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The effects of transcription factors on the maintenance and differentiation of human-induced or embryonic pluripotent stem cells (iPSCs/ESCs) have been well studied. However, the importance of posttranscriptional regulatory mechanisms, which cause the quantitative dissociation of mRNA and protein expression, has not been explored in detail. Here, by combining transcriptome and proteome profiling, we identified 228 posttranscriptionally regulated genes with strict upregulation of the protein level in iPSCs/ESCs. Among them, we found 84 genes were vital for the survival of iPSCs and HDFs, including 20 genes that were specifically necessary for iPSC survival. These 20 proteins were upregulated only in iPSCs/ESCs and not in differentiated cells derived from the three germ layers. Although there are still unknown mechanisms that downregulate protein levels in HDFs, these results reveal that posttranscriptionally regulated genes have a crucial role in iPSC survival.

Tricholoma matsutake is an ectomycorrhizal agaricomycete that produces matsutake mushrooms in association with conifers. Here, we isolated a pleiotropic mutant, designated as G1, following 7-ray irradiation of T. matsutake NBRC 33136. In addition to exhibiting increased cellulose- and amylose-degrading activities and altered mycelial morphology, G1 degenerated lateral roots and caused stunting or fatal wilting of seedlings of its symbiotic partner, Pinus densiflora, in vitro. A mutant, designated Ar 59, previously isolated after argon-ion beam irradiation, exhibited the same phenotypes as G1, but without its detrimental effects. Ar 59, like NBRC 33136, developed a Hartig net around healthy cortical cells that was composed of uniseriate hyphae. In G1-inoculated seedlings, the Hartig net was composed of heavily bundled hyphae penetrating the intercellular space, and it was accompanied by somewhat unusual forms of plant cortical cells. Sequences of rRNA gene-related markers, including four single nucleotide polymorphisms present within each strain, were 100% identical among NBRC 33136, G1, and Ar 59, indicating that they are mutants of the wild-type. Thus, 7-ray irradiation can convert the fungus from a beneficial to a harmful agent. These findings suggest the presence of an unknown mechanism in the fungal genome that can transform mutualism into parasitism. Key words: degrading enzymes, 7-ray irradiation mutagenesis, heavy-ion beam, phenotypic transformation, plant-microbe interactions. Tricholoma matsutake est un agaromycète ectomycorhize qui produit les champignons matsutake en association avec les conifères. Les auteurs ont isolé ici un mutant pléiotropique qu'ils ont désigné G1, à la suite d'une irradiation [gamma] de T. matsutake NBRC 33136. En plus de présenter une activité accrue de dégradation de la cellulose et de l'amylose et une morphologie mycéliale modifiée, G1 provoquait la dégénérescence des racines latérales et un retard de croissance ou une flétrissure fatale des jeunes plants de son partenaire symbiotique, Pinus densiflora, in vitro. Un mutant désigné Ar 59, isolé précédemment après une irradiation à un faisceau d'argon ionisé, présentait le même phénotype que G1, mais sans les effets néfastes. Ar 59, comme NBRC 33136, développait un réseau de Hartig autour des cellules corticales saines, composé d'hyphes unisériées. Chez les plantules inoculées avec G1, le réseau de Hartig était composé d'hyphes en faisceau pénétrant l'espace intercellulaire et était accompagné par des cellules corticales végétales de formes quelque peu inhabituelles. Les séquences de marqueurs reliés aux gènes de l'ARNr, y compris quatre polymorphismes de nucléotides uniques présents dans chaque souche, étaient 100% identiques entre NBRC 33136, G1 et Ar 59, indiquant qu'ils constituent des mutants de la souche sauvage. Ainsi, l'irradiation gamme peut convertir le champignon d'une forme bénéfique en un agent pathogène. Ces données suggèrent la présence d'un mécanisme inconnu dans le génome fongique qui peut transformer le mutualisme en parasitisme. [Traduit par la Rédaction] Mots-clés : enzymes de dégradation, mutagenèse par irradiation gamma, faisceau d'ions lourds, transformation phénotypique, interactions plante-microbe., Introduction Ectomycorrhizal symbiosis occurs belowground between woody plants, belonging mostly to Caesalpinioideae, Dipterocarpaceae, Fagaceae, and Pinaceae, and filamentous fungi, belonging mostly to Ascomycota and Basidiomycota, greatly contributing to healthy forest [...]

Fibrodysplasia ossificans progressiva (FOP) is a rare and intractable disease characterized by extraskeletal bone formation through endochondral ossification. Patients with FOP harbor point mutations in ACVR1, a type I receptor for BMPs. Although mutated ACVR1 (FOP-ACVR1) has been shown to render hyperactivity in BMP signaling, we and others have uncovered a mechanism by which FOP-ACVR1 mistransduces BMP signaling in response to Activin -A, a molecule that normally transduces TGF-[beta] signaling. Although Activin-A evokes enhanced chondrogenesis in vitro and heterotopic ossification (HO) in vivo, the underlying mechanisms have yet to be revealed. To this end, we developed a high -throughput screening (HTS) system using FOP patient-derived induced pluripotent stem cells (FOP-iPSCs) to identify pivotal pathways in enhanced chondrogenesis that are initiated by Activin-A. In a screen of 6,809 small-molecule compounds, we identified mTOR signaling as a critical pathway for the aberrant chondrogenesis of mesenchymal stromal cells derived from FOP-iPSCs (FOP-iMSCs). Two different HO mouse models, an FOP model mouse expressing FOP-ACVR1 and an FOP-iPSC-based HO model mouse, revealed critical roles for mTOR signaling in vivo. Moreover, we identified ENPP2, an enzyme that generates lysophosphatidic acid, as a linker of FOP-ACVR1 and mTOR signaling in chondrogenesis. These results uncovered the crucial role of the Activin-A/FOP-ACVR1/ ENPP2/mTOR axis in FOP pathogenesis., Introduction Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disease characterized by extraskeletal bone formation in soft tissue, where bone normally does not exist. Ectopic bones are formed through endochondral [...]

The third-order intermodulation distortions (IM3s) of class-F and inverse class-F heterojunction bipolar transistor amplifiers were compared experimentally. It was revealed that the IM3 of inverse class F is lower than that of class F at high input power ([P.sub.in]), although the better class for IM3 at low [P.sub.in] changes from class F to inverse class F according to the increase of the quiescent current ([I.sub.q]). The different IM3 behaviors are mainly caused by the different gain variations in both amplifiers. At a low [P.sub.in], the gain of class F is larger than that of inverse class F. The larger gain in class F causes a gradual gain decrease and a steep gain rise at high and low [I.sub.q], respectively. On the other hand, the gain of inverse class F is larger than that of class F at a high [P.sub.in]. The larger gain in inverse class F causes a gradual gain decrease at all [I.sub.q] values. These gradual gain decreases are one of main causes of a lower IM3. These phenomena can be explained by the output current ([I.sub.out]) and voltage ([V.sub.out]) waveforms, which differ according to the harmonic loads. The [I.sub.out] and [V.sub.out] positive half-sinusoidal waveforms, which consist of in-phase second harmonics, are effective for large-gain operations. The positive half-sinusoidal [I.sub.out] waveform of the class-F amplifier prevents a gain decrease at a low [P.sub.in] and high [I.sub.q], and the similar [V.sub.out] waveform in inverse class F prevents a gain decrease at a high [P.sub.in]. Index Terms--Code division multiple access (CDMA), hetero-junction bipolar transistor (HBT), intermodulation distortion, power amplifiers.