192 research outputs found

    Functional Genomics of Wood Formation

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    Intruder bands and configuration mixing in the lead isotopes

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    A three-configuration mixing calculation is performed in the context of the interacting boson model with the aim to describe recently observed collective bands built on low-lying 0+0^+ states in neutron-deficient lead isotopes. The configurations that are included correspond to the regular, spherical states as well as two-particle two-hole and four-particle four-hole excitations across the Z=82 shell gap.Comment: 20 pages, 4 figures, accepted by PRC, reference added for section 1 in this revised versio

    Collectivity and configuration mixing in 186,188Pb and 194Po

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    Lifetimes of prolate intruder states in 186Pb and oblate intruder states in 194Po have been determined by employing, for the first time, the recoil-decay tagging technique in recoil distance Doppler-shift lifetime measurements. In addition, lifetime measurements of prolate states in 188Pb up to the 8+ state were carried out using the recoil-gating method. The B(E2) values have been deduced from which deformation parameters |β2|=0.29(5) and |β2|=0.17(3) for the prolate and the oblate bands, respectively, have been extracted. The results also shed new light on the mixing between different shapes

    Collectivity and Configuration Mixing in \u3csup\u3e186,188\u3c/sup\u3ePb and \u3csup\u3e194\u3c/sup\u3ePo

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    Lifetimes of prolate intruder states in 186Pb and oblate intruder states in 194Po have been determined by employing, for the first time, the recoil-decay tagging technique in recoil distance Doppler-shift lifetime measurements. In addition, lifetime measurements of prolate states in 188Pb up to the 8+state were carried out using the recoil-gating method. The B(E2) values have been deduced from which deformation parameters lβ2l = 0.29(5) and lβ2l = 0.17(3) for the prolate and the oblate bands, respectively, have been extracted. The results also shed new light on the mixing between different shapes

    Lifetimes of intruder states in 186 Pb, 188 Pb and 194 Po

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    Lifetimes of prolate intruder states in 186Pb and 188Pb and oblate intruder states in 194Po have been determined through recoil distance Doppler-shift lifetime measurements. Deformation parameters of | β2 | = 0.29 (5) and | β2 | = 0.17(3) have been ext

    The AUXIN BINDING PROTEIN 1 Is Required for Differential Auxin Responses Mediating Root Growth

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    Background In plants, the phytohormone auxin is a crucial regulator sustaining growth and development. At the cellular level, auxin is interpreted differentially in a tissue- and dose-dependent manner. Mechanisms of auxin signalling are partially unknown and the contribution of the AUXIN BINDING PROTEIN 1 (ABP1) as an auxin receptor is still a matter of debate. Methodology/Principal Findings Here we took advantage of the present knowledge of the root biological system to demonstrate that ABP1 is required for auxin response. The use of conditional ABP1 defective plants reveals that the protein is essential for maintenance of the root meristem and acts at least on the D-type CYCLIN/RETINOBLASTOMA pathway to control entry into the cell cycle. ABP1 affects PLETHORA gradients and confers auxin sensitivity to root cells thus defining the competence of the cells to be maintained within the meristem or to elongate. ABP1 is also implicated in the regulation of gene expression in response to auxin. Conclusions/Significance Our data support that ABP1 is a key regulator for root growth and is required for auxin-mediated responses. Differential effects of ABP1 on various auxin responses support a model in which ABP1 is the major regulator for auxin action on the cell cycle and regulates auxin-mediated gene expression and cell elongation in addition to the already well known TIR1-mediated ubiquitination pathway

    A new vesicle trafficking regulator CTL1 plays a crucial role in ion homeostasis

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    Ion homeostasis is essential for plant growth and environmental adaptation, and maintaining ion homeostasis requires the precise regulation of various ion transporters, as well as correct root patterning. However, the mechanisms underlying these processes remain largely elusive. Here, we reported that a choline transporter gene, CTL1, controls ionome homeostasis by regulating the secretory trafficking of proteins required for plasmodesmata (PD) development, as well as the transport of some ion transporters. Map-based cloning studies revealed that CTL1 mutations alter the ion profile of Arabidopsis thaliana. We found that the phenotypes associated with these mutations are caused by a combination of PD defects and ion transporter misregulation. We also established that CTL1 is involved in regulating vesicle trafficking and is thus required for the trafficking of proteins essential for ion transport and PD development. Characterizing choline transporter-like 1 (CTL1) as a new regulator of protein sorting may enable researchers to understand not only ion homeostasis in plants but also vesicle trafficking in general

    Intercellular movement of the putative transcription factor SHR in root patterning

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    Positional information is pivotal for establishing developmental patterning in plants1,2,3, but little is known about the underlying signalling mechanisms. The Arabidopsis root radial pattern is generated through stereotyped division of initial cells and the subsequent acquisition of cell fate4. short-root (shr) mutants do not undergo the longitudinal cell division of the cortex/endodermis initial daughter cell, resulting in a single cell layer with only cortex attributes5,6. Thus, SHR is necessary for both cell division and endodermis specification5,6. SHR messenger RNA is found exclusively in the stele cells internal to the endodermis and cortex, indicating that it has a non-cell-autonomous mode of action6. Here we show that the SHR protein, a putative transcription factor, moves from the stele to a single layer of adjacent cells, where it enters the nucleus. Ectopic expression of SHR driven by the promoter of the downstream gene SCARECROW (SCR) results in autocatalytic reinforcement of SHR signalling, producing altered cell fates and multiplication of cell layers. These results support a model in which SHR protein acts both as a signal from the stele and as an activator of endodermal cell fate and SCR-mediated cell division
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