A Twist-like bHLH gene is a downstream factor of an endogenous FGF and determines mesenchymal fate in the ascidian embryos

Ascidian larvae develop mesenchyme cells in their trunk. A fibroblast growth factor (FGF9/16/20) is essential and sufficient for induction of the mesenchyme in Ciona savignyi. We have identified two basic helix-loop-helix (bHLH) genes named Twist-like1 and Twist-like2 as downstream factors of this FGF. These two genes are phylogenetically closely related to each other, and were expressed specifically in the mesenchymal cells after the 110-cell stage. Gene-knockdown experiments using a specific morpholino oligonucleotide demonstrated that Twist-like1 plays an essential role in determination of the mesenchyme and that Twist-like2 is a downstream factor of Twist-like1. In addition, both overexpression and misexpression of Twist-like1 converts non-mesenchymal cells to mesenchymal cells. We also demonstrate that the upstream regulatory mechanisms of Twist-like1 are different between B-line mesenchymal cells and the A-line mesenchymal cells called `trunk lateral cells'. FGF9/16/20 is required for the expression of Twist-like1 in B-line mesenchymal precursor cells, whereas FGF, FoxD and another novel bHLH factor called NoTrlc are required for Twist-like1 to be expressed in the A-line mesenchymal precursor cells. Therefore, two different but partially overlapping mechanisms are required for the expression of Twist-like1 in the mesenchymal precursors, which triggers the differentiation of the mesenchyme in Ciona embryos

N=1{\cal N}=1 superfield description of BPS solutions in 6D gauged SUGRA with 3-branes

We provide ${\cal N}=1$ superfield description of BPS backgrounds in six-dimensional supergravity (6D SUGRA) with 3-branes, which is compactified on a two-dimensional space. The brane terms induce the localized fluxes. We find a useful gauge in which the background equations become significantly simple. This is not the Wess-Zumino gauge, and the relation to the usual component-field expression of 6D SUGRA is not straightforward. One of the equations reduces to the Liouville equation. By moving to the Wess-Zumino gauge, we check that our expressions reproduce the known results of the previous works, which are expressed in the component fields. Our results help us develop the systematic derivation of four-dimensional effective theories that keeps the ${\cal N}=1$ SUSY structure.Comment: 32 pages, no figures, published versio

Zn-induced wipeout effect on Cu NQR spectra in La2−x_{2-x}Srx_xCu1−y_{1-y}Zny_yO4_4

We report a systematic study of Zn-substitution effect on Cu NQR spectrum for high $T_c$ superconductors La$_{2-x}$Sr$_x$Cu$_{1-y}$Zn$_y$O$_4$ from carrier-underdoped to -overdoped regimes (polycrystalline samples, $x$ =0.10, 0.15, and 0.20). We observed no appreciable wipeout effect for the overdoped samples, a gradual and partial wipeout effect below about 80 K for the optimally doped ones, and very abrupt and full wipeout effect below about 40 K for the underdoped ones. The wipeout effect indicates a highly enhanced spectral weight of Cu spin fluctuations at a low frequency. We associate the wipeout effect with a Zn-induced local magnetism far above 40 K and with a localization effect below 40 K.Comment: 2 pages, 3 figures, accepted for publication in Physica C (LT23, Hiroshima 2002

Requirement for Dicer in Maintenance of Monosynaptic Sensory-Motor Circuits in the Spinal Cord

SummaryIn contrast to our knowledge of mechanisms governing circuit formation, our understanding of how neural circuits are maintained is limited. Here, we show that Dicer, an RNaseIII protein required for processing microRNAs (miRNAs), is essential for maintenance of the spinal monosynaptic stretch reflex circuit in which group Ia proprioceptive sensory neurons form direct connections with motor neurons. In postnatal mice lacking Dicer in proprioceptor sensory neurons, there are no obvious defects in specificity or formation of monosynaptic sensory-motor connections. However, these circuits degrade through synapse loss and retraction of proprioceptive axonal projections from the ventral spinal cord. Peripheral terminals are also impaired without retracting from muscle targets. Interestingly, despite these central and peripheral axonal defects, proprioceptive neurons survive in the absence of Dicer-processed miRNAs. These findings reveal that Dicer, through its production of mature miRNAs, plays a key role in the maintenance of monosynaptic sensory-motor circuits