Protocol for universal gates in optimally biased superconducting qubits

We present a new experimental protocol for performing universal gates in a register of superconducting qubits coupled by fixed on-chip linear reactances. The qubits have fixed, detuned Larmor frequencies and can remain, during the entire gate operation, biased at their optimal working point where decoherence due to fluctuations in control parameters is suppressed to first order. Two-qubit gates are performed by simultaneously irradiating two qubits at their respective Larmor frequencies with appropriate amplitude and phase, while one-qubit gates are performed by the usual single-qubit irradiation pulses

State-dependent impedance of a strongly coupled oscillator-qubit system

We investigate the measurements of two-state quantum systems (qubits) at finite temperatures using a resonant harmonic oscillator as a quantum probe. The reduced density matrix and oscillator correlators are calculated by a scheme combining numerical methods with an analytical perturbation theory. Correlators provide us information about the system impedance, which depends on the qubit state. We show in detail how this property can be exploited in the qubit measurement.Comment: 8 pages, 16 image

Nuclear mRNA Degradation Pathway(s) Are Implicated in Xist Regulation and X Chromosome Inactivation

A critical step in X-chromosome inactivation (XCI), which results in the dosage compensation of X-linked gene expression in mammals, is the coating of the presumptive inactive X chromosome by the large noncoding Xist RNA, which then leads to the recruitment of other factors essential for the heterochromatinisation of the inactive X and its transcriptional silencing. In an approach aimed at identifying genes implicated in the X-inactivation process by comparative transcriptional profiling of female and male mouse gastrula, we identified the Eif1 gene involved in translation initiation and RNA degradation. We show here that female embryonic stem cell lines, silenced by RNA interference for the Eif1 gene, are unable to form Xist RNA domains upon differentiation and fail to undergo X-inactivation. To probe further an effect involving RNA degradation pathways, the inhibition by RNA interference of Rent1, a factor essential for nonsense-mediated decay and Exosc10, a specific nuclear component of the exosome, was analysed and shown to similarly impair Xist upregulation and XCI. In Eif1-, Rent1-, and Exosc10-interfered clones, Xist spliced form(s) are strongly downregulated, while the levels of unspliced form(s) of Xist and the stability of Xist RNA remain comparable to that of the control cell lines. Our data suggests a role for mRNA nuclear degradation pathways in the critical regulation of spliced Xist mRNA levels and the onset of the X-inactivation process

I-SceI-Mediated Double-Strand Break Does Not Increase the Frequency of Homologous Recombination at the Dct Locus in Mouse Embryonic Stem Cells

Targeted induction of double-strand breaks (DSBs) at natural endogenous loci was shown to increase the rate of gene replacement by homologous recombination in mouse embryonic stem cells. The gene encoding dopachrome tautomerase (Dct) is specifically expressed in melanocytes and their precursors. To construct a genetic tool allowing the replacement of Dct gene by any gene of interest, we generated an embryonic stem cell line carrying the recognition site for the yeast I-SceI meganuclease embedded in the Dct genomic segment. The embryonic stem cell line was electroporated with an I-SceI expression plasmid, and a template for the DSB-repair process that carried sequence homologies to the Dct target. The I-SceI meganuclease was indeed able to introduce a DSB at the Dct locus in live embryonic stem cells. However, the level of gene targeting was not improved by the DSB induction, indicating a limited capacity of I-SceI to mediate homologous recombination at the Dct locus. These data suggest that homologous recombination by meganuclease-induced DSB may be locus dependent in mammalian cells

[Nobel Prize 2007 for Medicine to Mario Capecchi, Martin Evans and Oliver Smithies: the mutant mice to order].

