F. We also find ~20-meV pseudogap-like features and signatures of superconducting gaps both in LaFeAsO:F and LaFePO:F. We discuss the possible origins of the unusual pseudogap-like features through comparison with the high-Tc cuprates

The Physics of the B Factories

This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C

TIF1β regulates the pluripotency of embryonic stem cells in a phosphorylation-dependent manner

Transcription networks composed of various transcriptional factors specifically expressed in undifferentiated embryonic stem (ES) cells have been implicated in the regulation of pluripotency in ES cells. However, the molecular mechanisms responsible for self-renewal, maintenance of pluripotency, and lineage specification during differentiation of ES cells are still unclear. The results of this study demonstrate that a phosphorylation-dependent chromatin relaxation factor, transcriptional intermediary factor–1β (TIF1β), is a unique regulator of the pluripotency of ES cells and regulates Oct3/4–dependent transcription in a phosphorylation-dependent manner. TIF1β is specifically phosphorylated in pluripotent mouse ES cells at the C-terminal serine 824, which has been previously shown to induce chromatin relaxation. Phosphorylated TIF1β is partially colocalized at the activated chromatin markers, and forms a complex with the pluripotency-specific transcription factor Oct3/4 and subunits of the switching defective/sucrose nonfermenting, ATP-dependent chromatin remodeling complex, Smarcad1, Brg-1, and BAF155, all of which are components of an ES-specific chromatin remodeling complex, esBAF. Phosphorylated TIF1β specifically induces ES cell–specific genes and enables prolonged main-tenance of an undifferentiated state in mouse ES cells. Moreover, TIF1β regulates the reprogramming process of somatic cells in a phosphorylation-dependent manner. Our results suggest that TIF1β provides a phosphorylation-dependent, bidirectional platform for specific transcriptional factors and chromatin remodeling enzymes that regulate the cell differentiation process and the pluripotency of stem cells

Prohibitin 2 regulates the proliferation and lineage-specific differentiation of mouse embryonic stem cells in mitochondria.

BACKGROUND: The pluripotent state of embryonic stem (ES) cells is controlled by a network of specific transcription factors. Recent studies also suggested the significant contribution of mitochondria on the regulation of pluripotent stem cells. However, the molecules involved in these regulations are still unknown. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we found that prohibitin 2 (PHB2), a pleiotrophic factor mainly localized in mitochondria, is a crucial regulatory factor for the homeostasis and differentiation of ES cells. PHB2 was highly expressed in undifferentiated mouse ES cells, and the expression was decreased during the differentiation of ES cells. Knockdown of PHB2 induced significant apoptosis in pluripotent ES cells, whereas enhanced expression of PHB2 contributed to the proliferation of ES cells. However, enhanced expression of PHB2 strongly inhibited ES cell differentiation into neuronal and endodermal cells. Interestingly, only PHB2 with intact mitochondrial targeting signal showed these specific effects on ES cells. Moreover, overexpression of PHB2 enhanced the processing of a dynamin-like GTPase (OPA1) that regulates mitochondrial fusion and cristae remodeling, which could induce partial dysfunction of mitochondria. CONCLUSIONS/SIGNIFICANCE: Our results suggest that PHB2 is a crucial mitochondrial regulator for homeostasis and lineage-specific differentiation of ES cells

Common and specific roles of the related CDK inhibitors p27 and p57 revealed by a knock-in mouse model

Although p27 and p57 are structurally related cyclin-dependent kinase inhibitors (CKIs), and are thought to perform similar functions, p27 knockout (p27KO) and p57KO mice show distinct phenotypes. To elucidate the in vivo functions of these CKIs, we have now generated a knock-in mouse model (p57p27KI), in which the p57 gene has been replaced with the p27 gene. The p57p27KI mice are viable and appear healthy, with most of the developmental defects characteristic of p57KO mice having been corrected by p27 knock-in. Such developmental defects of p57KO mice were also ameliorated in mice deficient in both p57 and the transcription factor E2F1, suggesting that loss of p57 promotes E2F1-dependent apoptosis. The developmental defects apparent in a few tissues of p57KO mice were unaffected or only partially corrected by knock-in expression of p27. Thus, these observations indicate that p57 and p27 share many characteristics in vivo, but that p57 also performs specific functions not amenable to substitution with p27

PHB2 inhibits the differentiation of ES cells into neuronal cells and endodermal cells but not into cardiomyocytes.

<p>(<b>A, C, E</b>) Effect of ectopic expression of PHB2 on the differentiation of mouse ES cells into cardiomyocytes (A), endoderm cells (C), or neuronal cells (E). EBRTcH3 cells were differentiated in the absence of Tc. The differentiated cells were immunostained with the indicated antibodies. The ectopic expression of PHB2 was monitored with the autofluorescence of the coexpressed Venus protein. (<b>B, D, F</b>) Quantification of the effect of PHB2 on the differentiation of ES cells. The number of Venus-positive PHB2-expressing cells and indicated marker-positive cells were counted. The bar graph shows the average numbers of immunofluorescently stained cells counted in 3 independent eye fields. 0: No Foxa2-positive cell was detected in Venus-positive cells. Scale bar, 50 µm. (<b>G</b>) Inhibitory effect of PHB2 on the differentiation of human iPS cells into Foxa2-positive endodermal cells. The human iPS cell line 201B7 stably expressing PHB2-Flag (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0081552#pone.0081552.s001" target="_blank">Fig. S1A</a> clone 9) was differentiated into the endodermal lineage. The differentiated cells were detected by immunofluorescence staining with Sox17 antibody. Scale bar, 50 µm. (<b>H</b>) Quantification of the inhibitory effect of PHB2 on the endodermal differentiation of human iPS cells. The number of Flag-positive PHB2-expressing cells and nuclear-localized Sox17-immunopositive cells were counted. Scale bar, 50 µm. P<0.01. (<b>I</b>) PHB2 does not inhibit the differentiation of ES cells into neural stem/progenitor cells. The EBRTcH3 cell line was differentiated as in (A) and immunostained with Nestin or MAP2 antibody. (<b>J, K</b>) Quantification of the inhibitory effect of PHB2 in (I).</p