International audienceLe prix Nobel de Médecine et Physiologie 2007 a été décerné à Mario Capecchi (University of Utah, Salt Lake City, États-Unis), Martin Evans (Cardiff University, Royaume-Uni) et Oliver Smithies (University of North Carolina, Chapel Hill, États- Unis) pour la mise au point de la technique du ciblage de gènes chez la souris. La possibilité de modifier de façon précise et contrôlée le génome de la souris a totalement bouleversé l’étude du développement et de la physiologie des mammifères. Au-delà des informations précieuses sur les fonctions physiologiques de plusieurs milliers de gènes, cette découverte a permis la création de nombreux modèles murins de maladies humaines, outils inestimables pour l’étude de la physiopathologie des maladies et pour la mise au point de nouvelles thérapeutiques

Cell cycle regulation during early mouse embryogenesis.

International audienceElaboration of a multicellular organism requires highly efficient coordination between proliferation and developmental processes. Accordingly, the embryonic cell cycle exhibits a high degree of plasticity; however, the mechanisms underlying its regulation in vivo remain largely unknown. The purpose of this review is to summarize the data on cell cycle regulation during the early mouse embryonic development, a period characterized by major variations in cell cycle parameters which correlate with important developmental transitions. In particular, we analyse the contribution of mutant mice to the study of in vivo cell cycle regulation during early development and discuss possible contributions of cell cycle regulators to developmental programs

Reconsidérer le rôle de la lignée germinale dans la différenciation et la fonction de l’ovaire

International audienceThe production of fertilizable ova is the consequence of multiple events that start as soon as ovarian development and culminate at the time of ovulation. Throughout their development, germ cells are associated with companion somatic cells, which ensure germ cell survival, growth and maturation. Data obtained in vitro and in vivo on several animal models of germ cell depletion have led to uncover the many roles of germ cells on both ovarian development and folliculogenesis. During ovarian development, germ cells become progressively enclosed within epithelial structures called "ovigerous cords" constituted by pregranulosa cells, lined by a basement membrane. At the end of ovarian development, ovigerous cords fragment into primordial follicles, which are epithelial units constituted by an oocyte surrounded by a single layer of granulosa cells. Germ cells are necessary for the fragmentation of ovigerous cords into follicles, since in their absence, no follicle will form. Germ cells also ensure the differentiation of the ovarian somatic lineage, and they may inhibit the testis-differentiating pathway by preventing the conversion of pregranulosa cells into Sertoli cells, their counterpart in the testis. Regularly, primordial follicles are recruited into the growing follicle pool and initiate their growth. They develop through primary, preantral, antral and preovulatory stages before being ovulated. Interestingly, the action of the oocyte on companion somatic cells tightly depends on the follicular stage. In primordial follicles, the oocyte prevents the transdifferentiation of granulosa cells into cells resembling Sertoli cells. By contrast, as soon as the follicle enters growth, the oocyte regulates the functional differentiation of granulosa cells and at the latest stages, it prevents their premature maturation into luteal cells. Overall, these data demonstrate that the female germ cell act on companion somatic cells to regulate ovarian development and folliculogenesis, thereby actively supporting its own maturation.Le stock de follicules primordiaux, chacun formé d’un ovocyte entouré par une assise de cellules somatiques folliculaires ou cellules de la granulosa, est définitivement constitué pendant la vie fœtale ou très peu de temps après la naissance chez la majorité des mammifères. Dès la constitution de cette réserve et jusqu'à son épuisement chez la femelle âgée, l’ovaire est le siège de la folliculogenèse qui est l’ensemble des processus de croissance et de maturation des follicules ovariens depuis le stade de follicule primordial jusqu’au stade préovulatoire. Sa finalité biologique est la production, lors de chaque cycle menstruel ou estrien, d’ovocytes aptes à la fécondation et au développement. L’obtention de tels ovocytes implique des régulations paracrines et endocrines complexes. Au cours de ces dernières décennies, de nombreuses données ont clairement établi l’importance des cellules somatiques ovariennes dans la survie, la croissance et la maturation ovocytaires. Mais ce n’est que plus récemment que des travaux ont mis en lumière le rôle clé joué par la cellule germinale dans la folliculogenèse et dans la différenciation ovarienne. Cette revue présente une synthèse des connaissances, basées principalement sur l’interprétation de travaux sur différents modèles animaux, ayant permis de reconsidérer le rôle des cellules germinales dans la différenciation et la fonction de l’ovaire